essay causes of cancer

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What are the causes of cancer?

There are an estimated 18.1 million new cancer cases globally, and cancer remains the second-leading cause of death in the United States, where more than 1.7 million people are diagnosed with cancer every year. Cancer is often discussed as if it’s one thing. But while unrestrained growth is the common denominator, cancer can develop in a variety of different ways, due to a variety of different factors. Some we inherit, and others we are exposed to throughout our lives. It can be categorized into hundreds of different diseases based on the cells in which it arises. And when each patient’s genetic background is taken into account, no two cases are identical.

To save more lives from cancer, therefore, it will be necessary to address this complexity. Through basic research into cancer biology and immunology, we can improve our understanding of how cancer develops and how it interacts with the immune system. In this way, it could enable us to discover new, more effective ways to treat cancer.

When does cancer occur?

Cellular definition of cancer.

Cancer begins when cells acquire the ability to grow uncontrollably and ultimately invade and damage the body’s normal tissues. Cancer development happens in multiple stages, from precancerous changes to malignant tumors. However, not all cancers form tumors, and different cancers can develop at different rates. Sometimes cancer cells spread from their original site to other places in the body through the bloodstream or lymphatic system—a process called metastasis .

Where does cancer occur?

Cancer’s point of origin.

Cancer can affect many different parts of the body, from the skin, bone, blood vessels, and muscle, to the lungs, kidneys, and many other organs. Cancer can also affect the immune system, which plays a key role during both the development and progression of cancer.

Can you inherit cancer?

Genetic causes of cancers.

Genes are segments of DNA located on chromosomes, and can mutate over time to become cancerous. These mutations can result from a variety of causes, including diet and lifestyle choices as well as exposure to certain environmental factors. Overall, only 5 to 10 percent of all cancers are genetically inherited, although these are the cancers that tend to occur earlier in life.

One such inheritable genetic disorder that is associated with increased cancer risk is Lynch syndrome , which prevents cells’ ability to repair their DNA when damage occurs. This can lead to cancers of the colon and uterus at an early age. Another such genetic factor is the BRCA family of genes, certain forms of which have been linked to breast and ovarian cancer .

Today, scientists and clinicians are using and developing new tests to search for biomarkers , which can help determine risks and appropriate treatment options based on an individual patient’s genetic profile.

Does behavior or lifestyle cause cancer?

Behavioral causes of cancer.

There are a number of behavioral factors that can lead to genetic mutations and, as a result, lead to the development of cancer.

• Tanning (excessive exposure to ultraviolet light)
• Diet (red, processed meats)
• Unsafe sex (leading to viral infection)
• Inflammatory conditions, such as ulcerative colitis or obesity

An example of a behavioral risk factor is smoking, which can lead to lung cancer, or excessive exposure to the sun’s ultraviolet (UV) rays, which can cause skin cancer. Some dietary choices, including red meat and alcohol, have also been linked to certain types of cancer, while obesity is associated with higher rates of cancer as well, a link that CRI investigators Harvard Medical School’s Lydia Lynch, PhD , and University of California, San Diego’s Zhenyu Zhong, PhD , are independently exploring further. One’s diet can also affect the bacteria that reside within our intestines, known as the gut microbiome, and recent research by scientists, such as Johns Hopkins University’s Cynthia Sears, MD , have revealed that certain bacteria can impact the likelihood of colorectal cancer development as well as patient responsiveness to treatment with immunotherapy.

Can where you live or work cause cancer?

Environmental causes of cancer.

Exposure to certain factors in the environment, such as chemicals like asbestos and benzene, as well as talcum powder and various sources of radiation (including excessive X-rays), can also cause cancer. These substances capable of damaging DNA and triggering cancer are referred to as carcinogens.

• Excessive sun exposure (UV)
• Chemical carcinogen exposure
• High-dose chemotherapy and radiation (mainly in children being treated for existing cancers)
• Hormonal drugs
• Immune-suppressing drugs (taken by transplant recipients)
• Radioactive materials, e.g., radon

In addition to other factors associated with aging and senescence, older individuals are more likely to have had exposure to environmental risk factors and are therefore diagnosed with cancer much more frequently than young people. When it comes to children with cancer, new immunotherapy approaches are providing for the possiblity of treating them not only more effectively, but also without some of the damaging side effects that can accompany conventional treatments.

Do viruses or bacteria cause cancer?

Viral and bacterial causes of cancer.

Theories surrounding bacterial causes of cancer date back over 100 years, put forth by the Father of Cancer Immunotherapy, Dr. William B. Coley . A person’s behavior and surroundings can expose them to bacteria and viruses known to cause cancer.

• Human papillomavirus (HPV)
• Hepatitis B (HBV) and hepatitis C (HCV) viruses
• Epstein–Barr virus (EBV)
• Human T-lymphotropic virus
• Kaposi's sarcoma-associated herpesvirus (KSHV)
• Merkel cell polyomavirus
• Helicobacter pylori

Exposure to the B and C strains of the hepatitis virus can result in liver cancer, and sexual transmission of certain strains of the human papillomavirus (HPV) can result in cervical cancer, anal and penile cancers, and several head and neck cancers .

A vaccine that protects against hepatitis B virus has been available since 1982; in fact, this vaccine was the first preventive cancer vaccine in existence. The Cancer Research Institute funds research into both preventive and therapeutic cancer vaccines, including Dr. Ian Frazer’s groundbreaking work on the development of Gardasil, the first preventive vaccine against cervical cancer.

Bacteria and viruses can also be engineered to fight cancer on our behalf. Oncolytic virus therapy uses modified viruses to infect tumor cells and cause them to produce chemicals that signal danger to the immune system before self-destructing. Antibodies that target cancer antigens can be engineered through a process called phage display, in which a bacteriophage (a virus that infects bacteria) can be used to evolve new proteins.

Although there are number of elements at play in the development of cancer, the treatments at our disposal are constsntly improving and adapting as new research provides insight into various risk factors. Learn more about why immunotherapy research matters and how CRI’s innovative approach has shaped the progress of cancer treatments . You can contribute to continued breakthroughs in cancer research and treatment options by making a donation to CRI today .

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Essay on Cancer for Students and Children

500+ words essay on cancer.

Cancer might just be one of the most feared and dreaded diseases. Globally, cancer is responsible for the death of nearly 9.5 million people in 2018. It is the second leading cause of death as per the world health organization. As per studies, in India, we see 1300 deaths due to cancer every day. These statistics are truly astonishing and scary. In the recent few decades, the number of cancer has been increasingly on the rise. So let us take a look at the meaning, causes, and types of cancer in this essay on cancer.

Cancer comes in many forms and types. Cancer is the collective name given to the disease where certain cells of the person’s body start dividing continuously, refusing to stop. These extra cells form when none are needed and they spread into the surrounding tissues and can even form malignant tumors. Cells may break away from such tumors and go and form tumors in other places of the patient’s body.

Types of Cancers

As we know, cancer can actually affect any part or organ of the human body. We all have come across various types of cancer – lung, blood, pancreas, stomach, skin, and so many others. Biologically, however, cancer can be divided into five types specifically – carcinoma, sarcoma, melanoma, lymphoma, leukemia.

Among these, carcinomas are the most diagnosed type. These cancers originate in organs or glands such as lungs, stomach, pancreas, breast, etc. Leukemia is the cancer of the blood, and this does not form any tumors. Sarcomas start in the muscles, bones, tissues or other connective tissues of the body. Lymphomas are the cancer of the white blood cells, i.e. the lymphocytes. And finally, melanoma is when cancer arises in the pigment of the skin.

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Causes of Cancer

In most cases, we can never attribute the cause of any cancer to one single factor. The main thing that causes cancer is a substance we know as carcinogens. But how these develop or enters a person’s body will depend on many factors. We can divide the main factors into the following types – biological factors, physical factors, and lifestyle-related factors.

Biological factors involve internal factors such as age, gender, genes, hereditary factors, blood type, skin type, etc. Physical factors refer to environmental exposure of any king to say X-rays, gamma rays, etc. Ad finally lifestyle-related factors refer to substances that introduced carcinogens into our body. These include tobacco, UV radiation, alcohol. smoke, etc. Next, in this essay on cancer lets learn about how we can treat cancer.

Treatment of Cancer

Early diagnosis and immediate medical care in cancer are of utmost importance. When diagnosed in the early stages, then the treatment becomes easier and has more chances of success. The three most common treatment plans are either surgery, radiation therapy or chemotherapy.

If there is a benign tumor, then surgery is performed to remove the mass from the body, hence removing cancer from the body. In radiation therapy, we use radiation (rays) to specially target and kill the cancer cells. Chemotherapy is similar, where we inject the patient with drugs that target and kill the cancer cells. All treatment plans, however, have various side-effects. And aftercare is one of the most important aspects of cancer treatment.

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• Fact sheets /
• Cancer is a leading cause of death worldwide, accounting for nearly 10 million deaths in 2020, or nearly one in six deaths.
• The most common cancers are breast, lung, colon and rectum and prostate cancers.
• Around one-third of deaths from cancer are due to tobacco use, high body mass index, alcohol consumption, low fruit and vegetable intake, and lack of physical activity. In addition, air pollution is an important risk factor for lung cancer.
• Cancer-causing infections, such as human papillomavirus (HPV) and hepatitis, are responsible for approximately 30% of cancer cases in low- and lower-middle-income countries.
• Many cancers can be cured if detected early and treated effectively.

Cancer is a generic term for a large group of diseases that can affect any part of the body. Other terms used are malignant tumours and neoplasms. One defining feature of cancer is the rapid creation of abnormal cells that grow beyond their usual boundaries, and which can then invade adjoining parts of the body and spread to other organs; the latter process is referred to as metastasis. Widespread metastases are the primary cause of death from cancer.

The problem

Cancer is a leading cause of death worldwide, accounting for nearly 10 million deaths in 2020 (1). The most common in 2020 (in terms of new cases of cancer) were:

• breast (2.26 million cases);
• lung (2.21 million cases);
• colon and rectum (1.93 million cases);
• prostate (1.41 million cases);
• skin (non-melanoma) (1.20 million cases); and
• stomach (1.09 million cases).

The most common causes of cancer death in 2020 were:

• lung (1.80 million deaths);
• colon and rectum (916 000 deaths);
• liver (830 000 deaths);
• stomach (769 000 deaths); and
• breast (685 000 deaths).

Each year, approximately 400 000 children develop cancer. The most common cancers vary between countries. Cervical cancer is the most common in 23 countries. 

Cancer arises from the transformation of normal cells into tumour cells in a multi-stage process that generally progresses from a pre-cancerous lesion to a malignant tumour. These changes are the result of the interaction between a person's genetic factors and three categories of external agents, including:

• physical carcinogens, such as ultraviolet and ionizing radiation;
• chemical carcinogens, such as asbestos, components of tobacco smoke, alcohol, aflatoxin (a food contaminant), and arsenic (a drinking water contaminant); and
• biological carcinogens, such as infections from certain viruses, bacteria, or parasites.

WHO, through its cancer research agency, the International Agency for Research on Cancer (IARC), maintains a classification of cancer-causing agents.

The incidence of cancer rises dramatically with age, most likely due to a build-up of risks for specific cancers that increase with age. The overall risk accumulation is combined with the tendency for cellular repair mechanisms to be less effective as a person grows older.

Risk factors

Tobacco use, alcohol consumption, unhealthy diet, physical inactivity and air pollution are risk factors for cancer and other noncommunicable diseases.  

Some chronic infections are risk factors for cancer; this is a particular issue in low- and middle-income countries. Approximately 13% of cancers diagnosed in 2018 globally were attributed to carcinogenic infections, including Helicobacter pylori, human papillomavirus (HPV), hepatitis B virus, hepatitis C virus, and Epstein-Barr virus (2).

Hepatitis B and C viruses and some types of HPV increase the risk for liver and cervical cancer, respectively. Infection with HIV increases the risk of developing cervical cancer six-fold and substantially increases the risk of developing select other cancers such as Kaposi sarcoma.

Reducing the burden

Between 30 and 50% of cancers can currently be prevented by avoiding risk factors and implementing existing evidence-based prevention strategies. The cancer burden can also be reduced through early detection of cancer and appropriate treatment and care of patients who develop cancer. Many cancers have a high chance of cure if diagnosed early and treated appropriately. 

Cancer risk can be reduced by:

• not using tobacco;
• maintaining a healthy body weight;
• eating a healthy diet, including fruit and vegetables;
• doing physical activity on a regular basis;
• avoiding or reducing consumption of alcohol;
• getting vaccinated against HPV and hepatitis B if you belong to a group for which vaccination is recommended;
• avoiding ultraviolet radiation exposure (which primarily results from exposure to the sun and artificial tanning devices) and/or using sun protection measures;
• ensuring safe and appropriate use of radiation in health care (for diagnostic and therapeutic purposes);
• minimizing occupational exposure to ionizing radiation; and
• reducing exposure to outdoor air pollution and indoor air pollution, including radon (a radioactive gas produced from the natural decay of uranium, which can accumulate in buildings — homes, schools and workplaces).

Early detection

Cancer mortality is reduced when cases are detected and treated early. There are two components of early detection: early diagnosis and screening.

Early diagnosis

When identified early, cancer is more likely to respond to treatment and can result in a greater probability of survival with less morbidity, as well as less expensive treatment. Significant improvements can be made in the lives of cancer patients by detecting cancer early and avoiding delays in care.

Early diagnosis consists of three components:

• being aware of the symptoms of different forms of cancer and of the importance of seeking medical advice when abnormal findings are observed;
• access to clinical evaluation and diagnostic services; and
• timely referral to treatment services.

Early diagnosis of symptomatic cancers is relevant in all settings and the majority of cancers. Cancer programmes should be designed to reduce delays in, and barriers to, diagnosis, treatment and supportive care. 

Screening aims to identify individuals with findings suggestive of a specific cancer or pre-cancer before they have developed symptoms. When abnormalities are identified during screening, further tests to establish a definitive diagnosis should follow, as should referral for treatment if cancer is proven to be present.

Screening programmes are effective for some but not all cancer types and in general are far more complex and resource-intensive than early diagnosis as they require special equipment and dedicated personnel. Even when screening programmes are established, early diagnosis programmes are still necessary to identify those cancer cases occurring in people who do not meet the age or risk factor criteria for screening.

Patient selection for screening programmes is based on age and risk factors to avoid excessive false positive studies. Examples of screening methods are:

• HPV test (including HPV DNA and mRNA test), as preferred modality for cervical cancer screening; and
• mammography screening for breast cancer for women aged 50–69 residing in settings with strong or relatively strong health systems.

Quality assurance is required for both screening and early diagnosis programmes.

A correct cancer diagnosis is essential for appropriate and effective treatment because every cancer type requires a specific treatment regimen. Treatment usually includes surgery, radiotherapy, and/or systemic therapy (chemotherapy, hormonal treatments, targeted biological therapies). Proper selection of a treatment regimen takes into consideration both the cancer and the individual being treated. Completion of the treatment protocol in a defined period of time is important to achieve the predicted therapeutic result.

Determining the goals of treatment is an important first step. The primary goal is generally to cure cancer or to considerably prolong life. Improving the patient's quality of life is also an important goal. This can be achieved by support for the patient’s physical, psychosocial and spiritual well-being and palliative care in terminal stages of cancer.  

Some of the most common cancer types, such as breast cancer, cervical cancer, oral cancer, and colorectal cancer, have high cure probabilities when detected early and treated according to best practices.

Some cancer types, such as testicular seminoma and different types of leukaemia and lymphoma in children, also have high cure rates if appropriate treatment is provided, even when cancerous cells are present in other areas of the body.

There is, however, a significant variation in treatment availability between countries of different income levels; comprehensive treatment is reportedly available in more than 90% of high-income countries but less than 15% of low-income countries (3).

Palliative care

Palliative care is treatment to relieve, rather than cure, symptoms and suffering caused by cancer and to improve the quality of life of patients and their families. Palliative care can help people live more comfortably. It is particularly needed in places with a high proportion of patients in advanced stages of cancer where there is little chance of cure.

Relief from physical, psychosocial, and spiritual problems through palliative care is possible for more than 90% of patients with advanced stages of cancer.

Effective public health strategies, comprising community- and home-based care, are essential to provide pain relief and palliative care for patients and their families.

WHO response

In 2017, the World Health Assembly passed the Resolution Cancer prevention and control in the context of an integrated approach (WHA70.12) that urges governments and WHO to accelerate action to achieve the targets specified in the Global Action Plan for the prevention and control of NCDs 2013-2020 and the 2030 UN Agenda for Sustainable Development to reduce premature mortality from cancer.

WHO and IARC collaborate with other UN organizations, inlcuing the International Atomic Energy Agency, and partners to:

• increase political commitment for cancer prevention and control;
• coordinate and conduct research on the causes of human cancer and the mechanisms of carcinogenesis;
• monitor the cancer burden (as part of the work of the Global Initiative on Cancer Registries);
• identify “best buys” and other cost-effective, priority strategies for cancer prevention and control;
• develop standards and tools to guide the planning and implementation of interventions for prevention, early diagnosis, screening, treatment and palliative and survivorship care for both adult and child cancers;
• strengthen health systems at national and local levels to help them improve access to cancer treatments;
• set the agenda for cancer prevention and control in the 2020 WHO Report on Cancer;
• provide global leadership as well as technical assistance to support governments and their partners build and sustain high-quality cervical cancer control programmes as part of the Global Strategy to Accelerate the Elimination of Cervical Cancer;
• improve breast cancer control and reduce avoidable deaths from breast cancer, focusing on health promotion, timely diagnosis and access to care in order to accelerate coordinated implementation through the WHO Global Breast Cancer Initiative;
• support governments to improve survival for childhood cancer through directed country support, regional networks and global action as part of the WHO Global Initiative for Childhood Cancer using the Cure All approach;
• increase access to essential cancer medicines, particularly through the Global Platform for Access to Childhood Cancer Medicines; and
• provide technical assistance for rapid, effective transfer of best practice interventions to countries.

(1) Ferlay J, Ervik M, Lam F, Colombet M, Mery L, Piñeros M, et al. Global Cancer Observatory: Cancer Today. Lyon: International Agency for Research on Cancer; 2020 ( https://gco.iarc.fr/today , accessed February 2021).

(2) de Martel C, Georges D, Bray F, Ferlay J, Clifford GM. Global burden of cancer attributable to infections in 2018: a worldwide incidence analysis. Lancet Glob Health. 2020;8(2):e180-e190.  

(3) Assessing national capacity for the prevention and control of noncommunicable diseases: report of the 2019 global survey. Geneva: World Health Organization; 2020.

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What Is Cancer?

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A dividing breast cancer cell.

The Definition of Cancer

Cancer is a disease in which some of the body’s cells grow uncontrollably and spread to other parts of the body. 

Cancer can start almost anywhere in the human body, which is made up of trillions of cells. Normally, human cells grow and multiply (through a process called cell division) to form new cells as the body needs them. When cells grow old or become damaged, they die, and new cells take their place.

Sometimes this orderly process breaks down, and abnormal or damaged cells grow and multiply when they shouldn’t. These cells may form tumors, which are lumps of tissue. Tumors can be cancerous or not cancerous ( benign ). 

Cancerous tumors spread into, or invade, nearby tissues and can travel to distant places in the body to form new tumors (a process called metastasis ). Cancerous tumors may also be called malignant tumors. Many cancers form solid tumors, but cancers of the blood, such as leukemias , generally do not.

Benign tumors do not spread into, or invade, nearby tissues. When removed, benign tumors usually don’t grow back, whereas cancerous tumors sometimes do. Benign tumors can sometimes be quite large, however. Some can cause serious symptoms or be life threatening, such as benign tumors in the brain.

Differences between Cancer Cells and Normal Cells

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Cancer cells differ from normal cells in many ways. For instance, cancer cells:

• grow in the absence of signals telling them to grow. Normal cells only grow when they receive such signals. 
• ignore signals that normally tell cells to stop dividing or to die (a process known as programmed cell death , or apoptosis ).
• invade into nearby areas and spread to other areas of the body. Normal cells stop growing when they encounter other cells, and most normal cells do not move around the body. 
• tell blood vessels to grow toward tumors.  These blood vessels supply tumors with oxygen and nutrients and remove waste products from tumors.
• hide from the immune system . The immune system normally eliminates damaged or abnormal cells. 
• trick the immune system into helping cancer cells stay alive and grow. For instance, some cancer cells convince immune cells to protect the tumor instead of attacking it.
• accumulate multiple changes in their chromosomes , such as duplications and deletions of chromosome parts. Some cancer cells have double the normal number of chromosomes.
• rely on different kinds of nutrients than normal cells. In addition, some cancer cells make energy from nutrients in a different way than most normal cells. This lets cancer cells grow more quickly. 

Many times, cancer cells rely so heavily on these abnormal behaviors that they can’t survive without them. Researchers have taken advantage of this fact, developing therapies that target the abnormal features of cancer cells. For example, some cancer therapies prevent blood vessels from growing toward tumors , essentially starving the tumor of needed nutrients.  

How Does Cancer Develop?

Cancer is caused by certain changes to genes, the basic physical units of inheritance. Genes are arranged in long strands of tightly packed DNA called chromosomes.

Cancer is a genetic disease—that is, it is caused by changes to genes that control the way our cells function, especially how they grow and divide.

Genetic changes that cause cancer can happen because:

• of errors that occur as cells divide. 
• of damage to DNA caused by harmful substances in the environment, such as the chemicals in tobacco smoke and ultraviolet rays from the sun. (Our Cancer Causes and Prevention section has more information.) 
• they were inherited from our parents. 

The body normally eliminates cells with damaged DNA before they turn cancerous. But the body’s ability to do so goes down as we age. This is part of the reason why there is a higher risk of cancer later in life.

Each person’s cancer has a unique combination of genetic changes. As the cancer continues to grow, additional changes will occur. Even within the same tumor, different cells may have different genetic changes.

Fundamentals of Cancer

Cancer is a disease caused when cells divide uncontrollably and spread into surrounding tissues.

Cancer is caused by changes to DNA. Most cancer-causing DNA changes occur in sections of DNA called genes. These changes are also called genetic changes.

A DNA change can cause genes involved in normal cell growth to become oncogenes. Unlike normal genes, oncogenes cannot be turned off, so they cause uncontrolled cell growth.

 In normal cells, tumor suppressor genes prevent cancer by slowing or stopping cell growth. DNA changes that inactivate tumor suppressor genes can lead to uncontrolled cell growth and cancer.

Within a tumor, cancer cells are surrounded by a variety of immune cells, fibroblasts, molecules, and blood vessels—what’s known as the tumor microenvironment. Cancer cells can change the microenvironment, which in turn can affect how cancer grows and spreads.

Immune system cells can detect and attack cancer cells. But some cancer cells can avoid detection or thwart an attack. Some cancer treatments can help the immune system better detect and kill cancer cells.

Each person’s cancer has a unique combination of genetic changes. Specific genetic changes may make a person’s cancer more or less likely to respond to certain treatments.

Genetic changes that cause cancer can be inherited or arise from certain environmental exposures. Genetic changes can also happen because of errors that occur as cells divide.

Most often, cancer-causing genetic changes accumulate slowly as a person ages, leading to a higher risk of cancer later in life.

Cancer cells can break away from the original tumor and travel through the blood or lymph system to distant locations in the body, where they exit the vessels to form additional tumors. This is called metastasis.

Types of Genes that Cause Cancer

The genetic changes that contribute to cancer tend to affect three main types of genes— proto-oncogenes , tumor suppressor genes , and DNA repair genes. These changes are sometimes called “drivers” of cancer.

Proto-oncogenes are involved in normal cell growth and division. However, when these genes are altered in certain ways or are more active than normal, they may become cancer-causing genes (or oncogenes), allowing cells to grow and survive when they should not.

Tumor suppressor genes are also involved in controlling cell growth and division. Cells with certain alterations in tumor suppressor genes may divide in an uncontrolled manner.

DNA repair genes are involved in fixing damaged DNA. Cells with mutations in these genes tend to develop additional mutations in other genes and changes in their chromosomes, such as duplications and deletions of chromosome parts. Together, these mutations may cause the cells to become cancerous.

As scientists have learned more about the molecular changes that lead to cancer, they have found that certain mutations commonly occur in many types of cancer. Now there are many cancer treatments available that target gene mutations found in cancer . A few of these treatments can be used by anyone with a cancer that has the targeted mutation, no matter where the cancer started growing .

When Cancer Spreads

In metastasis, cancer cells break away from where they first formed and form new tumors in other parts of the body. 

A cancer that has spread from the place where it first formed to another place in the body is called metastatic cancer. The process by which cancer cells spread to other parts of the body is called metastasis.

Metastatic cancer has the same name and the same type of cancer cells as the original, or primary, cancer. For example, breast cancer that forms a metastatic tumor in the lung is metastatic breast cancer, not lung cancer.

Under a microscope, metastatic cancer cells generally look the same as cells of the original cancer. Moreover, metastatic cancer cells and cells of the original cancer usually have some molecular features in common, such as the presence of specific chromosome changes.

In some cases, treatment may help prolong the lives of people with metastatic cancer. In other cases, the primary goal of treatment for metastatic cancer is to control the growth of the cancer or to relieve symptoms it is causing. Metastatic tumors can cause severe damage to how the body functions, and most people who die of cancer die of metastatic disease.  

Tissue Changes that Are Not Cancer

Not every change in the body’s tissues is cancer. Some tissue changes may develop into cancer if they are not treated, however. Here are some examples of tissue changes that are not cancer but, in some cases, are monitored because they could become cancer:

• Hyperplasia occurs when cells within a tissue multiply faster than normal and extra cells build up. However, the cells and the way the tissue is organized still look normal under a microscope. Hyperplasia can be caused by several factors or conditions, including chronic irritation.
• Dysplasia is a more advanced condition than hyperplasia. In dysplasia, there is also a buildup of extra cells. But the cells look abnormal and there are changes in how the tissue is organized. In general, the more abnormal the cells and tissue look, the greater the chance that cancer will form. Some types of dysplasia may need to be monitored or treated, but others do not. An example of dysplasia is an abnormal mole (called a dysplastic nevus ) that forms on the skin. A dysplastic nevus can turn into melanoma, although most do not.
• Carcinoma in situ  is an even more advanced condition. Although it is sometimes called stage 0 cancer, it is not cancer because the abnormal cells do not invade nearby tissue the way that cancer cells do. But because some carcinomas in situ may become cancer, they are usually treated.

Normal cells may become cancer cells. Before cancer cells form in tissues of the body, the cells go through abnormal changes called hyperplasia and dysplasia. In hyperplasia, there is an increase in the number of cells in an organ or tissue that appear normal under a microscope. In dysplasia, the cells look abnormal under a microscope but are not cancer. Hyperplasia and dysplasia may or may not become cancer.

Types of Cancer

There are more than 100 types of cancer. Types of cancer are usually named for the organs or tissues where the cancers form. For example, lung cancer starts in the lung, and brain cancer starts in the brain. Cancers also may be described by the type of cell that formed them, such as an epithelial cell or a squamous cell .

You can search NCI’s website for information on specific types of cancer based on the cancer’s location in the body or by using our A to Z List of Cancers . We also have information on childhood cancers and cancers in adolescents and young adults .

Here are some categories of cancers that begin in specific types of cells:

Carcinomas are the most common type of cancer. They are formed by epithelial cells, which are the cells that cover the inside and outside surfaces of the body. There are many types of epithelial cells, which often have a column-like shape when viewed under a microscope.

Carcinomas that begin in different epithelial cell types have specific names:

Adenocarcinoma is a cancer that forms in epithelial cells that produce fluids or mucus. Tissues with this type of epithelial cell are sometimes called glandular tissues. Most cancers of the breast, colon, and prostate are adenocarcinomas.

Basal cell carcinoma is a cancer that begins in the lower or basal (base) layer of the epidermis, which is a person’s outer layer of skin.

Squamous cell carcinoma is a cancer that forms in squamous cells, which are epithelial cells that lie just beneath the outer surface of the skin. Squamous cells also line many other organs, including the stomach, intestines, lungs, bladder, and kidneys. Squamous cells look flat, like fish scales, when viewed under a microscope. Squamous cell carcinomas are sometimes called epidermoid carcinomas.

Transitional cell carcinoma is a cancer that forms in a type of epithelial tissue called transitional epithelium, or urothelium. This tissue, which is made up of many layers of epithelial cells that can get bigger and smaller, is found in the linings of the bladder, ureters, and part of the kidneys (renal pelvis), and a few other organs. Some cancers of the bladder, ureters, and kidneys are transitional cell carcinomas.

Soft tissue sarcoma forms in soft tissues of the body, including muscle, tendons, fat, blood vessels, lymph vessels, nerves, and tissue around joints.

Sarcomas are cancers that form in bone and soft tissues, including muscle, fat, blood vessels, lymph vessels , and fibrous tissue (such as tendons and ligaments).

Osteosarcoma is the most common cancer of bone. The most common types of soft tissue sarcoma are leiomyosarcoma , Kaposi sarcoma , malignant fibrous histiocytoma , liposarcoma , and dermatofibrosarcoma protuberans .

Our page on soft tissue sarcoma has more information.

Cancers that begin in the blood-forming tissue of the bone marrow are called leukemias. These cancers do not form solid tumors. Instead, large numbers of abnormal white blood cells (leukemia cells and leukemic blast cells) build up in the blood and bone marrow, crowding out normal blood cells. The low level of normal blood cells can make it harder for the body to get oxygen to its tissues, control bleeding, or fight infections.  

There are four common types of leukemia, which are grouped based on how quickly the disease gets worse (acute or chronic) and on the type of blood cell the cancer starts in (lymphoblastic or myeloid). Acute forms of leukemia grow quickly and chronic forms grow more slowly.

Our page on leukemia has more information.

Lymphoma is cancer that begins in lymphocytes (T cells or B cells). These are disease-fighting white blood cells that are part of the immune system. In lymphoma, abnormal lymphocytes build up in lymph nodes and lymph vessels, as well as in other organs of the body.

There are two main types of lymphoma:

Hodgkin lymphoma – People with this disease have abnormal lymphocytes that are called Reed-Sternberg cells. These cells usually form from B cells.

Non-Hodgkin lymphoma – This is a large group of cancers that start in lymphocytes. The cancers can grow quickly or slowly and can form from B cells or T cells.

Our page on lymphoma has more information.

Multiple Myeloma

Multiple myeloma is cancer that begins in plasma cells , another type of immune cell. The abnormal plasma cells, called myeloma cells, build up in the bone marrow and form tumors in bones all through the body. Multiple myeloma is also called plasma cell myeloma and Kahler disease.

Our page on multiple myeloma and other plasma cell neoplasms has more information.

Melanoma is cancer that begins in cells that become melanocytes, which are specialized cells that make melanin (the pigment that gives skin its color). Most melanomas form on the skin, but melanomas can also form in other pigmented tissues, such as the eye.

Our pages on skin cancer and intraocular melanoma have more information.

Brain and Spinal Cord Tumors

There are different types of brain and spinal cord tumors. These tumors are named based on the type of cell in which they formed and where the tumor first formed in the central nervous system. For example, an astrocytic tumor begins in star-shaped brain cells called astrocytes , which help keep nerve cells healthy. Brain tumors can be benign (not cancer) or malignant (cancer).

Our page on brain and spinal cord tumors has more information.

Other Types of Tumors

Germ cell tumors.

Germ cell tumors are a type of tumor that begins in the cells that give rise to sperm or eggs. These tumors can occur almost anywhere in the body and can be either benign or malignant.

Our page of cancers by body location/system includes a list of germ cell tumors with links to more information.

Neuroendocrine Tumors

Neuroendocrine tumors form from cells that release hormones into the blood in response to a signal from the nervous system. These tumors, which may make higher-than-normal amounts of hormones, can cause many different symptoms. Neuroendocrine tumors may be benign or malignant.

Our definition of neuroendocrine tumors has more information.

Carcinoid Tumors

Carcinoid tumors are a type of neuroendocrine tumor. They are slow-growing tumors that are usually found in the gastrointestinal system (most often in the rectum and small intestine). Carcinoid tumors may spread to the liver or other sites in the body, and they may secrete substances such as serotonin or prostaglandins, causing carcinoid syndrome .

Our page on gastrointestinal neuroendocrine tumors has more information.

The Unique Hell of Getting Cancer as a Young Adult

W hen I got diagnosed with Stage 3b Hodgkin Lymphoma at age 32, it was almost impossible to process. Without a family history or lifestyle risk factors that put cancer on my radar, I stared at the emergency room doctor in utter disbelief when he said the CT scan of my swollen lymph node showed what appeared to be cancer—and lots of it. A few days away from a bucket list trip to Japan, I’d only gone to the emergency room because the antibiotics CityMD prescribed to me when I was sick weren’t working.I didn’t want to be sick in a foreign country. So when the doctor told me of my diagnosis, the  only question I could conjure was: “So Tokyo is a no-go?”

Around the world, cancer rates in people under 50 are surging, with a recent study in BMJ Oncology showing that new cases for young adults have risen 79% overall over the past three decades. In the U.S. alone, new cancer diagnoses in people under 50 hit 3.26 million, with the most common types being breast, windpipe, lung, bowel, and stomach. A new feature in the Wall Street Journal highlights the mad dash among doctors and researchers to determine what’s causing this troubling rise. Strangely, overall cancer rates in the U.S. have dropped over the past three decades, while young people—particularly with colorectal cancers—are increasingly diagnosed at late stages. “We need to make it easier for adolescents and young adults to participate in clinical trials to improve outcomes and study the factors contributing to earlier onset cancers so we can develop new cures,” says Julia Glade Bender, MD, co-lead of the Stuart Center for Adolescent and Young Adult (AYA) Cancers at Memorial Sloan Kettering in New York City (where I am currently a patient.)

Doctors suspect that lifestyle factors and environmental elements, from microplastics to ultra-processed foods, could be to blame. But many adults in their 20s and 30s, such as myself, were otherwise healthy before their diagnoses. It felt like all those years of forcing myself to run, eat high-fiber foods, and choke down kombucha were for nothing. 

Cancer is hell at any age, but the challenges facing young adults are especially steep, as the disease disrupts a formative period for building a career, family, and even healthy self-esteem, from body image to gender identity. It’s critical that our approach to treating and supporting these patients reflects the severity of this disruption. In recent years, a growing number of cancer hospitals have developed young adult-specific programming like support groups, information sessions on dating and sexual health, and even mobile apps to help counter social alienation. But there is still a long way to go.

Read more: Why I Stopped Being A “Good” Cancer Patient

Shockingly enough, canceling my trip to Japan was the least of my worries. Beyond the excruciating physical side effects of high-dose chemotherapy and a number of life-threatening complications, cancer pulverized my self-esteem into nothingness, as I watched peers get married and promoted from my bed. Thankfully, after switching to a new hospital, I found support groups that connected me with a community of peers who got it, as well as social workers who work exclusively with young adults and thus recognized many of my biggest challenges, like social isolation, financial strain, the dating nightmare, and hating my bald head.

Perhaps the biggest reason I resented cancer was for disrupting a milestone I’d worked for my whole life: a book launch. (My diagnosis came two months before my first book was published.) Young adulthood is meant to be littered with these kinds of professional and personal benchmarks, many of which are hard enough to accomplish without tumors; dating, for instance, is impossible for me even as a healthy person. Now I have to re-enter the pool older, weaker, and more traumatized? 

“Young adult patients may be trying to assert independence from parents, establish a career or intimate relationship, or even be parents themselves,” says Bender. “Most will be naïve to the medical system or a serious health condition.” And so they require flexible, creative clinicians who can help navigate them “to and through the best available therapy and back to their lives, inevitably ‘changed’ but intact.” Not only do these patients need specialized psychosocial support, but research initiatives should prioritize developing treatments that minimize long-term toxicities.

Given that many young patients haven’t yet built financial stability and are often in some form of debt, organizations like Young Adults Survivors United (YASU) have emerged to support young adult survivors and patients through the financial overwhelm. Stephanie Samolovitch, MSW and founder of YASU, says that there’s still an enormous need for resources supporting young adult cancer patients and survivors.

“Cancer causes a young adult to be dependent again, whether it’s moving back in with parents, getting rides to appointments, or asking for financial help,” says Samolovitch, who was diagnosed with leukemia in 2005, two weeks before her 20th birthday. “Young adults never expect to apply for Medicaid or Social Security Disability during our twenties or thirties, yet cancer doesn't give us a choice sometimes. That causes stress, shame, depression, and anxiety when trying to navigate the healthcare system.”

Read more: How to Create an Action Plan After a Cancer Diagnosis

When Ana Calderone, a 33-year-old magazine editor, was diagnosed with stage 2 breast cancer at 30, the most challenging part of getting diagnosed so young was “everything.”

“I felt like it set my whole life back, which sounds stupid because I was literally fighting for my life,” she says. “Who cares if I had to delay my wedding a year because I was still getting radiation treatment? But it was really hard at the time. Everything was delayed, and still is.”

During chemo, Calderone’s doctors gave her a shot that she still receives to try and preserve her ovaries, and she’s been able to try IVF twice. She says she had to proactively advocate for those things with her care team. While Calderone is currently cancer free, she still must take medication that has further delayed her plans to build a family. “I’m fairly confident I’d have a child by now if I didn’t get cancer. That’s been the most devastating part,” she says. “My oncologist would consider letting me get pregnant in two more years, which would be 4.5 years post-diagnosis, and even that is still a risk.”

For 32-year-old Megan Koehler, whose son was one and a half when she was diagnosed with Hodgkin Lymphoma, the hardest part “was knowing the world continued on while I spent days in bed,” she says. “My coworkers still worked on projects I was supposed to be part of, and the worst was knowing my son was growing up, learning to speak sentences, and just becoming a toddler without me – or so it felt that way.” 

She remembers crying for most of his second birthday because she was in bed post chemo, feeling devastated that she didn’t have the energy to spend the day with him. During a 50-plus day hospital stay caused by an adverse reaction to a chemotherapy drug, she would Facetime him and cry when he spoke in sentences, because he wasn’t doing that before she was admitted. While she’s grateful for the support she had from her husband and mother, she felt alienated. “I spoke to a few people my age via social media, but no one in person. My center mostly catered to the older generations, so it was somewhat isolating. I did have a great relationship with a few of the infusion nurses who were around my age.”

While oncologists may be rightly focused on saving patients’ lives, there must be more consideration for quality of life during and after treatment – both physical and mental. “More questions need to be asked about their relationships, fertility options, and any mental health concerns or symptoms,” says Samolovitch. From a research perspective, initiatives must expand to pinpoint not only the reason for the rise of cancer in young adults, but find ways to screen and diagnose earlier.

Towards the beginning of my treatment, before I switched hospitals, my oncologist seemed to treat my concerns about self-esteem and hair loss as trivial compared to the real work of saving my life. At my weakest, I had to advocate repeatedly to get accurate information on cold capping, a process of scalp cooling that can preserve most of your hair during chemotherapy, and I had to beg again and again for a social worker to reach out to me, which took weeks. 

It’s a beautiful thing that more young adults with cancer are surviving their illnesses. But that means they’ll have decades of life ahead of them. Providers must do a better job supporting young adult patients through all the collateral damage that comes with cancer and its treatment.  

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Cancer causes: popular myths about the causes of cancer.

Misconceptions about cancer causes can lead to unnecessary worry about your health. Find out whether there's any truth to these common myths about the causes of cancer.

Scary claims circulate on the internet that everyday objects and products, such as plastic and deodorant, cause cancer. Beyond being wrong, many of these myths may cause you to worry unnecessarily about your own health and the health of your family.

Before you panic, take a look at the reality behind these common myths.

Myth: Antiperspirants or deodorants can cause breast cancer.

Fact: There's no conclusive evidence linking the use of underarm antiperspirants or deodorants with breast cancer.

Some reports have suggested that these products contain harmful substances such as aluminum compounds and parabens that can be absorbed through the skin or enter the body through nicks caused by shaving. No clinical studies have yet given a definitive answer to the question of whether these products cause breast cancer. But the evidence to date suggests these products don't cause cancer.

If you're still concerned that your underarm antiperspirant or deodorant could increase your risk of cancer, choose products that don't contain chemicals that worry you.

Myth: Microwaving food in plastic containers and wraps releases harmful, cancer-causing substances.

Fact: Plastic containers and wraps labeled as safe for use in the microwave don't pose a threat.

There is some evidence that plastic containers that aren't intended for use in the microwave could melt and potentially leak chemicals into your food. Avoid microwaving plastic containers that were never intended for the microwave, such as margarine tubs, takeout containers or whipped topping bowls.

Check to see that any container you use in the microwave is labeled as microwave-safe.

Myth: People who have cancer shouldn't eat sugar, since it can cause cancer to grow faster.

Fact: More research is needed to understand the relationship between sugar in the diet and cancer. All kinds of cells, including cancer cells, depend on blood sugar (glucose) for energy. But giving more sugar to cancer cells doesn't make them grow faster. Likewise, depriving cancer cells of sugar doesn't make them grow more slowly.

This misconception may be based in part on a misunderstanding of positron emission tomography (PET) scans, which use a small amount of radioactive tracer — typically a form of glucose. All tissues in your body absorb some of this tracer, but tissues that are using more energy — including cancer cells — absorb greater amounts. For this reason, some people have concluded that cancer cells grow faster on sugar. But this isn't true.

There is some evidence that consuming large amounts of sugar is associated with an increased risk of certain cancers, including esophageal cancer. Eating too much sugar can also lead to weight gain and increase the risk of obesity and diabetes, which may increase the risk of cancer.

Myth: Cancer is contagious.

Fact: There's no need to avoid someone who has cancer. You can't catch it. It's OK to touch and spend time with someone who has cancer. In fact, your support may never be more valuable.

Though cancer itself isn't contagious, sometimes viruses, which are contagious, can lead to the development of cancer. Examples of viruses that can cause cancer include:

• Human papillomavirus (HPV) — a sexually transmitted infection — that can cause cervical cancer and other forms of cancer
• Hepatitis B or C — viruses transmitted through sexual intercourse or use of infected IV needles — that can cause liver cancer

Talk to your doctor about vaccines and other ways to protect yourself from these viruses.

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• Golemis EA, et al. Molecular mechanisms of the preventable causes of cancer in the United States. Genes & Development. 2018; doi:10.1101/gad.314849.118.
• Common cancer myths and misconceptions. National Cancer Institute. https://www.cancer.gov/about-cancer/causes-prevention/risk/myths. Accessed Feb. 4, 2020.
• Food safety: What you should know. World Health Organization. https://apps.who.int/iris/handle/10665/160165. Accessed Feb. 5, 2020.
• Tse LA, et al. Bisphenol A and other environmental risk factors for prostate cancer in Hong Kong. Environment International. 2017; doi:10.1016/j.envint.2017.06.012.
• Goncalves MD, et al. Dietary fat and sugar in promoting cancer development and progression. Annual Review of Cancer Biology. 2019; doi:10.1146/annurev-cancerbio-030518-055855.
• Li N, et al. Dietary sugar/starches intake and Barrett's esophagus: A pooled analysis. European Journal of Epidemiology. 2017; doi:10.1007/s10654-017-0301-8.
• Tashiro H, et al. Immunotherapy against cancer-related viruses. Cell Research. 2017; doi:10.1038/cr.2016.153.

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Essay on Cancer

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Cancer is a disease which is related to the abnormal growth of cells in a particular part of the body. Since the last decade, cancer has become one of the most feared diseases of all times, particularly due to the difficult treatment one has to undergo and the limitations of the treatment in curing this disease during later stages of cancer.

Audience: The below given essays are exclusively written for school and college students. Furthermore, those students preparing for IAS, IPS, UPSC, Civil Services and other competitive exams can also increase their knowledge by studying these essays.

Introduction:

Cancer is a group of more than 100 diseases that can develop in almost anywhere in the body. Cancer is a group of diseases involving abnormal cell growth with the potential to invade or spread to other parts of the body.

Types of Cancer:

There are various types of cancer. They include:

1] Breast cancer: This is type of cancer that forms in the cells of the breast.

2] Prostate cancer: This is type of cancer that occurs in a man’s prostate. This is a small walnut sized gland that has the duty of producing seminal fluid.

3] Lung cancer: This is a type of cancer that begins in the lungs and this occurs mostly in people who smoke.

4] Leukemia: A cancer of blood forming tissues, hindering the body’s ability to fight infection.

Conclusion:

We have seen various types of cancer but the types of cancer we have are hundreds but we had mentioned just a few. Each type of cancer comes with various symptoms and various ways of curbing it.

Cancer is a disease that has been around for centuries, but it has never had such an impact on public health as it has now. Cancer is the increase in the number of cells in human beings at an abnormal rate. Doctors have been discussing the reasons behind this increase for the past fifty years. One is tempted to think that there are no reasons behind this occurrence and that it is just a natural phenomenon, people die all the time. Right?

The thing is that the number of cancer cases has increased in the past decades and a lot of this increase is attributed to the influence of different types of radiation. Even though most of the really dangerous substances (or sources of radiation) are not allowed near people. What else can be causing such an increase in cancer cases?

Some doctors have made a discovery regarding cancer that can really help us get rid of this problem. Following down the line of the argumentation presented in the famous “China Study” more doctors are advising their patients to change their diet because it can help  in their fight against cancer. Not only that but a proper diet can also be the best prevention.

When you are a student your metabolism is young so you do not feel the bad effect of your habits as much as older people do but as we age the side effects of our bad choices will become obvious. We can teach ourselves to listen to our bodies and to prevent cancer but to do that we, first of all, have to defeat our habits.

Cancer is uncontrolled and unchecked development of abnormal cells in a part of the body. Cancerous cells develop just like another cell in the body. They, however, keep growing and can form a mass then subsequently becomes tumors. Since cells are present in every part of our body, cancer can also grow in all parts of our body.

Causes of Cancer:

One great scientific mystery in our world is the cause of cancer. Scientists from all over have tried and failed in isolating any particular action, substance or environmental factors that can lead to cancer.

However, scientists all over the world agree that cancer is caused by substances known as carcinogens. These substances are introduced to the body when we are exposed to or consume materials containing them. One of the confirmed sources of carcinogens is exposure to radiation from x-ray machines.

Cancer Treatment:

There are various ways to treat a person infected with cancer. These modes of treatment are chosen depending on the type of cancer, the stage of development and the health peculiarities of the cancer patient. In other cases, several modes of treatment are combined to treat a single patient.

Some of the modes of treating cancer are in fly highlighted below:

1. Surgery to remove Cancerous tumors from the body.

2. Radiation therapy to reduce the growth of cells.

3. Chemotherapy for destroying cancer cells.

4. Stem cell transplant.

Prevention of Cancer:

Just as there are no agreed actions, materials and exposure that causes cancer, there are no generally accepted means of preventing cancer. However, there are certain habits that can limit a person’s exposure.

Some of them are highlighted below:

1. Healthy environment and diet.

2. Reduction of exposure from the sun.

3. Keep your weight low.

4. Avoid the use of tobacco.

Early detection of cancer has been hailed as the most potent way of treating this menace. Though scientists are still in the business of searching for a cure, we as humans can prevent cancer by regular medical check-ups.

Cancer is one of the second largest fatal illnesses across the world. One of the horrific words a human being can listen to is being diagnosed with Cancer. The word Cancer brings alarm and anxiety to the listener. Cancer is the abnormal growth of cells in one part of the body which can even spread to other parts if not treated at an early stage. Neoplasms or tumour are the subset of these abnormally grown-up cells which often results in a mass or lump.

What causes Cancer?

Those agents which cause cancer are termed as Carcinogens . These can be classified into physical, chemical and biological. Physical Carcinogens include ultra violet and other ionizing radiations. Food adulterants such as aflatoxin, tobacco smoke, drinking water contaminant such as Arsenic, asbestos etc., are termed as Chemical Carcinogens. Viruses, Bacteria and other parasites which cause infections and eventually lead to Cancer are categorized under Biological Carcinogens. Ageing also causes cancer as the risk of the cellular repair mechanism weakens as we age.

Significant Symptoms of Cancer:

Some of the major symptoms of cancer include unexplained weight loss, extreme fatigue, persistent sores that do not heal, changes in the bladder and bowel movements, odd bleeding and discharges, change in voice due to cancer indication in larynx and lumps and bumps on the skin.

Preventive Measures:

Some of the risk factors which needs to be addressed to prevent cancer may include avoidance of tobacco, being overweight or obese, unhealthy eating with less vegetables and greens, physical in-activity, avoiding pollution etc. Apart from the mentioned, vaccination against HPV and Hepatitis B Virus, controlling hazards while at work, reducing exposure to ultra violet and ionizing radiation etc., can help prevent being infected by Cancer.

Assessing the type of cancer and the stage is very important because every cancer type has a different pattern of treatment from surgery, radiotherapy and chemotherapy . The treatment that is used to relieve the cancer patient from their pain and enhance the quality of life for the patients and their families is termed as Palliative care.

World Health Organization has partnered with UNO and other non-profit organizations to ensure every country is being made aware of the non-communicable diseases and the prevention of cancer and its control. Insights to develop Centers of Excellence to provide quality treatments and to conduct research on the carcinogenesis should be provided to governments and to help the people.

The abnormal cell growth in our body which spreads to other parts as well is what is termed as cancer. Around four lakh of people in India are known to be affected by this disease every year. More so, around half of them are not able to survive as they are usually detected in the last stages of cancer. Hence it is all the more important to educate the people about this disease and its symptoms so that it can be detected early and the lives of the people suffering from it can be saved.

Cancer can affect any body part. The part that is affected gives it the name, for instance, lung cancer which affects the lungs, skin cancer in which the skin is affected and so on. However, we can broadly divide cancer into four types. The first one is Sarcoma which is known to affect the blood vessels, bones, muscles cartilages and connective tissues. The second type of cancer is Carcinoma which affects the internal organs of the body or the skin. The third type is the Lymphoma. This cancer affects the lymph glands and the lymph nodes. The last type in which cancer can be categorised is Leukaemia which largely affects the parts forming blood such as the bone marrow.

Symptoms of Cancer:

Although no particular cause is known to trigger this disease, some activities have been associated as the cause of different types of cancer. The first and foremost is smoking. Excess smoking affects the entire respiratory system thereby leading to the onset of lung cancer. More so chewing tobacco is also attributed to giving rise to mouth and throat cancer. Similarly, alcohol is attributed to be the cause of stomach, liver and gallbladder cancer. Summarising it, all the ill habits of society and urbanisation have been attributed to this disease. Even radiations coming from X-ray machines can prove harmful and lead to cancer. That is why there are proper laws an protection in place when exposing people to these harmful radiations.

Treatments Available:

If detected in early stages, cancer can surely be curable. Surgery is one of the primary steps of curing this disease. If required, doctors remove the body part affected such as the uterus, gallbladder or the breast. Thereafter, through radiotherapy, the cancerous cells on the other affected parts of the body are killed so that they don’t spread to other parts. Chemotherapy is done using the strong chemical in order to kill the cancerous cells. Other methods such as tumour suppressing genes are used in different types of cancer as may be the need advised by the doctors. Whatever the method, it is extremely difficult to go through the pain and social stigma such as loss hair which comes alongside the treatment of cancer.

Living with this Disease:

It is indeed very difficult to live with this disease as not only this disease is not fully curable but the treatment is so tough that it scares even the toughest of individuals. We, as a society, must support the people suffering from cancer and help in their difficult times. We must not discriminate them and must understand that is already suffering a lot and must not do anything which further aggravates their sufferings.

Cancer is a severe disease in which there is abnormal growth of cell that spreads around the human body. Many people in the world are struggling with this disease. Consistently around 10 million cases are analyzed. These number of cases are expected to increase around 20 million by 2020. It turns into the most widely recognized reasons for death. Due to abnormal cell growth, it develops & affects the overall body weight. Prolonged cough and abnormal bleeding are some symptoms of this severe disease. The developed abnormal cells first make their impact on organs then slowly moved as poison. Cancer disease can be identified in the beginning periods. The medical professionals are still trying to catch this disease.

One of the main causes of cancer is smoking. Other causes include tobacco, consumption of alcohol, obesity, lack of physical activities, exposure to UV radiations, etc. Age factor and changes in genes are yet other factors that cause cancer.

Cancer has different types which can be divided into various forms:

i. Skin Cancer:

It is the most common type of cancer which can be seen in many people. Every year more than 1 million people are affected by skin cancer. Skin cancer happens due to the overexposure from the sun. The thicker ozone layers directly harms our skin, which increases the chances of skin cancer.

ii. Lung Cancer:

This type of cancer is related to the cells inside the lungs. The symptoms of this type of cancer are chest pain & sudden weight loss. It is also known as lung carcinoma. As a process of metastasis, the growth of abnormal cell growth spread inside the lungs. Smoking is a fundamental driver of Lung cases.

iii. Kidney Cancer:

Another name of kidney cancer is renal cancer. Renal Cell Carcinoma and Transitional Cell Carcinoma are the types of kidney cancer. This development of cancer happens after the age of 40 years. Smoking can twofold the danger of kidney malignant growth.

iv. Leukemia:

This cancer starts developing in the bone marrow, which leads to a high number of abnormal white cells. Acute myeloid leukemia or acute lymphocytic leukemia are the sorts of leukemia. Chemotherapy or radiation therapy can be used as the treatment for Leukemia.

Cancer Staging:

It is important to understand the staging factor of this severe disease. Diagnosis of cancer in early stages helps to tackle this disease by proper treatments. During the initial stages of cancer, proper surgeries or radiotherapy can help to overcome cancer. When the broken cancer cells move to other parts of the human body, then advance treatment is suggested by the professionals. But when a patient is in the final stages of cancer, he needs a treatment which covers his whole body. Chemotherapy is a therapy which is used to circulate the bloodstream. Professional doctors use various test techniques to identify the stages of cancer. Stages are used to describe the severity of cancer.

In the initial stage, cancer can be prevented through medication, proper surgeries and light treatment. In the advance stages of cancer, chemotherapy and radiation therapy is useful. Above all, the best way to keep cancer away is to stay away from smoking and tobacco, eat healthy food and a lot of green vegetables, and do some physical exercise daily.

It is very difficult for a cancer patient to fight with the final stages of cancer. To deal with this severe problem cancer symptoms should never be ignored. More than 70% of cases are seen only due to smoking. At every stage, it is essential that everyone must adopt a healthy diet plan & exercise daily to prevent this disease. A person who has a good and healthy lifestyle can fight with cancer more strongly.

Current trends in global health mention cancer. Cancer is currently one of the leading causes of death globally. It is an illness in which abnormal cell growth develops and affects parts of the human body as it advances, it has the potential to spread from one part of the body to the other. It is a chronic illness that imposes a great economic burden on a nation because its management is costly. Cancer occurs in different parts of the body and are classified according to where it has affected. In India, men are mostly acted by lung, oral, lip and neck cancers whereas women are affected by cervical, breast and ovarian cancer. The detection procedure varies with the type of cancer while the treatment varies with the stage of the cancer progression. Mostly early stages of cancer have better prognosis compared to late stages of cancer.

There are modifiable and non-modifiable factors that predispose an individual to cancer. Non modifiable factors include age and genetics. With an increase in age, the rate of cancer incidence increases. The genetic predisposition to cancer increases the incidences of suffering the disease. Modifiable factors include lifestyle habits like drinking and smoking tobacco which increase the incidences of lung, oral, esophageal among other cancers. Diet is also a predisposing factor especially one that is less in vitamin supplements.

Physical inactivity and obesity predispose to cancers of the colon, breast and others. Sexual activity in women with multiple sexual partners predisposes them to cervical cancer due to the transmission of HPV (Human Papilloma Virus). The environment also predisposes to cancer because of the chemicals, radicals and radiations that interact with human beings.

Detection of Cancer:

The detection varies with the type of cancer and so screening is done for each type differently. It is advisable that people get regular checkups of the whole body so that early detection facilitates effective and curative treatment. Screening of cancer is done using detailed examination of the physique, laboratory and histology tests, radiological and magnetic imaging techniques among other methods.

The campaigns against cancer advocate for early detection by teaching the public on the early signs of cancer. In breast cancer awareness for example, the public is made aware of physical examination of the breast and if they detect any abnormal growth or lump, they are to seek further investigation. Early detection is important because it results in successful treatment. In the detection, the cancer staging is done, which is usually four stages, stage one, two, three and four. Stage one has the best prognosis whereas stage four has the poorest prognosis.

Treatment of Cancer:

Once cancer is detected, a range of treatment options is provided. Treatment depends on the types of cancer and the staging. It can be treated by surgery whereby excision of the abnormal growth is done. Surgery is done for non-hematological cancers and those that have not metastasized to other parts of the body. An example of surgery is mastectomy to treat breast cancer.

Chemotherapy is another treatment option that involves the administration of anticancer medication that eliminate the abnormal cells in the body. Another treatment option is radiation therapy that uses ionizing radiations to destroy cancer cells. Radiation is also used to make tumors small. It is used to treat solid tumors and it depends on the sensitivity of the tumor to the radiations. It is targeted at the nucleic acid destruction in the tumor cells.

Consequences of Cancer:

Cancer is a chronic illness that could result in very serious consequences even with treatment. Cachexia is the extreme wasting of the body that causes death in cancer patients. Economic burden to both the individual and the nation is experienced in cancer treatment because the treatment modalities are costly. The economic burden results in decline of the nation’s economy and increased healthcare costs to the population.

Mental illnesses result from cancer because it is a terminal illness and most patients become mentally unstable upon diagnosis. The quality of health is affected in a country when there is high incidences of cancer and the performance is greatly affected, which cause poverty and economic crisis for individuals.

Cancer is a serious illness that impacts the lives of people and the nation negatively. It is evident that cancer has diverse treatment options but the problem is that people do not go for checkups. Checkups are important in early detection, which usually results in successful treatment and less burden of cancer in a nation and in individuals.

Cancer is basically an agglomeration of various diseases that involves the abnormal growth of cells with the ability to spread or invade other body parts. Cancers are quite different from benign tumours in that the latter does not spread or invade other body parts. Some of the many symptoms and signs of cancer include abnormal bleeding, a lump, weight loss that is unusual, prolonged cough and bowel movement change. Even though these listed symptoms and signs of cancer, they might be caused by other things so it is necessary to be diagnosed. Today, we have more than 100 various kinds of cancer that affect us humans.

History of Cancer:

It is believed that cancer has been in existence for a majority if not all of the history of man. Breast cancer was the first form of cancer that was recorded and this happened around 1600 BC in Egypt. Between 460 BC and 370 BC, Hippocrates spent time analysing various types of cancer and referred to them as crayfish or crab. The name was as a result of the crab-like look of the malignant tumour and the lateral extension of the distended veins and tumours.

Factors Causing Cancer:

It has been discovered that the major cause of deaths as a result of cancer is the use of tobacco and it accounts for about 22 percent of the total number of deaths due to cancer. Poor diet, obesity, excessive alcohol consumption and a lack of exercise and physical activities accounts for another 10 percent of deaths caused by cancer. Some other causes and factors that contribute to cancer include environmental pollutants, ionizing radiation exposure and certain infections.

In most developing countries, infections like hepatitis B, Helicobacter pylori, papillomavirus infection of humans, Hepatitis C, HIV and Epstein Barr contribute to fifteen percent of all cancers. All of the factors listed above change the cell genes. There are always a lot of genetic changes before the development of cancer. About 10% of all cancers are as a result of genetic defects that are inherited from a parent. Asides the symptoms and signs that are used to detect cancer, screening tests are also a good way of detecting cancer. Cancer is normally thoroughly investigated using medical imaging; it is then confirmed through biopsy.

Development of Cancer:

A tumour or neoplasm is a collection of cells which have gone through growth that is not regulated and most times form a lump or mass. Every tumour cell exhibits the six important characters that are necessary for the production of the malignant tumour.

The six characteristics are:

1. Cell division and growth without all the signals that are proper.

2. Continuous division and growth even though the signals given are contrary.

3. Cell death that is usually programmed is avoided.

4. The divisions of the cell are quite limitless in number.

5. The construction of blood vessel is promoted.

6. The tissues are invaded and metastases are formed.

Cancer Prevention:

The prevention of a lot of cancers can be ensured by trying to maintain a weight that is healthy, not smoking, consuming a lot of whole grains, fruits and vegetable, avoiding the consumption of a lot of alcohol, reduction in the amount of red and processed meat that is consumed, getting vaccinated against some infectious diseases and the avoidance of too much exposure to sunlight. It is sometimes useful that there is early detection in cases of colorectal and cervical cancer and this can be achieved through screening. The usefulness of breast cancer screening is highly controversial.

The treatment of cancer is usually done by combining surgery, radiation therapy, targeted therapy and chemotherapy. A very important element of care is the management of symptoms and pain. In cases of advanced disease, palliative care is of utmost importance. The extent of the disease at the commencement of treatment and also the form of cancer that is involved go a long way to determine the odds of survival. Using the adopted survival rate at five years, children that were under the age of 15 when they were diagnosed have an average rate of survival of 80% in most developed countries. In the US, the average rate of survival for the five year period is 66%.

90.5 million  people were living with different cancers in 2015. It has been reported that every year, close to 15 million reports of new cancer cases are filed. These do not include the cases of skin cancer. Cancer results in more than eight million deaths every year which is about 15.7% of the total number of deaths every year.

In males, prostate cancer, lung cancer, stomach cancer and colorectal cancer are the most widespread cancer types. In females, colorectal cancer, breast cancer, cervical cancer and lung cancer are the most widespread cancer types. Apart from melanoma, if we include skin cancer in the amount of new cases of cancer every year, it is going to be 40% of the total number of cases.

Brain tumours and lymphoblastic leukemia that is acute are the most widespread cancer types in children but in Africa, lymphoma that is no-Hodgkin is the most widespread. The total number of children that are under the age of 15 that ended up being diagnosed with one type of cancer or the other in 2012 is around 165,000.

With an increase in age, it has been seen that the risk of getting cancer also increases significantly and the number and occurrence of cases of cancer in developed countries in more than the number and occurrence of cancer cases in other countries. The change in lifestyle and increase in the number of people living to a very old age in countries that are developing contributes to the increase in the rate of the occurrence of cancer. Cancer is believed to have a financial cost of up to 1.16 trillion dollars every year.

Cancer can be extremely dangerous when it is not discovered early and when adequate and proper care and attention is not given to the treatment. Therefore it is very important to go for regularly screening to find out if there is need for caution or treatment.

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Cancer Essay

500+ words cancer essay.

Cancer is a leading cause of death globally. The World Health Organisation estimates that 10 million people will die of cancer in 2020, and more people will die in the coming years if action is not taken. More than 70% of all cancer deaths occur in low and middle-income countries, where resources available for prevention, diagnosis and treatment of cancer are limited or nonexistent. This essay on cancer will help students know about this disease and the prevention method.

Students can also go through the list of CBSE Essays on different topics. It will help them to improve their writing skills and also increase their scores on the English exam. Moreover, they can participate in different essay writing competitions which are conducted at the school level.

What Is Cancer?

Cancer is a group of diseases characterised by the uncontrolled growth and spread of abnormal cells. Cancer cells develop because of multiple changes in their genes. These changes can have many possible causes. If the spread of cells is not controlled, it can result in death. There are many known causes of cancer; they include tobacco use, smoking, alcohol, excess body weight, inherited genetic mutations, hormones, and immune conditions. These risk factors may act simultaneously or in sequence to initiate and/or promote cancer growth. There are many types of cancer. Cancer can develop anywhere in the body and is named after the part of the body where it started. For instance, breast cancer that starts in the breast is still called breast cancer, even if it spreads (metastasises) to other parts of the body.

Cancer Prevention

Cancer prevention is achieved through primary, secondary, and tertiary methods. Primary cancer prevention is achieved through two mechanisms: the promotion of health and wellness and the reduction of risks known to contribute to cancer development. Primary prevention aims to reverse or inhibit the carcinogenic process through modifications in a patient’s diet or environment. Secondary cancer prevention includes screening and early detection. Screening for cancer refers to checking for the presence of disease in populations at risk, and early detection is defined as testing for cancer when no symptoms are present.

Secondary prevention seeks to detect cancer at the earliest possible stage when the disease is most likely to be treated successfully. Tertiary cancer prevention is applied to those individuals who have already been diagnosed with malignancy but are now candidates for screening and early detection of secondary malignancies.

How to Fight Cancer?

The promotion of a healthy diet and physical activity is one of the best ways to fight against cancer. Avoid the use of alcohol, tobacco, cigarettes and such items which are hazardous to health. Cancer mortality can be reduced if cases are detected and treated early. So, early diagnosis, screening and treatment reduce the severity of cancer; and it can be cured.

Apart from spreading awareness among people and educating them to know the early signs of this disease. Also, the education will upgrade the information about exercise, dietary habits, sun exposure, smoking cessation, and recommended screening practices. We all can together fight against this disease and make our country cancer-free.

Cancer is a dangerous disease, but it can be cured. Required instruments should be provided to the hospitals so that the screening and initial detection of cancer can be done at the early stage. In national health insurance, the treatment of cancer should be included with an emphasis on providing financial support to the patient and his family. The expensive immune and targeted therapies should not only be for those upper-income people. These facilities should be made accessible to all people at affordable costs. Thus, it will increase access to health services and strengthen the health systems for low and middle-income people.

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Essay on the Causes of Cancer (962 Words) | Cancer

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Read this essay on the main causes of cancer!

Cancer is a disease involving heritable defects in cellular control mechanisms.

As a result of this, cancer cells proliferate uncontrollably forming malignant tumors which grow irregular. Besides, these cells spread to surrounding tissues (metastases) therefore infecting several parts of the body.

These cancer cells have a tendency to exhibit an abnormal number of chromosome (aneuploidy), ability to divide indefinitely, disorganized cytoskeleton and lack of responsiveness to neighbouring cells.

Image Courtesy : 2.bp.blogspot.com/cancer+cells.jpg

Causes of Cancer :

Normal cells can be converted to cancer cells by treatment with a wide variety of chemicals, ionizing radiations and several DNA and RNA-containing viruses. Broadly speaking, two large groups of viruses appear to be carcinogenic.

They include DNA tumor viruses and RNA tumor viruses, depending on the type of nucleic acid present within the mature virus particle. Among DNA tumor viruses, there are simian virus 40 (SV 40), adenovirus, polyoma virus and herpes like virus. The RNA tumor viruses include retroviruses similar to HIV.

Two kinds of genes have been found to be associated with carcinogenesis:

These comprise tumor – suppressor genes and oncogenes.

1. Tumor – suppressor genes:

These are anti-oncogenes and encode proteins which restrain cell growth and prevent cells from becoming malignant. First tumor – suppressor gene resulting in eye cancer called retinoblastoma was discovered, designated as RB. It was caused due to deletion in one member of 13th pair of chromosome. Other cancers caused by tumor-suppressor genes include colon carcinoma, nephroblastoma, neurofibromas and thyroid carcinoma etc.

Proto-oncogene:

All 20 viral oncogenes derive from cellular genes in normal cells. The normal cellular version of the gene is called a proto-oncogene. Retroviruses pick up into their genome sequences from mRNA population that will increase viral production (by increasing cell proliferation). These viruses can transmit genes from one species to another, thus breaking evolutionary barriers (Bishop, 1983).

Another agent that stimulates proliferation, epidermal growth factor (EGF), like Svc, increases phosphorylation of membrane proteins at tyrosines. It is thought that this tyrosine phosphorylation somehow controls cell proliferation. Cancer cells (also called transformed cells) contain ten times more phosphotyrosine than normal cells.

About half of the oncogenes code for Tyr protein kinases and in all cases the proteins are integral components of the cell membrane. Most oncogenes seem to be related in one way or another with the same pathway of regulation of cell proliferation by protein growth factors.

EGF stimulates lung development and differentiation. In intact organisms, the production of growth factor induces multiplication at a short distance only, stimulating the cell that secretes it and the nearby cells. This is sometimes called autocrine secretion. When EGF reaches the membrane of a target cell it binds to a specific receptor protein of 170,000 Daltons, and the complex is subsequently internalized.

The receptor protein becomes phosphorylated during this process and the phosphorus binds to tyrosine. Phosphorylation of tyrosine is rare in proteins except in cells that have been transformed by retroviruses and become cancerous. Both in EGF and in viral transformation phosphorylation of tyrosine results in increased cell proliferation. Cells start dividing only after many hours of adding the growth factors.

Growth inhibitors, called chalones (Gr., to slow down) are numerous, which have been isolated from tissues. These are also numerous and important as growth factors.

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• Published: 19 June 2024

Why do patients with cancer die?

• Adrienne Boire   ORCID: orcid.org/0000-0002-9029-1248 1   na1 ,
• Katy Burke 2   na1 ,
• Thomas R. Cox   ORCID: orcid.org/0000-0001-9294-1745 3 , 4   na1 ,
• Theresa Guise 5   na1 ,
• Mariam Jamal-Hanjani 6 , 7 , 8   na1 ,
• Tobias Janowitz   ORCID: orcid.org/0000-0002-7820-3727 9 , 10   na1 ,
• Rosandra Kaplan 11   na1 ,
• Rebecca Lee   ORCID: orcid.org/0000-0003-2540-2009 12 , 13   na1 ,
• Charles Swanton   ORCID: orcid.org/0000-0002-4299-3018 7 , 8 , 14   na1 ,
• Matthew G. Vander Heiden   ORCID: orcid.org/0000-0002-6702-4192 15 , 16   na1 &
• Erik Sahai   ORCID: orcid.org/0000-0002-3932-5086 12   na1  

Nature Reviews Cancer ( 2024 ) Cite this article

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Cancer is a major cause of global mortality, both in affluent countries and increasingly in developing nations. Many patients with cancer experience reduced life expectancy and have metastatic disease at the time of death. However, the more precise causes of mortality and patient deterioration before death remain poorly understood. This scarcity of information, particularly the lack of mechanistic insights, presents a challenge for the development of novel treatment strategies to improve the quality of, and potentially extend, life for patients with late-stage cancer. In addition, earlier deployment of existing strategies to prolong quality of life is highly desirable. In this Roadmap, we review the proximal causes of mortality in patients with cancer and discuss current knowledge about the interconnections between mechanisms that contribute to mortality, before finally proposing new and improved avenues for data collection, research and the development of treatment strategies that may improve quality of life for patients.

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Acknowledgements

A.B. is funded by National Institutes of Health/National Cancer Institute P30 CA008748 and R01-CA245499. K.B. is employed by the UK National Health Service. T.R.C. acknowledges funding support from the National Health and Medical Research Council (NHMRC) Ideas (2000937), Project (1129766, 1140125), Development (2013881) and Fellowship (1158590) schemes, a Cancer Institute NSW Career Development Fellowship (CDF171105), Cancer Council NSW project support (RG19-09, RG23-11) and Susan G. Komen for the Cure (CCR17483294). T.G. is funded by the Cancer Prevention and Research Institute of Texas Grant 00011633. M.J.-H. has received funding from CRUK, NIH National Cancer Institute, IASLC International Lung Cancer Foundation, Lung Cancer Research Foundation, Rosetrees Trust, UKI NETs and NIHR. T.J. acknowledges funding from Cancer Grand Challenges (NIH: 1OT2CA278690-01; CRUK: CGCATF-2021/100019), the Mark Foundation for Cancer Research (20-028-EDV), the Osprey Foundation, Fortune Footwear, Cold Spring Harbour Laboratory (CSHL) and developmental funds from CSHL Cancer Center Support Grant 5P30CA045508. R.K. is funded by the Intramural Research Program, the National Cancer Institute, NIH Clinical Center and the National Institutes of Health (NIH NCI ZIABC011332-06 and NIH NCI ZIABC011334-10). R.L. is supported by a Wellcome Early Career Investigator Award (225724/Z/22/Z). E.S. is supported by the Francis Crick Institute, which receives its core funding from Cancer Research UK (CC2040), the UK Medical Research Council (CC2040) and the Wellcome Trust (CC2040) and the European Research Council (ERC Advanced Grant CAN_ORGANISE, Grant agreement number 101019366). E.S. reports personal grants from Mark Foundation and the European Research Council. C.S. is a Royal Society Napier Research Professor (RSRP\R\210001). His work is supported by the Francis Crick Institute that receives its core funding from Cancer Research UK (CC2041), the UK Medical Research Council (CC2041) and the Wellcome Trust (CC2041) and the European Research Council under the European Union’s Horizon 2020 research and innovation programme (ERC Advanced Grant PROTEUS Grant agreement number 835297). M.G.V.H. reports support from the Lustgarten Foundation, the MIT Center for Precision Cancer Medicine, the Ludwig Center at MIT and NIH grants R35 CA242379 and P30 CA1405141.

Author information

These authors contributed equally: Adrienne Boire, Katy Burke, Thomas R. Cox, Theresa Guise, Mariam Jamal-Hanjani, Tobias Janowitz, Rosandra Kaplan, Rebecca Lee, Charles Swanton, Matthew G. Vander Heiden, Erik Sahai.

Authors and Affiliations

Memorial Sloan Kettering Cancer Center, New York, NY, USA

Adrienne Boire

University College London Hospitals NHS Foundation Trust and Central and North West London NHS Foundation Trust Palliative Care Team, London, UK

Cancer Ecosystems Program, The Garvan Institute of Medical Research and The Kinghorn Cancer Centre, Darlinghurst, New South Wales, Australia

Thomas R. Cox

School of Clinical Medicine, St Vincent’s Healthcare Clinical Campus, UNSW Medicine and Health, UNSW Sydney, Sydney, New South Wales, Australia

Department of Endocrine Neoplasia and Hormonal Disorders, The University of Texas MD Anderson Cancer Center, Houston, TX, USA

Theresa Guise

Cancer Metastasis Laboratory, University College London Cancer Institute, London, UK

Mariam Jamal-Hanjani

Department of Oncology, University College London Hospitals, London, UK

Mariam Jamal-Hanjani & Charles Swanton

Cancer Research UK Lung Centre of Excellence, University College London Cancer Institute, London, UK

Cold Spring Harbour Laboratory, Cold Spring Harbour, New York, NY, USA

Tobias Janowitz

Northwell Health Cancer Institute, New York, NY, USA

Paediatric Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA

Rosandra Kaplan

Tumour Cell Biology Laboratory, The Francis Crick Institute, London, UK

Rebecca Lee & Erik Sahai

Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UK

Rebecca Lee

Cancer Evolution and Genome Instability Laboratory, The Francis Crick Institute, London, UK

Charles Swanton

Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, USA

Matthew G. Vander Heiden

Dana-Farber Cancer Institute, Boston, MA, USA

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Contributions

All authors researched data for the article. A.B., K.B., T.R.C., T.G., T.J., C.S., M.G.V.H, R.K., M.J.-H. and E.S. contributed substantially to discussion of the content. T.C., R.L. and E.S. wrote the article. All authors reviewed and/or edited the manuscript before submission.

Corresponding authors

Correspondence to Thomas R. Cox or Erik Sahai .

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Competing interests.

A.B. is an inventor on pending patents 63/449,817, 63/052,139 as well as awarded patents 11,305,014 and 10,413,522; all issued to the Sloan Kettering Institute. She has received personal fees from Apelis Pharmaceuticals and serves as an unpaid member of the Evren Technologies SAB. K.B., T.R.C., T.G., T.J. and R.K. declare no competing interests. M.J.-H. reports support from Achilles Therapeutics Scientific Advisory Board and Steering Committee, Pfizer, Astex Pharmaceuticals, Oslo Cancer Cluster and Bristol Myers Squibb outside the submitted work. R.L. reports personal fees from Pierre Fabre and has research funding from BMS, Astra Zeneca and Pierre Fabre outside the submitted work. E.S. reports grants from Novartis, Merck Sharp Dohme, AstraZeneca and personal fees from Phenomic outside the submitted work. C.S. reports grants and personal fees from Bristol Myers Squibb, AstraZeneca, Boehringer-Ingelheim, Roche-Ventana, personal fees from Pfizer, grants from Ono Pharmaceutical, Personalis, grants, personal fees and other support from GRAIL, other support from AstraZeneca and GRAIL, personal fees and other support from Achilles Therapeutics, Bicycle Therapeutics, personal fees from Genentech, Medixci, China Innovation Centre of Roche (CiCoR) formerly Roche Innovation Centre, Metabomed, Relay Therapeutics, Saga Diagnostics, Sarah Canon Research Institute, Amgen, GlaxoSmithKline, Illumina, MSD, Novartis, other support from Apogen Biotechnologies and Epic Bioscience outside the submitted work; in addition, C.S. has a patent for PCT/US2017/028013 licensed to Natera Inc., UCL Business, a patent for PCT/EP2016/059401 licensed to Cancer Research Technology, a patent for PCT/EP2016/071471 issued to Cancer Research Technology, a patent for PCT/GB2018/051912 pending, a patent for PCT/GB2018/052004 issued to Francis Crick Institute, University College London, Cancer Research Technology Ltd, a patent for PCT/GB2020/050221 issued to Francis Crick Institute, University College London, a patent for PCT/EP2022/077987 pending to Cancer Research Technology, a patent for PCT/GB2017/053289 licensed, a patent for PCT/EP2022/077987 pending to Francis Crick Institute, a patent for PCT/EP2023/059039 pending to Francis Crick Institute and a patent for PCT/GB2018/051892 pending to Francis Crick Institute. C.S. is Co-chief Investigator of the NHS Galleri trial funded by GRAIL. He is Chief Investigator for the AstraZeneca MeRmaiD I and II clinical trials and Chair of the Steering Committee. C.S. is cofounder of Achilles Therapeutics and holds stock options. M.G.V.H. is a scientific adviser for Agios Pharmaceuticals, iTeos Therapeutics, Sage Therapeutics, Faeth Therapeutics, Droia Ventures and Auron Therapeutics on topics unrelated to the presented work.

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Nature Reviews Cancer thanks Vickie Baracos, Clare M. Isacke, who co-reviewed with Amanda Fitzpatrick and Erica Sloan and the other, anonymous, reviewer(s) for their contribution to the peer review of this work.

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An autoimmune encephalitis characterized by complex neuropsychiatric features and the presence of immunoglobulin G (IgG) antibodies against the NR1 subunit of the NMDA receptors in the central nervous system.

Partial collapse or incomplete inflation of the lung.

Pressure-induced movement of brain tissue.

An ageing-associated process in which haematopoiesis becomes dominated by one or a small number of genetically distinct stem or progenitor cells. Clonal haematopoiesis is linked to an increased risk of haematological malignancies.

Inability of the heart to pump blood properly.

Constriction of the arteries that supply blood to the heart.

(CRH). One of the major factors that drives the response of the body to stress.

(DIC). A rare but serious condition in which abnormal blood clotting occurs throughout the blood vessels of the body.

Inflammation of the brain.

An abnormal connection that forms between two body parts, such as an organ or blood vessel and another often unrelated structure in close proximity.

A rare disorder in which the immune system of a body attacks the nerves, which can lead to paralysis.

The stopping of flow of blood, typically associated with the bodies response to prevent and stop bleeding.

A build-up of fluid within the cavities of the brain.

Elevated calcium levels in the blood, often caused by overactive parathyroid glands. Hypercalcaemia is linked to kidney stones, weakened bones, altered digestion and potentially altered cardiac and brain function.

(HPD). Rapid tumour progression sometimes observed during immune checkpoint inhibitor treatment.

The condition that occurs when the level of sodium in the blood is low.

Harm, which is often unavoidable, caused by cancer treatments.

The marked suppression of polyclonal immunoglobulins in the body.

(LEMS). A neuromuscular junction disorder affecting communication between nerves and muscles, which manifests as a result of a paraneoplastic syndrome or a primary autoimmune disorder. Many cases are associated with small-cell lung cancer.

When cancer cells spread to the tissue layers covering the brain and spinal cord (the leptomeninges).

Also known as pulmonary oedema is a condition caused by excess fluid in the lungs. This fluid collects in the alveoli compromising function and making it difficult to breathe.

The observation of displacement of brain tissue across the centre line of the brain, suggestive of uneven intracranial pressure.

Decreased blood flow to the myocardium, commonly called a heart attack.

Inflammation specifically of the middle layer of the heart wall.

A group of rare disorders that occur when the immune system reacts to changes in the body triggered by the presence of a neoplasm.

A dense network of nerves that transmit information from the brain (efferent neurons) to the periphery and conversely transmit information from the periphery to the brain (afferent neurons). A component of the peripheral nervous system is the autonomic nervous system.

A build-up of fluid between the tissues that line the lungs and the chest wall.

A condition characterized by loss of skeletal muscle mass and function.

The lodging of a circulating blood clot within a vessel leading to obstruction. Thromboembolisms may occur in veins (venous thromboembolism) and arteries (arterial thromboembolism).

A key component of the pathway regulating blood clotting, specifically the receptor and cofactor for factor VII/VIIa.

A syndrome occurs when tumour cells release their contents into the bloodstream, either spontaneously or more typically, in response to therapeutic intervention.

Devices worn on the body, typically in the form of accessories or clothing, that incorporate advanced electronics and technology to monitor, track or enhance various aspects of human life. Examples include smartwatches and fitness trackers.

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Boire, A., Burke, K., Cox, T.R. et al. Why do patients with cancer die?. Nat Rev Cancer (2024). https://doi.org/10.1038/s41568-024-00708-4

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DOI : https://doi.org/10.1038/s41568-024-00708-4

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Melanoma Brain Metastases: New Study Offers Insight for More Effective Cancer Treatment

For those living with advanced melanoma , brain metastases— malignant growths that occur when cancer cells travel to the brain—are particularly challenging to treat. New findings, published April 18 in Cellular and Molecular Life Sciences , could help clinicians improve treatments for this form of late-stage cancer and reduce the risk of recurrence.

Brain metastases are a risk from any cancer but are especially prevalent in certain types, including melanoma. Researchers estimate as many as 40% to 60% of those with late-stage melanoma will develop brain metastases, often resulting in death. In some cases, cancer growth is supported by a process known as vascular mimicry, in which tumors form their own vasculature, allowing nutrient flow to the tumor. Now, a team of researchers has investigated the underlying mechanisms of vascular mimicry to better understand how this process may drive the outgrowth of melanoma brain metastases and their poor response to current cancer treatments. The researchers also hope to discover how inhibiting this process could lead to a potential novel therapy.

“Brain metastasis patients are often excluded from clinical trials [due to concerns regarding drug penetration, toxicity, and their historical poor prognosis], which has slowed the development of systemic therapies for these patients,” says Lucia Jilaveanu, MD, PhD , associate professor of medicine (medical oncology), member of Yale Cancer Center, and the study’s principal investigator. “Our team is hoping to provide proof-of principle of the therapeutic value of inhibiting vascular mimicry as a strategy for treating melanoma brain metastases.”

Do angiogenesis and vascular mimicry cause tumor growth?

Cancers, including melanoma, can remain dormant in the body for long periods of time. This dormancy is often followed by an aggressive outbreak in which the melanoma rapidly spreads and is difficult to control with existing therapies.

Scientists have long believed that the reactivation of dormant cancers can be triggered by a process known as angiogenesis (the development of new blood vessels). Each of our organs has a local vasculature system; through angiogenesis, tumors stimulate existing nearby blood vessels to create new vessels which facilitate the tumors’ growth.

There is emerging evidence that the cancer reactivation may also be triggered by vascular mimicry. Through this process, cancer stem cells differentiate into cells that mimic vascular endothelial cells—the cells that line blood vessels. These cells form tubular structures that connect to our normal vasculature, allowing for the active circulation of blood within the tumor.

Jilaveanu has been focusing on the biology of brain metastasis for more than a decade. Part of her research includes the development of mouse models to help her team better understand how to treat the disease. One of the models developed in her lab replicated the transition from dormant micro-metastasis to macro-metastasis. Through this work, they uncovered a link between brain metastasis and several previously undiscovered molecules. This inspired further studies, which found that these molecules were linked to the regulation of vascular mimicry.

How does vascular mimicry drive melanoma brain metastasis?

In their latest investigation on the mechanisms of vascular mimicry in melanoma brain metastasis, the team integrated several approaches. First, they analyzed tumor tissues from both on and outside the brains of patients who had undergone surgery for melanoma. They found an increased density of vascular mimicry in brain metastases compared to tissue collected from other kinds of tumors. Furthermore, they uncovered a positive correlation between vascular mimicry density and tumor volume, as well as cerebral edema [brain swelling].

Next, they cultured human melanoma cell lines taken from tumors of the brain and from other anatomical sites of patients treated at Yale New Haven Hospital, as well as mouse melanoma cell lines. Once again, they found that cells taken from brain metastases had developed structures of vascular mimicry, whereas cells of tumors from outside the brain had not. This evidence suggests that brain metastases are more likely than tumors outside the brain to utilize vascular mimicry over angiogenesis.

Are YAP/TAZ inhibitors a potential treatment for melanoma brain metastasis?

Through previous work in her lab, Jilaveanu and her team have pinpointed a signaling pathway, known as YAP/TAZ, that is involved with the regulation of vascular mimicry. “YAP and TAZ are two transcription cofactors [proteins involved in the transcription of genetic information] that are widely expressed in melanoma and involved in melanoma progression,” she says.

In their current study, the researchers studied the effects of applying drugs that target YAP/TAZ on the vascular mimicry in their models. They applied verteporfin, a macular degeneration drug that treats the abnormal blood vessel growth, and CA3, another YAP/TAZ inhibitor, to their brain metastatic cell lines. They also used TED347, a newer drug that is more specific and better tolerated. They found that the drugs inhibited vascular mimicry and reduced cancer cell growth.

Furthermore, the team employed their previously developed mouse models of metastatic melanoma to study the disease in vivo. Treated mice lived longer than the controls, the researchers found. “Vascular mimicry can be specifically targeted, and this impacts metastatic growth,” says Jilaveanu.

Some current therapies for treating malignant tumors target mechanisms underlying angiogenesis. Thus, tumors that preferentially utilize vascular mimicry may be resistant to these treatments. Jilaveanu hopes that her work will show clinicians the potential therapeutic value of inhibiting both angiogenesis and vascular mimicry when treating melanoma. “Brain metastases pose a major challenge in the clinic due to a lack of effective therapy,” she says. “Focusing on vascular mimicry as a mechanism of treatment resistance will be very significant for our patients.”

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• Lucia Jilaveanu, MD, PhD Associate Professor of Medicine (Medical Oncology)

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Understanding cancer.

In simple terms, cancer is a group of more than 100 diseases that develop across time and involve the uncontrolled division of the body's cells. Although cancer can develop in virtually any of the body's tissues, and each type of cancer has its unique features, the basic processes that produce cancer are quite similar in all forms of the disease.

Cancer begins when a cell breaks free from the normal restraints on cell division and begins to follow its own agenda for proliferation ( Figure 3 ). All of the cells produced by division of this first, ancestral cell and its progeny also display inappropriate proliferation. A tumor , or mass of cells, formed of these abnormal cells may remain within the tissue in which it originated (a condition called in situ cancer), or it may begin to invade nearby tissues (a condition called invasive cancer). An invasive tumor is said to be malignant , and cells shed into the blood or lymph from a malignant tumor are likely to establish new tumors ( metastases ) throughout the body. Tumors threaten an individual's life when their growth disrupts the tissues and organs needed for survival.

The stages of tumor development. A malignant tumor develops across time, as shown in this diagram. This tumor develops as a result of four mutations, but the number of mutations involved in other types of tumors can vary. We do not know the exact number (more...)

What happens to cause a cell to become cancerous? Thirty years ago, scientists could not offer a coherent answer to this question. They knew that cancer arose from cells that began to proliferate uncontrollably within the body, and they knew that chemicals, radiation, and viruses could trigger this change. But exactly how it happened was a mystery.

Research across the last three decades, however, has revolutionized our understanding of cancer. In large part, this success was made possible by the development and application of the techniques of molecular biology, techniques that enabled researchers to probe and describe features of individual cells in ways unimaginable a century ago. Today, we know that cancer is a disease of molecules and genes, and we even know many of the molecules and genes involved. In fact, our increasing understanding of these genes is making possible the development of exciting new strategies for avoiding, forestalling, and even correcting the changes that lead to cancer.

• Unraveling the Mystery of Cancer

People likely have wondered about the cause of cancer for centuries. Its name derives from an observation by Hippocrates more than 2,300 years ago that the long, distended veins that radiate out from some breast tumors look like the limbs of a crab. From that observation came the term karkinoma in Greek, and later, cancer in Latin.

With the work of Hooke in the 1600s, and then Virchow in the 1800s, came the understanding that living tissues are composed of cells, and that all cells arise as direct descendants of other cells. Yet, this understanding raised more questions about cancer than it answered. Now scientists began to ask from what kinds of normal cells cancer cells arise, how cancer cells differ from their normal counterparts, and what events promote the proliferation of these abnormal cells. And physicians began to ask how cancer could be prevented or cured.

Clues from epidemiology

One of the most important early observations that people made about cancer was that its incidence varies between different populations. For example, in 1775, an extraordinarily high incidence of scrotal cancer was described among men who worked as chimney sweeps as boys. In the mid-1800s, lung cancer was observed at alarmingly high rates among pitch blende miners in Germany. And by the end of the 19th century, using snuff and cigars was thought by some physicians to be closely associated with cancers of the mouth and throat.

These observations and others suggested that the origin or causes of cancer may lie outside the body and, more important, that cancer could be linked to identifiable and even preventable causes. These ideas led to a widespread search for agents that might cause cancer. One early notion, prompted by the discovery that bacteria cause a variety of important human diseases, was that cancer is an infectious disease. Another idea was that cancer arises from the chronic irritation of tissues. This view received strong support with the discovery of X-rays in 1895 and the observation that exposure to this form of radiation could induce localized tissue damage, which could lead in turn to the development of cancer. A conflicting view, prompted by the observation that cancer sometimes seems to run in families, was that cancer is hereditary.

Such explanations, based as they were on fragmentary evidence and incomplete understanding, helped create the very considerable confusion about cancer that existed among scientists well into the mid-twentieth century. The obvious question facing researchers—and no one could seem to answer it—was how agents as diverse as this could all cause cancer. Far from bringing science closer to understanding cancer, each new observation seemed to add to the confusion.

Yet each new observation also, ultimately, contributed to scientists' eventual understanding of the disease. For example, the discovery in 1910 that a defined, submicroscopic agent isolated from a chicken tumor could induce new tumors in healthy chickens showed that a tumor could be traced simply and definitively back to a single cause. Today, scientists know this agent as Roussarcoma virus, one of several viruses that can act as causative factors in the development of cancer.

Although cancer-causing viruses are not prime agents in promoting most human cancers, their intensive study focused researchers' attention on cellular genes as playing a central role in the development of the disease.

Likewise, investigations into the association between cancer and tissue damage, particularly that induced by radiation, revealed that while visible damage sometimes occurs, something more subtle happens in cells exposed to cancer-causing agents. One clue to what happens came from the work of Herman Muller, who noticed in 1927 that X-irradiation of fruit flies often resulted in mutant offspring. Might the two known effects of X-rays, promotion of cancer and genetic mutation, be related to one another? And might chemical carcinogens induce cancer through a similar ability to damage genes?

Support for this idea came from the work of Bruce Ames and others who showed in 1975 that com pounds known to be potent carcinogens (cancer-causing agents) generally also were potent mutagens (mutation-inducing agents), and that compounds known to be only weak carcinogens were only weak mutagens. Although scientists know today that many chemicals do not follow this correlation precisely, this initial, dramatic association between mutagenicity and carcinogenicity had widespread influence on the development of a unified view of the origin and development of cancer.

Finally, a simple genetic model, proposed by Alfred Knudson in 1971, provided both a compelling explanation for the origins of retinoblastoma, a rare tumor that occurs early in life, and a convincing way to reconcile the view of cancer as a disease produced by external agents that damage cells with the observation that some cancers run in families. Knudson's model states that children with sporadic retinoblastoma (children whose parents have no history of the disease) are genetically normal at the moment of conception, but experience two somatic mutations that lead to the development of an eye tumor. Children with familial retinoblastoma (children whose parents have a history of the disease) already carry one mutation at conception and thus must experience only one more mutation to reach the doubly mutated configuration required for a tumor to form. In effect, in familial retinoblastoma, each retinal cell is already primed for tumor development, needing only a second mutational event to trigger the cancerous state. The difference in probabilities between the requirement for one or two mutational events, happening randomly, explains why in sporadic retinoblastoma, the affected children have only one tumor focus, in one eye, while in familial retinoblastoma, the affected children usually have multiple tumor foci growing in both eyes.

Although it was years before Knudson's explanation was confirmed, it had great impact on scientists' understanding of cancer. Retinoblastoma, and by extension, other familial tumors, appeared to be linked to the inheritance of mutated versions of growth-suppressing genes. This idea led to the notion that cells in sporadically arising tumors might also have experienced damage to these critical genes as the cells moved along the path from the normal to the cancerous state.

Clues from cell biology

Another field of study that contributed to scientists' growing understanding of cancer was cell biology. Cell biologists studied the characteristics of cancer cells, through observations in the laboratory and by inferences from their appearance in the whole organism. Not unexpectedly, these investigations yielded a wealth of information about normal cellular processes. But they also led to several key understandings about cancer, understandings that ultimately allowed scientists to construct a unified view of the disease.

One such understanding is that cancer cells are indigenous cells—abnormal cells that arise from the body's normal tissues. Furthermore, virtually all malignant tumors are monoclonal in origin, that is, derived from a single ancestral cell that somehow underwent conversion from a normal to a cancerous state. These insights, as straight for ward as they seem, were surprisingly difficult to reach. How could biologists describe the cell pedigree of a mass of cells that eventually is recognized as a tumor?

One approach to identifying the origin of cancer cells came from attempts to transplant tissues from one person to another. Such transplants work well between identical twins, but less well as the people involved are more distantly related. The barrier to successful transplantation exists because the recipient's immune system can distinguish between cells that have always lived inside the self and cells of foreign origin. One practical application of this discovery is that tissues can be classified as matching or nonmatching before a doctor attempts to graft a tissue or organ into another person's body. Such tissue-typing tests, when done on cancer cells, reveal that the tumor cells of a particular cancer patient are always of the same transplantation type as the cells of normal tissues located elsewhere in the person's body. Tumors, therefore, arise from one's own tissues, not from cells introduced into the body by infection from another person.

How do we know that tumors are monoclonal? Two distinct scenarios might explain how cancers develop within normal tissues. In the first, many individual cells become cancerous, and the resulting tumor represents the descendants of these original cells. In this case, the tumor is polyclonal in nature ( Figure 4 ). In the second scenario, only one cell experiences the original transformation from a normal cell to a cancerous cell, and all of the cells in the tumor are descendants of that cell.

Two schemes by which tumors can develop. Most—if not all—human cancer appears to be monoclonal.

Direct evidence supporting the monoclonal origin of virtually all malignant tumors has been difficult to acquire because most tumor cells lack obvious distinguishing marks that scientists can use to demonstrate their clonal relationship. There is, however, one cellular marker that scientists can use as an indication of such relationships: the inactivated X chromosome that occurs in almost all of the body cells of a human female. X-chromosome inactivation occurs randomly in all cells during female embryonic development. Because the inactivation is random, the female is like a mosaic in terms of the X chromosome, with different copies of the X turned on or off in different cells of the body. Once inactivation occurs in a cell, all of the future generations of cells coming from that cell have the same chromosome inactivated in them as well (either the maternal or the paternal X). The observation that all the cells within a given tumor invariably have the same X chromosome inactivated suggests that all cells in the tumor must have descended from a single ancestral cell.

Cancer, then, is a disease in which a single normal body cell undergoes a genetic transformation into a cancer cell. This cell and its descendants, proliferating across many years, produce the population of cells that we recognize as a tumor, and tumors produce the symptoms that an individual experiences as cancer.

Even this picture, although accurate in its essence, did not represent a complete description of the events involved in tumor formation. Additional research revealed that as a tumor develops, the cells of which it is composed become different from one another as they acquire new traits and form distinct subpopulations of cells within the tumor. As shown in Figure 5 , these changes allow the cells that experience them to compete with increasing success against cells that lack the full set of changes. The development of cancer, then, occurs as a result of a series of clonal expansions from a single ancestral cell.

A series of changes leads to tumor formation. Tumor formation occurs as a result of successive clonal expansions. This figure illustrates only three such changes; the development of many cancers likely involves more than three.

A second critical understanding that emerged from studying the biology of cancer cells is that these cells show a wide range of important differences from normal cells. For example, cancer cells are genetically unstable and prone to rearrangements, duplications, and deletions of their chromosomes that cause their progeny to display unusual traits. Thus, although a tumor as a whole is monoclonal in origin, it may contain a large number of cells with diverse characteristics.

Cancerous cells also look and act differently from normal cells. In most normal cells, the nucleus is only about one-fifth the size of the cell; in cancerous cells, the nucleus may occupy most of the cell's volume. Tumor cells also often lack the differentiated traits of the normal cell from which they arose. Whereas normal secretory cells pro duce and release mucus, cancers derived from these cells may have lost this characteristic. Likewise, epithelial cells usually contain large amounts of keratin, but the cells that make up skin cancer may no longer accumulate this protein in their cytoplasms.

The key difference between normal and cancerous cells, however, is that cancer cells have lost the restraints on growth that characterize normal cells. Significantly, a large number of cells in a tumor are engaged in mitosis, whereas mitosis is a relatively rare event in most normal tissues. Cancer cells also demonstrate a variety of unusual characteristics when grown in culture; two such examples are a lack of contact inhibition and a reduced dependence on the presence of growth factors in the environment. In contrast to normal cells, cancer cells do not cooperate with other cells in their environment. They often proliferate indefinitely in tissue culture. The ability to divide for an apparently unlimited number of generations is another important characteristic of the cancerous state, allowing a tumor composed of such cells to grow without the constraints that normally limit cell growth.

A unified view

By the mid-1970s, scientists had started to develop the basis of our modern molecular understanding of cancer. In particular, the relationship Ames and others had established between mutagenicity and carcinogenicity pro vided substantial support for the idea that chemical carcinogens act directly through their ability to damage cellular genes. This idea led to a straightforward model for the initiation of cancer: Carcinogens induce mutations in critical genes, and these mutations direct the cell in which they occur, as well as all of its progeny cells, to grow abnormally. The result of this abnormal growth appears years later as a tumor. The model could even explain the observation that cancer sometimes appears to run in families: If cancer is caused by mutations in critical genes, then people who inherit such mutations would be more susceptible to cancer's development than people who do not.

As exciting as it was to see a unified view of cancer begin to emerge from the earlier confusion, cancer researchers knew their work was not finished. The primary flaw in their emerging explanation was that the nature of these cancer-causing mutations was unknown. Indeed, their very existence had yet to be proven. Evidence from work with cancer-causing viruses suggested that only a small number of genes were involved, and evidence from cell biology pointed to genes that normally control cell division. But now scientists asked new questions: Exactly which genes are involved? What are their specific roles in the cell? and How do their functions change as a result of mutation?

It would take another 20 years and a revolution in the techniques of biological research to answer these questions. However, today our picture of the causes and development of cancer is so detailed that scientists find themselves in the extraordinary position of not only knowing many of the genes involved but also being able to target prevention, detection, and treatment efforts directly at these genes.

• Cancer as a Multistep Process

A central feature of today's molecular view of cancer is that cancer does not develop all at once, but across time, as a long and complex succession of genetic changes. Each change enables precancerous cells to acquire some of the traits that together create the malignant growth of cancer cells.

Two categories of genes play major roles in triggering cancer. In their normal forms, these genes control the cell cycle , the sequence of events by which cells enlarge and divide. One category of genes, called proto-oncogenes , encourages cell division. The other category, called tumor suppressor genes , inhibits it. Together, proto-oncogenes and tumor suppressor genes coordinate the regulated growth that normally ensures that each tissue and organ in the body maintains a size and structure that meets the body's needs.

What happens when proto-oncogenes or tumor suppressor genes are mutated? Mutated proto oncogenes become oncogenes, genes that stimulate excessive division. And mutations in tumor suppressor genes inactivate these genes, eliminating the critical inhibition of cell division that normally prevents excessive growth. Collectively, mutations in these two categories of genes account for much of the uncontrolled cell division that occurs in human cancers ( Figure 6 ).

Some Genes Involved in Human Cancer

The role of oncogenes

How do proto-oncogenes, or more accurately, the oncogenes they become after mutation, contribute to the development of cancer? Most proto-oncogenes code for proteins that are involved in molecular pathways that receive and process growth-stimulating signals from other cells in a tissue. Typically, such signaling begins with the production of a growth factor, a protein that stimulates division. These growth factors move through the spaces between cells and attach to specific receptor proteins located on the surfaces of neighboring cells. When a growth-stimulating factor binds to such a receptor, the receptor conveys a stimulatory signal to proteins in the cytoplasm. These proteins emit stimulatory signals to other proteins in the cell until the division-promoting message reaches the cell's nucleus and activates a set of genes that help move the cell through its growth cycle.

Oncogenes, the mutated forms of these proto oncogenes, cause the proteins involved in these growth-promoting pathways to be overactive. Thus, the cell proliferates much faster than it would if the mutation had not occurred. Some oncogenes cause cells to overproduce growth factors. These factors stimulate the growth of neighboring cells, but they also may drive excessive division of the cells that just produced them. Other oncogenes produce aberrant receptor proteins that release stimulatory signals into the cytoplasm even when no growth factors are present in the environment. Still other oncogenes disrupt parts of the signal cascade that occurs in a cell's cytoplasm such that the cell's nucleus receives stimulatory messages continuously, even when growth factor receptors are not prompting them.

The role of tumor suppressor genes

To become cancerous, cells also must break free from the inhibitory messages that normally counterbalance these growth-stimulating pathways. In normal cells, inhibitory messages flow to a cell's nucleus much like stimulatory messages do. But when this flow is interrupted, the cell can ignore the normally powerful inhibitory messages at its surface.

Scientists are still trying to identify the normal functions of many known tumor suppressor genes. Some of these genes apparently code for proteins that operate as parts of specific inhibitory pathways. When a mutation causes such proteins to be inactivate or absent, these inhibitory pathways no longer function normally. Other tumor suppressor genes appear to block the flow of signals through growth-stimulating pathways; when these genes no longer function properly, such growth-promoting pathways may operate without normal restraint. Mutations in all tumor suppressor genes, however, apparently inactivate critical tumor suppressor proteins, depriving cells of this restraint on cell division.

The body's back-up systems

In addition to the controls on proliferation afforded by the coordinated action of proto-oncogenes and tumor suppressor genes, cells also have at least three other systems that can help them avoid runaway cell division. The first of these systems is the DNA repair system. This system operates in virtually every cell in the body, detecting and correcting errors in DNA. Across a lifetime, a person's genes are under constant attack, both by carcinogens imported from the environment and by chemicals produced in the cell itself. Errors also occur during DNA replication. In most cases, such errors are rapidly corrected by the cell's DNA repair system. Should the system fail, however, the error (now a mutation) becomes a permanent feature in that cell and in all of its descendants.

The system's normally high efficiency is one reason why many years typically must pass before all the mutations required for cancer to develop occur together in one cell. Mutations in DNA repair genes themselves, however, can undermine this repair system in a particularly devastating way: They damage a cell's ability to repair errors in its DNA. As a result, mutations appear in the cell (including mutations in genes that control cell growth) much more frequently than normal.

A second cellular back-up system prompts a cell to commit suicide (undergo apoptosis ) if some essential component is damaged or its control system is deregulated. This observation suggests that tumors arise from cells that have managed to evade such death. One way of avoiding apoptosis involves the p53 protein. In its normal form, this protein not only halts cell division, but induces apoptosis in abnormal cells. The product of a tumor suppressor gene, p53 is inactivated in many types of cancers.

This ability to avoid apoptosis endangers cancer patients in two ways. First, it contributes to the growth of tumors. Second, it makes cancer cells resistant to treatment. Scientists used to think that radiation and chemotherapeutic drugs killed cancer cells directly by harming their DNA. It seems clear now that such therapy only slightly damages the DNA in cells; the damaged cells, in response, actively kill themselves. This discovery suggests that cancer cells able to evade apoptosis will be less responsive to treatment than other cells.

A third back-up system limits the number of times a cell can divide, and so assures that cells cannot reproduce endlessly. This system is governed by a counting mechanism that involves the DNA segments at the ends of chromosomes. Called telomeres, these segments shorten each time a chromo some replicates. Once the telomeres are shorter than some threshold length, they trigger an internal signal that causes the cell to stop dividing. If the cells continue dividing, further shortening of the telomeres eventually causes the chromosomes to break apart or fuse with one another, a genetic crisis that is inevitably fatal to the cell.

Early observations of cancer cells grown in culture revealed that, unlike normal cells, cancer cells can proliferate indefinitely. Scientists have recently discovered the molecular basis for this characteristic—an enzyme called telomerase, that systematically replaces telomeric segments that are trimmed away during each round of cell division. Telomerase is virtually absent from most mature cells, but is present in most cancer cells, where its action enables the cells to proliferate endlessly.

The multistep development of cancer

Cancer, then, does not develop all at once as a massive shift in cellular functions that results from a mutation in one or two wayward genes. Instead, it develops step-by-step, across time, as an accumulation of many molecular changes, each contributing some of the characteristics that eventually pro duce the malignant state. The number of cell divisions that occur during this process can be astronomically large—human tumors often become apparent only after they have grown to a size of 10 billion to 100 billion cells. As you might expect, the time frame involved also is very long— it normally takes decades to accumulate enough mutations to reach a malignant state.

Understanding cancer as a multistep process that occurs across long periods of time explains a number of long-standing observations. A key observation is the increase in incidence with age. Cancer is, for the most part, a disease of people who have lived long enough to have experienced a complex and extended succession of events. Because each change is a rare accident requiring years to occur, the whole process takes a very long time, and most of us die from other causes before it is complete.

Understanding cancer in this way also explains the increase in cancer incidence in people who experience unusual exposure to carcinogens, as well as the increased cancer risk of people who inherit predisposing mutations. Exposure to carcinogens increases the likelihood that certain harmful changes will occur, greatly increasing the probability of developing cancer during a normal life span. Similarly, inheriting a cancer -susceptibility mutation means that instead of that mutation being a rare event, it already has occurred, and not just in one or two cells, but in all the body's cells. In other words, the process of tumor formation has leapfrogged over one of its early steps. Now the accumulation of changes required to reach the malignant state, which usually requires several decades to occur, may take place in one or two.

Finally, understanding the development of cancer as a multistep process also explains the lag time that often separates exposure to a cancer-causing agent and the development of cancer. This explains, for example, the observation that severe sunburns in children can lead to the development of skin cancer decades later. It also explains the 20-to 25-year lag between the onset of widespread cigarette smoking among women after World War II and the massive increase in lung cancer that occurred among women in the 1970s.

• The Human Face of Cancer

For most Americans, the real issues associated with cancer are personal. More than 8 million Americans alive today have a history of cancer (National Cancer Institute, 1998; Rennie, 1996). In fact, cancer is the second leading cause of death in the United States, exceeded only by heart disease.

Who are these people who develop cancer and what are their chances for surviving it? Scientists measure the impact of cancer in a population by looking at a combination of three elements: (1) the number of new cases per year per 100,000 persons ( incidence rate ), (2) the number of deaths per 100,000 persons per year ( mortality rate ), and (3) the proportion of patients alive at some point after their diagnosis of cancer ( survival rate ). Data on incidence, mortality, and survival are collected from a variety of sources. For example, in the United States there are many statewide cancer registries and some regional registries based on groups of counties, many of which surround large metropolitan areas. Some of these population-based registries keep track of cancer incidence in their geographic areas only; others also collect follow-up information to calculate survival rates.

In 1973, the National Cancer Institute began the Surveillance, Epidemiology, and End Results (SEER) Program to estimate cancer incidence and patient survival in the United States. SEER collects cancer incidence data in 11 geographic areas and two supplemental registries, for a combined population of approximately 14 percent of the entire U.S. population. Data from SEER are used to track cancer incidence in the United States by primary cancer site, race, sex, age, and year of diagnosis. For example, Figure 7 shows SEER data for the age-adjusted cancer incidence rates for the 10 most common sites for Caucasian and African-American males and females for the period 1987–1991.

Age-Adjusted Cancer Incidence Rates, 1987–1991

Cancer among children is relatively rare. SEER data from 1991 showed an incidence of only 14.1 cases per 100,000 children under age 15. Nevertheless, after accidents, cancer is the second leading cause of childhood death in the United States. Leukemias (4.3 per 100,000) and cancer of the brain and other nervous system organs (3.4 per 100,000) account for more than one-half of the cancers among children.

Everyone is at some risk of developing cancer. Cancer researchers use the term lifetime risk to indicate the probability that a person will develop cancer over the course of a lifetime. In the United States, men have a 1 in 2 lifetime risk of developing cancer, and women have a 1 in 3 risk.

For a specific individual, however, the risk of developing a particular type of cancer may be quite different from his or her lifetime risk of developing any type of cancer. Relative risk compares the risk of developing cancer between persons with a certain exposure or characteristic and persons who do not have this exposure or characteristic. For example, a person who smokes has a 10- to 20-fold higher relative risk of developing lung cancer compared with a person who does not smoke. This means that a smoker is 10- to 20-times more likely to develop lung cancer than a nonsmoker.

Scientists rely heavily on epidemiology to help them identify factors associated with the development of cancer. Epidemiologists look for factors that are common to cancer victims' histories and lives and evaluate these factors in the light of current understandings of the disease. With enough study, researchers may assemble evidence that a particular factor "causes" cancer, that is, that exposure to it increases significantly the probability of the disease developing. Although this information cannot be used to predict what will happen to any one individual exposed to this risk factor, it can help people make choices that reduce their exposure to known carcinogens (cancer-causing agents) and increase the probability that if cancer develops, it will be detected early (for example, by getting regular check-ups and participating in cancer screening programs).

As noted above, hereditary factors also can contribute to the development of cancer. Some people are born with mutations that directly promote the unrestrained growth of certain cells or the occurrence of more mutations. These mutations, such as the mutation identified in the 1980s that causes retinoblastoma, confer a high relative cancer risk. Such mutations are rare in the population, however, accounting for the development of fewer than 5 percent of the cases of fatal cancer.

Hereditary factors also contribute to the development of cancer by dictating a person's general physiological traits. For example, a person with fair skin is more susceptible to the development of skin cancer than a person with a darker complexion. Likewise, a person whose body metabolizes and eliminates a particular carcinogen relatively inefficiently is more likely to develop types of cancer associated with that carcinogen than a person who has more efficient forms of the genes involved in that particular metabolic process. These inherited characteristics do not directly promote the development of cancer; each person, susceptible or not, still must be exposed to the related environ mental carcinogen for cancer to develop. Nevertheless, genes probably do contribute in some way to the vast majority of cancers.

One question often asked about cancer is "How many cases of cancer would be expected to occur naturally in a population of individuals who somehow had managed to avoid all environmental carcinogens and also had no mutations that predisposed them to developing cancer?" Comparing populations around the world with very different cancer patterns has led epidemiologists to suggest that perhaps only about 25 percent of all cancers are "hard core"—that is, would develop anyway, even in a world free of external influences. These cancers would occur simply because of the production of carcinogens within the body and because of the random occurrence of unrepaired genetic mistakes.

Although cancer continues to be a significant health issue in the United States, a recent report from the American Cancer Society (ACS), National Cancer Institute (NCI), and Centers for Disease Control and Prevention (CDC) indicates that health officials are making progress in controlling the disease. In a news bulletin released on 12 March 1998, the ACS, NCI, and CDC announced the first sustained decline in the cancer death rate, a turning point from the steady increase observed throughout much of the century. The report showed that after increasing 1.2 percent per year from 1973 to 1990, the incidence for all cancers combined declined an average of 0.7 percent per year from 1990 to 1995. The overall cancer death rate also declined by about 0.5 percent per year across this period.

The overall survival rate for all cancer sites combined also continues to increase steadily, from 49.3 percent in 1974–1976 to 53.9 percent in 1983–1990 ( Figure 8 ). In some cases—for example, among children age 15 and younger—survival rates have increased dramatically.

Five-Year Relative Survival Rates for Selected Cancer Sites, All Races

• New Hope for Treating Cancer

What explanation can we offer for the steady increase in survival rates among cancer patients? One answer likely is the improvements scientists have made in cancer detection. These improvements include a variety of new imaging techniques as well as blood and other tests that can help physicians detect and diagnose cancer early. Although many Americans regularly watch for the early symptoms of cancer, by the time symptoms occur many tumors already have grown quite large and may have metastasized. Likewise, many cancers have no symptoms. Clearly, great effort is needed to educate Americans that cancer screening (checking for cancer in people with no symptoms) is key to early detection.

Another explanation for increased survival is improved treatment. Today, the traditional workhorses of cancer treatment—surgery, radiation, and chemotherapy—are being used in ways that are increasingly specific to the type of cancer involved. In fact, many cases of cancer now are being fully cured.

But is this the best we can do? What will the future bring? Hellman and Vokes, in their 1996 article in Scientific American , note that war often serves as a metaphor for cancer research. In 1971, two days before Christmas, President Richard M. Nixon signed the National Cancer Act, committing the United States to a "war" on cancer. Although the analogy is not perfect, Hellman and Vokes suggest that it can help us understand our current position with respect to cancer prevention, detection, and treatment. Looking at the "map" of cancer research after almost 30 years of "war," we can see that we have made some modest advances. But these successes do not reveal the tremendous developments that lie ahead of us by virtue of the new, strategic position we have achieved. In fact, most scientists expect that our newly gained understanding of the molecular basis of cancer will eventually give rise to a whole generation of exciting new techniques, not only for detecting and treating cancer but also for preventing it.

A key area of interest lies in learning how to exploit the molecular abnormalities of cancer cells to bring about their destruction. For example, understanding the role of oncogenes in the development of cancer suggests new targets for anticancer therapies. Some drug companies are working on drugs designed to shut down abnormal receptor proteins. Other potential targets are the aberrant proteins within the cytoplasm that transmit stimulatory signals even without being stimulated by surface receptors.

As in the case of oncogenes, a better understanding of the role of tumor suppressor genes in preventing runaway cell division may help scientists develop new therapies directed at these genes. For example, various studies have shown that introducing a normal tumor suppressor gene into a cell can help restore the cell to normalcy. Similarly, a therapy capable of restoring a cell's capacity for apoptosis would improve significantly the effectiveness of current cancer treatments. Even telomerase represents an important potential target for scientists looking for new and more powerful treatments for cancer. If telomerase could be blocked in cancer cells, their telomeres would continue to shorten with each division until their own proliferation pushed them into a genetic crisis and death.

One bold new research initiative that offers significant promise is the Cancer Genome Anatomy Project (CGAP). The project's goal is to identify all the genes responsible for the establishment and growth of human cancer. The work is based on a simple concept: Although almost every cell in the body contains the full set of human genes, only about one-tenth of them are expressed in any particular type of cell. Thus, different types of cells— for example, muscle cells and skin cells—can be distinguished by their patterns of gene expression.

Establishing for a particular cell the repertoire of genes expressed, together with the amount of nor mal or altered gene product produced by each expressed gene, yields a powerful "fingerprint" or "signature" for that cell type. Not unexpectedly, during the transformation of a normal cell to a cancer cell, this signature changes. Some changes are quantitative. That is, gene A may be expressed in both cells, but at greatly different levels, or it may be expressed in one cell but not the other. Other changes are qualitative: Gene B may be expressed at the same level in both cells, but pro duce an altered product in the cancerous cell.

Scientists expect that being able to "read" these signatures—in other words, being able to compare the signatures of cells in their normal and cancerous states—will change cancer detection, diagnosis, and treatment in many exciting ways. Specifically, studying the exact sequence of molecular changes a cell undergoes during its transformation to a cancerous state will help scientists identify new molecular-level targets for prevention, detection, and treatment. One observation scientists have recently made is that cells surrounding an incipient tumor also may undergo changes that indicate that cancer is present. For example, early tobacco-induced molecular changes in the mouth may predict the risk of developing lung cancer, and cancers of the urinary tract may be signaled by molecularly-altered cells that are shed in the urine. Reading the signatures of these easily accessed cells may enable scientists to develop simple, non-invasive tests that will allow early detection of cancerous or precancerous cells hidden deep within the body.

Reading such signatures will also enhance the specificity of cancer diagnosis by allowing scientists to differentiate among tumors at the molecular level. By assessing the meaning of individual changes in a cell's signature, scientists will be able to determine which cancers are most likely to progress and which are not—a dilemma that confronts doctors in the treatment of prostate cancer—thereby allowing patients to avoid the harmful consequences of unnecessary treatment.

Finally, molecular fingerprinting will allow researchers to develop new treatments specifically targeted at cellular subtypes of different cancers. Often, patients suffering from tumors that by traditional criteria are indistinguishable, nevertheless experience quite different outcomes despite having received the same treatment. Research indicates that these different outcomes sometimes are related to the presence or absence of particular gene products. In the future, such molecular characteristics likely will be used to identify patients who would benefit from one type of treatment as compared with another.

The ultimate goal of such work, of course, is to push back the detection and diagnosis of cancer to its earliest stages of development. For the first time in the history of humankind, scientists can now envision the day when medical intervention for cancer will become focused at identifying incipient disease and preventing its progression to overt disease, rather than treating the cancer after it is well established.

• Cancer and Society

But what does this mean for society? The financial costs of cancer loom large, not only for the individual but also for the community. The NCI estimates overall annual costs for cancer at about $107 billion. This cost includes $37 billion for direct medical costs, $11 billion for morbidity costs (cost of lost productivity), and $59 billion for mortality costs. Interestingly, treatment for breast, lung, and prostate cancers account for more than one-half of the direct medical costs.

Although early detection and successful treatment can reduce cancer deaths, the most desirable way to reduce them is prevention. In fact, scientists estimate that as many as one-half of the deaths from cancer in the United States and Europe, two areas with closely tracked cancer rates, could theoretically be prevented.

Nevertheless, the widespread persistence of unhealthful habits suggests that many Americans remain unconvinced about the power of prevention as a defense against cancer. Part of the reason may be that the only data we have about factors related to cancer are drawn from whole populations. These data cannot tell us who will develop cancer. Nor can they tell us whether healthful choices prevented its appearance in a particular individual.

Unhealthful habits also may persist because of the long time that elapses between the exposures that trigger the development of cancer and its actual appearance as disease. Conversely, there is a time lag between the institution of a beneficial personal habit (such as quitting smoking) or public policy (such as banning use of a known carcinogen) and its positive impact on personal and public health.

In their article "Strategies for Minimizing Cancer Risk," Willett, Colditz, and Mueller propose four levels on which to focus cancer prevention efforts. The first level is that of the individual. These authors argue that because most of the actions that can prevent cancer must be taken by individuals, dissemination of accurate information directly to the American public, together with peer support for behavioral changes, are critical.

A second level is health care providers, who are in a position to provide both counseling and screening to individuals under their care. Here, dissemination of accurate and timely information also is key.

A third level of prevention is the national level, where government agencies can impose regulations that help minimize the public's exposure to known carcinogens and implement policies that improve public health. Examples include regulating industries to cease using potent carcinogens and providing community facilities for safe physical activity.

Finally, a fourth level of prevention is at the international level, where the actions of developed countries can affect the incidence of cancer worldwide. Unfortunate examples of this include promoting the exportation of tobacco products and moving hazardous manufacturing processes to unregulated developing countries.

How do we think about devising and implementing measures to improve personal and public health in a pluralist society? One way to address this question is by attending to the ethical and public policy issues raised by our understanding and treatment of cancer.

A history of severe sunburns is strongly linked to the development of skin cancer later in life.

Ethics is the study of good and bad, right and wrong. It has to do with the actions and character of individuals, families, communities, institutions, and societies. During the last 2,500 years, Western philosophy has developed a variety of powerful methods and a reliable set of concepts and technical terms for studying and talking about the ethical life. Generally speaking, we apply the terms "right" and "good" to actions and qualities that foster the interests of individuals, families, communities, institutions, and society. Here, an "interest" refers to a participant's share in a situation. The terms "wrong" or "bad" apply to actions and qualities that impair interests. Often there are competing, well-reasoned answers to questions about what is right and wrong and good and bad about an individual's or group's conduct or actions.

Ethical considerations are complex, multifaceted, and raise many questions. In the United States, for example, we value protecting individuals from preventable harms. We support restrictions on who can purchase cigarettes and where smoking can occur. We inform pregnant women of the risks of drinking and smoking. However, we also value individual freedom and autonomy. We do not ban cigarettes outright; instead, we allow individuals over 18 years of age to take personal risks and be exposed to the related consequences. We permit pregnant women to buy and use liquor and cigarettes.

The inevitability of ethical tradeoffs is not simply a mark of the discussions in the United States. When considering differing health policy issues between and among countries, one cannot avoid encountering a pluralism of ethical considerations. Developing countries, whose health standards often differ from those in the United States, provide different cultural approaches to cancer and different standards for marketing and using tobacco and other known carcinogens. These different approaches raise a variety of ethical questions. For example, is there any legal and ethical way for people in the United States to prevent the widespread use of tobacco in other countries, a practice that contributes to the rise of lung cancer worldwide? Is there any legal and ethical way to govern other choices of individuals (for example, poor diet and lack of exercise) that contribute to cancer?

Typically, answers to such questions all involve an appeal to values. A value is something that has significance or worth in a given situation. One of the exciting events to witness in any discussion in ethics in a pluralist society is the varying ways in which the individuals involved assign value to things, persons, and states of affairs. Examples of values that students may appeal to in discussions of ethical issues include autonomy, freedom, privacy, sanctity of life, protecting another from harm, promoting another's good, justice, fairness, relationships, scientific knowledge, and technological progress.

Acknowledging the complex, multifaceted nature of ethical discussions is not to suggest that "anything goes." Experts generally agree on the following features of ethics. First, ethics is a process of rational inquiry. It involves posing clearly formulated questions and seeking well-reasoned answers to those questions. Well-reasoned answers to ethical questions constitute arguments . Ethical analysis and argument, then, result from successful ethical inquiry.

Second, ethics requires a solid foundation of information and rigorous interpretation of that information. For example, one must have a solid understanding of cancer to discuss the ethics of requiring protective covering to be worn to prevent skin cancer. Ethics is not strictly a theoretical discipline but is concerned in vital ways with practical matters.

Third, because tradeoffs among interests are complex, constantly changing, and sometimes uncertain, there are often competing, well-reasoned answers to questions about what is right and wrong and good and bad. This is especially true in a pluralist society.

Public policy is a set of guidelines or rules that results from the actions or lack of actions of government entities. Government entities act by making laws. In the United States, laws can be made by each of the three branches of government: by legislatures (statutory law), by courts (case law), and by regulatory agencies (regulatory law). Regulatory laws are written by the executive branch of the government, under authorization by the legislative branch. All three types of law are pertinent to how we respond to cancer. When laws exist to regulate behavior, public policy is called de jure public policy.

Whether one makes public policy involves at least the following five considerations:

• -the costs of implementing particular policies (including financial, social, and personal costs),
• the urgency of implementing a new policy,
• how effective a particular policy is likely to be,
• -whether appropriate means exist to implement the policy, and
• social, cultural, and political factors.

For example, many argue that there is overwhelming evidence to support increased public policy restrictions on access to and use of cigarettes. Cigarette smoking is said to be linked to 85–90 percent of lung cancer cases. In 1998, 171,500 new cases of lung cancer were predicted. Of these, 160,100 were expected to end in death. Public policy prohibitions on cigarette use and access may be seen to satisfy four of the five criteria: (1) the cost of the policy would be minimal because cigarette access and use restrictions are in place, (2) the urgency of the situation is serious given the large number of deaths, (3) prohibiting purchase by minors and raising the prices (through taxation) are seen as effective, and (4) means are already in place for additional restrictions. The challenge in this era of high economic interest in cigarette production is the social, cultural, and political considerations (5).

Where do we spend our money? A consequence of allowing unhealthful habits, such as smoking, is that public funds may be spent on cancer treatments instead of on other societal benefits, such as improved school facilities.

It is important to recognize that sometimes the best public policy is not to enact a law in response to a controversy, but rather to allow individuals, families, communities, and societies to act in the manner they choose. Clearly, de jure public policy can only go so far in regulating people's behaviors. De jure public policy in the United States offers no match for the addictive power of nicotine and the marketing clout of the tobacco industry. In addition, any decline in cigarette use brought about by de jure public policy in the United States has been more than offset in recent years by a rapid increase of cigarette consumption elsewhere in the world.

When no laws exist to regulate behavior, public policy is called de facto (actual) public policy. With regard to lung cancer prevention programs, many think that other approaches are needed: improved general education and cultivation of an antismoking ethos. In any discussion of society's response to a social problem, it is important to think about other ways to address the problem.

Knowledge, choice, behavior, and human welfare

We can conclude that science plays an important role in assisting individuals to make choices about enhancing personal and public welfare. Science provides evidence that can be used to support ways of understanding and treating human disease, ill ness, deformity, and dysfunction. But the relationships between scientific information and human choices, and between choices and behaviors, are not linear. Human choice allows individuals to choose against sound knowledge, and choice does not necessarily lead to particular actions.

Nevertheless, it is increasingly difficult for most of us to deny the claims of science. We are continually presented with great amounts of relevant scientific and medical knowledge that is publicly accessible. We are fortunate to have available a large amount of convincing data about the development, nature, and treatment of particular cancers. As a consequence, we might be encouraged to think about the relationships among knowledge, choice, behavior, and human welfare in the following ways:

One of the goals of this module is to encourage students to think in terms of these relationships, now and as they grow older.

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The following glossary was modified from the glossary on the National Cancer Institute's Web site, available from http://www.nci.nih.gov .

Type of blood cancer that originates in lymphatic cells of the bone marrow.

Type of blood cancer that involves accumulation of myeloid cells in the bone marrow and bloodstream.

Cancer that begins in cells that line certain internal organs.

Noncancerous tumor.

Protein often found in abnormal amounts in the blood of patients with liver cancer.

Mutagenesis assay (a measure of mutagenic ability) that involves specially engineered strains of bacteria. Because of the relationship between mutagenicity and carcinogenicity, the test is used as a rapid and relatively inexpensive first screening of untested chemicals that are suspected to be carcinogens.

Term used to describe cancer cells that divide rapidly and bear little or no resemblance to normal cells.

Blood vessel formation, which usually accompanies the growth of malignant tissue.

Type of cancer that begins in the lining of blood vessels.

Normal cellular process involving a genetically programmed series of events leading to the death of a cell.

Presenting no signs or symptoms of disease.

Hereditary disorder characterized by problems with muscle coordination, immunodeficiency, inadequate DNA repair, and an increased risk of developing cancer.

Benign (noncancerous) condition in which tissue has certain abnormal features.

Small, round cell found in the lower part, or base, of the epidermis, the outer layer of the skin.

Type of skin cancer that arises from the basal cells.

Not cancerous; does not invade nearby tissue or spread to other parts of the body.

A noncancerous growth that does not spread to other parts of the body.

Use of the body's immune system, either directly or indirectly, to fight cancer or to lessen side effects that may be caused by some cancer treatments. Also known as immuno-therapy, biotherapy, or biological response modifier therapy.

Removal of a sample of tissue, which is then examined under a microscope to check for cancer cells.

Soft, spongy tissue in the center of large bones that produces white blood cells, red blood cells, and platelets.

Removal of a small sample of bone marrow (usually from the hip) through a needle for examination under a microscope to see whether cancer cells are present.

Removal of a sample of tissue from the bone marrow with a large needle. The cells are checked to see whether they are cancerous. If cancerous plasma cells are found, the pathologist estimates how much of the bone marrow is affected. Bone marrow biopsy is usually done at the same time as bone marrow aspiration.

Procedure in which doctors replace marrow destroyed by treatment with high doses of anticancer drugs or radiation. The replacement marrow may be taken from the patient before treatment or may be donated by another person.

Technique to create images of bones on a computer screen or on film. A small amount of radioactive material is injected and travels through the bloodstream. It collects in the bones, especially in abnormal areas of the bones, and is detected by a scanner.

Internal radiation therapy using an implant of radioactive material placed directly into or near the tumor.

Gene located on chromosome 17 that normally helps restrain cell growth. Inheriting an altered version of BRCA1 predisposes an individual to breast, ovarian, or prostate cancer.

Gene located on chromosome 13 that scientists believe may account for 30 to 40 percent of all inherited breast cancer.

Surgery to rebuild a breast's shape after a mastectomy.

Type of non-Hodgkin lymphoma that most often occurs in young people between the ages of 12 and 30. The disease usually causes a rapidly growing tumor in the abdomen.

Term for a group of more than 100 diseases in which abnormal cells divide without control. Cancer cells can invade nearby tissues and can spread through the bloodstream and lymphocytic system to other parts of the body.

Any substance that is known to cause cancer.

Process by which normal cells are transformed into cancer cells.

Cancer that begins in the lining or covering of an organ.

Cancer that involves only the cells in which it began and has not spread to other tissues.

Laboratory test to measure the level of carcinoembryonic antigen (CEA), a substance that is sometimes found in an increased amount in the blood of patients with certain cancers.

Sequence of events by which cells enlarge and divide. Includes stages typically named G1, S, G2, and M.

Use of natural or laboratory-made substances to prevent cancer.

Treatment with anticancer drugs.

Type of blood cancer that involves overproduction of mature lymphocytes.

Type of blood cancer that involves accumulation of granulocytes (a type of white blood cell) in the bone marrow and bloodstream.

Research study that involves patients. Each study is designed to find better ways to prevent, detect, diagnose, or treat cancer and to answer scientific questions.

Procedure that uses a flexible fiber optic endoscope to examine the internal surface of the colon along its entire length.

Treatment in which two or more chemicals are used to obtain more effective results.

X-ray procedure that uses a computer to produce a detailed picture of a cross section of the body; also called CAT or CT scan.

Inhibition of cell division in normal (noncancerous) cells when they contact a neighboring cell.

See computed tomography.

Poisonous to cells. In chemotherapy, used to describe an agent that is poisonous to cancer cells.

Process of identifying a disease by the signs and symptoms.

Abnormal cells that are not cancer.

Atypical moles; moles whose appearance is different from that of common moles. Dysplastic nevi are generally larger than ordinary moles and have irregular and indistinct borders. Their color often is not uniform and ranges from pink or even white to dark brown or black; they usually are flat, but parts may be raised above the skin surface.

Confined to a specific area; an encapsulated tumor remains in a compact form.

Having to do with the mucous membrane that lines the cavity of the uterus.

Smoke that comes from the burning end of a cigarette and smoke that is exhaled by smokers. Also called ETS or secondhand smoke. Inhaling ETS is called involuntary or passive smoking.

Study of the factors that affect the prevalence, distribution, and control of disease.

Upper or outer layer of the two main layers of cells that make up the skin.

Virus that has been associated with the development of infectious mononucleosis and also with Burkitt lymphoma.

Female hormone produced by the ovary. Responsible for secondary sex characteristics and cyclic changes in the lining of the uterus and vagina.

Study of the causes of abnormal condition or disease.

Inherited condition in which several hundred polyps develop in the colon and rectum. These polyps have a high potential to become malignant.

Test to reveal blood hidden in the feces, which may be a sign of colon cancer.

Parts of fruits and vegetables that cannot be digested. Also called bulk or roughage.

Benign uterine tumor made up of fibrous and muscular tissue.

Treatment that alters genes (the basic units of heredity found in all cells in the body). In studies of gene therapy for cancer, researchers are trying to improve the body's natural ability to fight the disease or to make the tumor more sensitive to other kinds of therapy.

Inherited; having to do with information that is passed from parents to children through DNA in the genes.

Describes how closely a cancer resembles normal tissue of its same type, along with the cancer's probable rate of growth.

System for classifying cancer cells in terms of how malignant or aggressive they appear microscopically. The grading of a tumor indicates how quickly cancer cells are likely to spread and plays a role in treatment decisions.

Member of the herpes family of viruses. One type of herpes virus is sexually transmitted and causes sores on the genitals.

Treatment of cancer by removing, blocking, or adding hormones.

Viruses that generally cause warts. Some papillomaviruses are sexually transmitted. Some of these sexually transmitted viruses cause wartlike growths on the genitals, and some are thought to cause abnormal changes in cells of the cervix.

Precancerous condition in which there is an increase in the number of normal cells lining an organ.

Tests that produce pictures of areas inside the body.

Treatment that uses the body's natural defenses to fight cancer. Also called biotherapy or biological modifier response therapy.

Number of new cases of a disease diagnosed each year.

Number of new cases per year per 100,000 persons.

Preneoplastic change in the genetic material of cells caused by a chemical carcinogen. Cancer develops when initiated cells are subsequently exposed to the same or another carcinogen.

Cancer that has remained within the tissue in which it originated.

As related to cancer, the spread of cancer cells into healthy tissue adjacent to the tumor.

Cancer that has spread beyond the layer of tissue in which it developed.

Insoluble protein that is the major constituent of the outer layer of the skin, nails, and hair.

Area of abnormal tissue change.

Cancer of the blood cells.

Probability that a person, over the course of a lifetime, will develop cancer.

Rare family predisposition to multiple cancers, caused by an alteration in the p53 tumor suppressor gene.

An enclosed space bounded by an epithelial membrane; for example, the lumen of the gut.

Cancerous; can invade nearby tissue and spread to other parts of the body.

Skin pigment (substance that gives the skin its color). Dark-skinned people have more melanin than light-skinned people.

Cell in the skin that produces and contains the pigment called melanin.

Cancer of the cells that produce pigment in the skin. Melanoma usually begins in a mole.

Cancer growth (secondary tumors) that is anatomically separated from the site at which the original cancer developed.

To spread from one part of the body to another. When cancer cells metastasize and form secondary tumors, the cells in the metastatic tumor are like those in the original (primary) tumor.

Area on the skin (usually dark in color) that contains a cluster of melanocytes. See also nevus.

Population of cells that was derived by cell division from a single ancestral cell.

Number of deaths per 100,000 persons per year.

Any substance that is known to cause mutations.

Process by which mutations occur.

Change in the way cells function or develop, caused by an inherited genetic defect or an environmental exposure. Such changes may lead to cancer.

The largest of the 24 separate institutes, centers, and divisions of the National Institutes of Health. The NCI coordinates the federal government's cancer research program.

One of eight health agencies of the Public Health Service (the Public Health Service is part of the U.S. Department of Health and Human Services). Composed of 24 separate institutes, centers, and divisions, NIH is the largest biomedical research facility in the world.

Cell death.

Abnormal new growth of cells.

New growth of tissue. Can be referred to as benign or malignant.

Medical term for a spot on the skin, such as a mole. A mole is a cluster of melanocytes that usually appears as a dark spot on the skin.

One of the several types of lymphoma (cancer that develops in the lymphocytic system) that are not Hodgkin lymphoma. Hodgkin lymphoma is rare and occurs most often in people aged 15 to 34 and in people over 55. All other lymphomas are grouped together and called non-Hodgkin lymphoma.

Skin cancer that does not involve melanocytes. Basal cell cancer and squamous cell cancer are nonmelanoma skin cancers.

The Office of Science Education of the National Institutes of Health (NIH) coordinates science education activities at NIH and sponsors science education projects in-house.

Gene that normally directs cell growth but also can promote or allow the uncontrolled growth of cancer if damaged (mutated) by an environmental exposure to carcinogens or if damaged or missing because of an inherited defect.

Having the capacity to cause cancer.

Doctor who specializes in treating cancer. Some oncologists specialize in a particular type of cancer treatment. For example, a radiation oncologist specializes in treating cancer with radiation.

Study of tumors encompassing their physical, chemical, and biologic properties.

Surgical removal of one or both ovaries.

Gene that normally inhibits the growth of tumors, which can prevent or slow the spread of cancer.

Treatment that does not alter the course of a disease, but improves the quality of life.

Population of cells that was derived by cell division from more than one ancestral cell.

Mass of tissue that projects into the colon.

Term used to describe a condition that may or is likely to become cancer.

Growths in the colon that often become cancerous.

Female hormone produced by the ovaries and placenta; responsible for preparing the uterine lining for implantation of an early embryo.

Probable outcome or course of a disease; the chance of recovery.

Expression of the cancerous potential of initiated cells after exposure to the same or a different carcinogen.

Treatment administered or taken to prevent disease.

Gene that, when converted to an oncogene by a mutation or other change, can cause a normal cell to become malignant. Normal oncogenes function to control normal cell growth and differentiation.

Treatment with high-energy rays (such as X-rays) to kill cancer cells. The radiation may come from outside the body (external radiation) or from radioactive materials placed directly in the tumor (implant radiation). Also called radiotherapy.

Giving off radiation.

Radioactive gas that is released by uranium, a substance found in soil and rock. When too much radon is breathed in, it can damage lung cells and lead to lung cancer.

Comparison of the risk of developing cancer in persons with a certain type of exposure or characteristic with the risk in persons who do not have this exposure or characteristic.

Disappearance of the signs and symptoms of cancer. When this happens, the disease is said to be "in remission." A remission can be temporary or permanent.

Eye cancer caused by the loss of both copies of the tumor suppressor gene RB ; the inherited form typically occurs in childhood because one gene is missing from the time of birth.

Small RNA virus that has an RNA genome. Acts as a template for the production of the DNA that is integrated into the DNA of the host cell. Many retroviruses are believed to be oncogenic.

Something that increases the chance of developing a disease.

Chicken retrovirus that was the first virus shown to cause a malignancy.

Malignant tumor that begins in connective and supportive tissue.

Checking for disease when there are no symptoms.

Metastasis.

Surveillance, Epidemiology, and End Results Program of the National Cancer Institute. Started in 1973, SEER collects cancer incidence data in nine geographic areas with a combined population of approximately 9.6 percent of the total population of the United States.

Problem that occurs when treatment affects healthy cells. Common side effects of cancer treatment are fatigue, nausea, vomiting, decreased blood cell counts, hair loss, and mouth sores.

Any of the body cells except the reproductive cells.

Scale for rating sun-screens. Sunscreens with an SPF of 15 or higher provide the best protection from the sun's harmful rays.

Type of skin cancer that arises from the squamous cells.

Extent of a cancer, especially whether the disease has spread from the original site to other parts of the body.

Doing exams and tests to learn the extent of the cancer, especially whether it has spread from its original site to other parts of the body.

Cells from which all blood cells develop.

Substance that blocks the effect of the sun's harmful rays. Using lotions or creams that contain sunscreens can protect the skin from damage that may lead to cancer. See also SPF.

Proportion of patients alive at some point after their diagnosis of a disease.

Enzyme that is present and active in cells that can divide without apparent limit (for example, cancer cells and cells of the germ line). Telomerase replaces the missing repeated sequences of each telomere.

End of a chromosome. In vertebrate cells, each telomere consists of thousands of copies of the same DNA sequence, repeated again and again. Telomeres become shorter each time a cell divides; when one or more telomeres reaches a minimum length, cell division stops. This mechanism limits the number of times a cell can divide.

Male sex hormone.

Change that a normal cell undergoes as it becomes malignant.

Abnormal mass of tissue that results from excessive cell division. Tumors perform no useful body function. They may be either benign (not cancerous) or malignant (cancerous).

Substance in blood or other body fluids that may suggest that a person has cancer.

Gene in the body that can suppress or block the development of cancer.

Invisible rays that are part of the energy that comes from the sun. UV radiation can burn the skin and cause melanoma and other types of skin cancer. UV radiation that reaches the earth's surface is made up of two types of rays, UVA and UVB rays. UVB rays are more likely than UVA rays to cause sunburn, but UVA rays pass further into the skin. Scientists have long thought that UVB radiation can cause melanoma and other types of skin cancer. They now think that UVA radiation also may add to skin damage that can lead to cancer. For this reason, skin specialists recommend that people use sunscreens that block or absorb both kinds of UV radiation.

Process by which one of the two X chromosomes in each cell from a female mammal becomes condensed and inactive. This process assures that most genes on the X chromosome are expressed to the same extent in both males and females.

High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer.

Hereditary disease characterized by extreme sensitivity to the sun and a tendency to develop skin cancers. Caused by inadequate DNA repair.

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Groundbreaking cancer treatment may trigger more cancer – but here’s why you shouldn’t worry

Professor of Biomedical Sciences, Anglia Ruskin University

Disclosure statement

Justin Stebbing does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

Anglia Ruskin University (ARU) provides funding as a member of The Conversation UK.

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In the last few decades, scientists have finally learned to harness the immune system to successfully treat cancer . Although doctors often use immunotherapy drugs, another type of treatment uses patient’s cells to treat their own cancers.

Car-T therapy, short for “chimeric antigen receptor T-cell”, is a cutting-edge treatment that reprogrammes a patient’s immune cells to fight their cancer. This innovative approach involves taking T-cells, a type of white blood cell that plays a crucial role in the immune system, from a patient and modifying them in a laboratory to better recognise and attack cancer cells.

These enhanced T-cells are then multiplied and infused back into the patient, where they seek out and destroy cancer cells. Lots of data shows that in difficult-to-treat lymphomas, a type of cancer, patients can do so well.

In November 2023, the US Food and Drug Administration (FDA) announced an investigation into this celebrated cancer treatment. They were looking into whether Car-T therapy might be causing new cancers in some patients who had undergone the treatment . This was a significant concern given the therapy’s reputation as a revolutionary cancer-fighting strategy.

Initially, the FDA mentioned that it had observed 20 cases where patients developed new immune-cell cancers, such as lymphomas or leukaemias, which are types of blood cell cancer, after receiving Car-T therapy. This prompted questions about who these patients were, how many such cases existed and what other treatments they might have received before Car-T therapy.

By March 2024, the FDA had documented 33 such cases among around 30,000 treated patients. Consequently, all Car-T therapies now carry a boxed warning about the potential risk of developing secondary cancers. The European Medicines Agency also started its own investigation into the matter .

Despite these concerns, it is still unclear whether the new cancers are directly caused by the Car-T cells or whether other factors are involved. It is also important to note that these cancers are very rare – as data published this month shows .

Many cancer treatments come with a risk of secondary malignancies and, of course, the cancer returning. And patients receiving Car-T therapy often have had several other treatments that could also contribute to the risk. Researchers are now working to determine if Car-T therapy is a contributing factor or the primary cause of these new cancers.

Car-T therapy was initially used for patients with no other treatment options, but it has since been approved as a second-line treatment for certain types of blood cancers, like lymphoma and multiple myeloma . Scientists are also exploring its potential for treating solid tumours including hard to treat brain cancers , autoimmune diseases , ageing , HIV and other conditions.

The process of creating Car-T cells involves using viruses to insert new genetic material into T-cells. These viruses, called retroviruses, are engineered to carry the gene for a chimeric antigen receptor (Car) into the T-cells.

Massive benefits

While these retroviruses are modified to be safe, there is always a risk that the new genetic material could disrupt other important genes and potentially lead to cancer – a phenomenon known as “insertional mutagenesis”. This means new genetic material is added to a cell .

This risk isn’t new. About 20 years ago, gene therapy treatments for severe combined immunodeficiency syndrome using similar retroviruses led to leukaemia in some patients . As a result, scientists have worked to improve the safety of these viral vectors. The FDA now requires thorough testing to ensure that the viruses used in Car-T therapy cannot replicate and cause harm.

Despite these findings, the most important thing to emphasise is that secondary cancers remain rare and these cell therapies can have massive benefits in very sick people.

The new review of patients treated with Car-T therapies at various centres found that only a small percentage developed secondary cancers, and most were not the type directly linked to the Car-T treatment . This suggests that while there is a risk, it is relatively low compared to the immediate threat posed by the patient’s existing cancer.

Medical professionals now inform patients about the potential but rare risk of secondary cancers when discussing Car-T therapy. For most patients, especially those with advanced cancers, the potential benefits of Car-T therapy far outweigh these risks.

As mentioned, Car-T therapy is also being investigated for other applications beyond cancer. For instance, it has shown promise in treating autoimmune diseases such as lupus and even in preventing organ transplant rejection . The potential uses for Car-T cells are continually expanding, offering hope for treating a wide range of diseases.

Ultimately, while the risk of secondary cancers from Car-T therapy is a serious consideration, the benefits for many patients are significant and far outweigh this small risk. Research will continue to refine these treatments and improve their safety.

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• DOI: 10.1158/1055-9965.EPI-24-0305
• Corpus ID: 270617384

Use of non-steroidal anti-inflammatory drugs and pancreatic cancer risk in the Women's Health Initiative.

• Theodore M. Brasky , Leah R Jager , +5 authors Juhua Luo
• Published in Cancer Epidemiology… 20 June 2024

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Environmental Factor

Your online source for niehs news, papers of the month.

Extramural By Julie Leibach

Increased wildfire activity could contribute to more infectious marine bacteria

Exposure to ash from wildfires that occur where nature meets development may enhance the growth of more infectious marine bacteria, NIEHS-funded researchers reported. Their findings provide insight into how extreme weather associated with climate change may contribute to disease spread.

Climate change is fueling wildfires that are encroaching into urban areas, producing ash containing metals that could eventually infiltrate aquatic ecosystems. However, little research exists on how wildfire ash might affect the growth and toxicity of Vibrio vulnificus, a bacterium responsible for most seafood-related deaths in the U.S.

The researchers collected ash from a burned vegetated area and a burned residential structure. Next, they treated batches of V. vulnificus with increasing concentrations of either vegetation ash, characterized by its iron levels, or structural ash, containing chromium, copper, and arsenic. In a separate experiment, they exposed the microorganisms to structural ash or vegetation ash for 24 hours and analyzed gene expression, or activity.

For vegetation and structural ash, higher metal content corresponded to slower V. vulnificus growth rates, suggesting that certain compositions of wildfire ash are toxic to the bacteria. However, V. vulnificus growth initially spiked after several hours of exposure to vegetation ash with low iron levels, indicating the bacteria could proliferate under the right conditions. Additionally, both types of ash increased expression of genes related to antibiotic and metal resistance, with more prominent effects tied to structural ash exposure.

The findings suggest that ash from fires occurring where wildlands mingle with buildings could contribute to the spread of more infectious strains of V. vulnificus, according to the authors. A better understanding of the effects of mixed ash on bacterial adaptation could inform models for predicting potential V. vulnificus outbreaks, they added.

Citation : Correa Velez KE, Alam M, Baalousha MA, Norman RS. 2024. Wildfire ashes from the wildland-urban interface alter Vibrio vulnificus growth and gene expression . Environ Sci Technol 58(19):8169-8181.

Health intervention shows reduced arsenic exposures among tribes

Exposure to arsenic from private wells declined among American Indian communities that received free kitchen faucet filters and periodic health check-ins through phone calls and home visits, according to NIEHS-funded researchers. Participants also reported greater use of filtered water for cooking and drinking, and an increased understanding of vulnerability to arsenic in drinking water.

Studies have found connections between chronic arsenic exposure and health problems, such as cardiovascular disease, diabetes, and some cancers among American Indians, who often live in rural communities that rely on private wells. However, little research has focused on developing and evaluating effective interventions to reduce those exposures among private well users.

The team recruited participants from a Northern Great Plains American Indian Nation whose private wells contained high arsenic levels. After receiving community input on study design and implementation, the researchers randomly divided 50 households into two groups. Both received free filter installation at the kitchen faucet, as well as three check-in phone calls from a mobile health program. One group also received three home visits from a local health promoter.

The team measured urinary arsenic levels in participants before filter installation and during a two-year follow-up period. By the end of the study, urinary arsenic levels had decreased by 47% across groups, with no significant difference between interventions. Self-reported exclusive use of filtered water for cooking and drinking tripled over that time.

The results show that point-of-use filter installation, combined with mobile health check-ins, can reduce arsenic exposure among American Indian communities, according to the authors. Given that public health interventions involving in-person visits can be costly and difficult to implement in rural areas, the findings could inform feasible arsenic mitigation programs among other private well users.

Citation : George CM, Zacher T, Endres K, Richards F, Bear Robe L, Harvey D, Best LG, Red Cloud R, Black Bear A, Skinner L, Cuny C, Rule A, Schwab KJ, Gittelsohn J, Glabonjat RA, Schilling K, O'Leary M, Thomas ED, Umans J, Zhu J, Moulton LH, Navas-Acien A. 2024. Effect of an arsenic mitigation program on arsenic exposure in American Indian communities: a cluster randomized controlled trial of the community-led Strong Heart Water Study program . Environ Health Perspect 132(3):37007.

New cell-based approach identifies genetic sensitivity to toxic exposures

NIEHS-funded researchers developed a new cell-based approach for studying how environmental contaminants, like arsenic, interact with our genes to affect health. The results could help identify molecular pathways underlying genetic sensitivity and resistance to environmental toxicants.

Arsenic is a widespread groundwater contaminant that can damage DNA and cells through a process called oxidative stress. However, the likelihood and severity of health outcomes associated with exposure depend on a person’s genetic makeup. Because studying genetic susceptibility in humans is difficult, research with genetically diverse rodent cells can shed light on gene-environment interactions.

The researchers used a minimally invasive method to collect mouse cells representing 226 genetically distinct lines. Next, they exposed the cells to a metabolic byproduct of arsenic at eight increasing concentrations for 24 hours. After exposure, the team stained the cells with fluorescent dyes so they could easily track morphological changes, which signified sensitivity to the exposure. Using a genetic mapping technique, they linked genetic variation in the cell lines to variation in the morphological responses to arsenic.

In parallel, the team evaluated gene expression in the cells and examined previously published findings to identify variation in genes and molecular pathways that regulate sensitivity to arsenic. Those variations related to arsenic transport, oxidative stress, and DNA damage. Although some of the identified genes had known ties to arsenic exposure, other genes — such as Xrcc2, involved in DNA damage repair — were new associations.

The findings provide a novel approach for studying interactions between environmental exposures and genes within a genetically diverse population, according to the authors. The technique could minimize the reliance on animal testing in chemical risk assessments, they added.

Citation : O’Connor C, Keele GR, Martin W, Stodola T, Gatti D, Hoffman BR, Korstanje R, Churchill GA, Reinholdt LG. 2024. Unraveling the genetics of arsenic toxicity with cellular morphology QTL . PLoS Genet 20(4):e1011248.

Cancer-preventive mechanisms of omega-3 fatty acids uncovered

Researchers funded by NIEHS identified mechanisms through which omega-3 fatty acids (omega-3s) may protect against lung cancer caused by exposure to polycyclic aromatic hydrocarbons (PAHs) in mice. The findings could inform lung cancer prevention strategies.

Extensive research has shown that lung cancer stems from exposure to cancer-causing chemicals in the environment, including PAHs found in air pollution and cigarette smoke. Studies suggest that omega-3s have anticancer effects, partially by inhibiting certain proteins called cytochrome P450 enzymes (CYP). Those proteins can convert PAHs to harmful derivatives that can damage DNA, potentially resulting in genetic mutations, or changes, that cause cancer. However, the mechanisms of omega-3 protection are not well understood.

Building on earlier work, the researchers explored how omega-3s might prevent cancer in mice exposed to PAHs. First, they fed omega-3 diets to regular mice and to groups of mice missing one of three CYP genes, then exposed them to PAHs. Next, the team used regular mice to examine how omega-3s might stop DNA damage. Finally, they investigated whether omega-3s interact with other cancer-related genes.

Following PAH exposure, levels of DNA damage declined in all mice fed omega-3s, including in those missing the cytochrome gene Cyp1b1. In mice with intact CYP genes, molecular analysis showed that omega-3s inhibited expression of CYP1B1, which reportedly plays a key role in converting PAHs to DNA-damaging derivatives, according to the authors. Additional experiments showed that omega-3s increased expression of a tumor-suppressing gene called RUNX3.

Taken together, the results suggest that omega-3s inhibit DNA damage via a CYP pathway and also promote tumor suppression. Future studies should explore the possibility of incorporating supplemental omega-3s into cancer prevention efforts, according to the authors.

Citation : Xia G, Zhou G, Jiang W, Chu C, Wang L, Moorthy B. 2024. Attenuation of polycyclic aromatic hydrocarbon (PAH)-induced carcinogenesis and tumorigenesis by omega-3 fatty acids in mice in vivo . Int J Mol Sci 25(7):3781.

(Julie Leibach is a senior science writer at MDB, Inc., a contractor for the NIEHS Division of Extramural Research and Training.)

Read the current Superfund Research Program Research Brief . New issues are published on the first Wednesday of every month.

Why you can get sunburnt through a window but it won't help with your vitamin D needs

A warm spot by a sunny window can be the ideal place to ride out a winter cold snap. 

But exposure to sunlight through a window has implications for your health. Here's what you need to know.

First, how does sunlight affect the skin? Damage and vitamin D

Sunlight is the main source of ultraviolet (UV) radiation. Made up of UVA and UVB rays, UV radiation penetrates the skin and can cause sunburn, skin cancer, skin ageing and eye damage.

Professor Anne Cust, chair of Cancer Council's National Skin Cancer Committee, says UV radiation is often confused with infrared radiation, which we feel as heat from the sun.

"The temperature does not affect UV levels , and in fact, the UV can be as high on a cool day as it is on a hot one."

Both longer-wavelength UVA and shorter-wavelength UVB cause sunburn and skin cancer.

UVA is primarily responsible for photo-ageing, penetrating deeper into the dermis, breaking down collagen and elastin and causing cellular damage.

"UVB is a shorter wavelength than UVA, so it penetrates the skin more superficially," dermatologist Leona Yip says.

Our bodies also need UVB rays for vitamin D synthesis , which occurs in the skin's epidermis and is essential for calcium absorption and bone health.

Can you get sunburnt through a window?

Yes — although it depends on the type of window glass .

"While all types of commercial and automobile glass block the majority of UVB (vitamin D-generating) radiation, the degree of UVA radiation transmission depends on the type of glass," Professor Cust says.

"Laminated glass used on car windscreens provides better UV protection than tempered glass, blocking 98 per cent of UVA radiation compared to 79 per cent. Similarly, laminated glass used in buildings blocks UVA radiation completely, while tempered building glass can allow around 70 per cent of UVA transmissions.

"While untinted glass can reduce the transmission of UV radiation, it does not completely block it, which means you can still get sunburnt if you spend a lot of time next to an untinted window when the UV [Index] is three or above" (which it regularly is in Australia).

Cancer Council recommends people who spend long periods in a vehicle or close to a window use sun protection , such as a long-sleeved shirt, sunglasses and an SPF 30 or higher sunscreen.

Dr Yip recommends applying sunscreen every morning , even if you spend most of the day indoors.

"For people who work from home … sitting a few metres away from a glass window or a glass door, you still get UVA penetrating through it," she says.

"Or you might go out and get the mail, or go out and walk your dog, or hang out the washing — it might be 10 or 15 minutes, but for many fair-skinned people, 10 to 15 minutes is all you need to start getting a sunburn."

Can you get vitamin D from the sun through a window?

The short answer is no .

Glass blocks 95 per cent of UVB rays , which means sun exposure through a window won't trigger vitamin D production.

This matters for your health. Vitamin D is a pro-hormone — a molecule the body turns into a hormone required for calcium absorption.

Vitamin D deficiency can cause rickets, osteoporosis and osteomalacia and affects more than one in three Australian adults.

So, what is a safe way to get enough sun to meet our vitamin D needs?

While small amounts of vitamin D can be found in foods such as oily fish and eggs, the best source is sunlight.

How much time you need in the sun to generate vitamin D depends on several factors , including your skin colour, what you're wearing, where you live, the time of year and the UV index.

"When the UV is three or above, which is almost every day in summer, most Australians maintain adequate vitamin D levels just by spending a few minutes outdoors on most days of the week," Professor Cust says.

"In the cooler months in some southern parts of Australia, when the UV drops below three, it is safe to go outside without sun protection early in the morning and later afternoon, however sun protection is recommended once the UV level reaches three or above."

Dr Yip says a supplement is an option for people with a deficiency in vitamin D, particularly those with very fair skin or a family history of skin cancer.

But for most healthy adults, according to a 2019 review published in the Medical Journal of Australia, they are of little benefit.

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What Causes Blood in Urine With No Pain in Females?

• Common Causes

Other Possible Causes

• Risk Factors
• When to See a Provider

Hematuria is the medical term for blood in the urine. The two types, which can occur with or without pain, are:

• Gross hematuria means blood in the urine is visible to the naked eye, making it look orange, pink, bright or dark red, or tea-colored.
• Microscopic hematuria means the urine looks normal—yellow or clear—but blood can be seen under a microscope.

Painless hematuria in females has many potential causes, like vigorous exercise, infection, kidney disease, or a side effect of a medication. Most seriously, it can be a sign of a urinary tract cancer like bladder or kidney cancer.

This article reviews the possible causes of painless hematuria in females and when to see a healthcare provider. It also briefly explores risk factors for bladder and kidney cancer.

TravelCouples / Getty Images

A Note on Gender and Sex Terminology

Verywell Health acknowledges that  sex and gender  are related concepts, but they are not the same. To accurately reflect our sources, this article uses terms like “female,” “male,” “woman,” and “man” as the sources use them.

Common Causes of Blood in Urine With No Pain

Hematuria occurs when red blood cells enter the urine from an organ within the urinary tract system in the following ways:

• The kidneys are bean-shaped organs that serve several vital functions, including removing extra salt, water, and waste products from the body through urine.
• The ureters are thin muscular tubes that carry urine from the kidneys to the bladder.
• The bladder is a hollow organ in the lower abdomen that stores urine.
• The urethra is a short tube that carries urine from the lower part of the bladder to the outside of the body.

Potential causes of painless hematuria in females include the following.

Strenuous or prolonged exercises, such as long-distance running, rowing, or swimming, can cause painless hematuria.

Experts suspect blood vessels feeding the kidney narrow to improve blood supply to the exercising muscles. As a result of this blood vessel narrowing, red blood cells leak into the urine.

Hematuria following exercise can be gross or microscopic and is related to the intensity or degree of the activity rather than its duration.

It's generally short-lived, resolving within a day or two, although it can last up to a week.

Other causes of exercise-induced hematuria are:

• Direct trauma to the kidney or bladder from contact sports (e.g., boxing or karate)
• Biking-related hematuria in females that's caused by the repeated collision of the perineum (the area between the anus and vagina) with the bicycle seat
• Bladder bruising from long-distance running, as the bladder walls repeatedly get bumped during the impact of running

While relatively common, exercise-induced hematuria should be investigated to rule out injury to the urinary tract system or concerning, although less common, findings like urinary tract cancer.

Seeking evaluation is especially crucial if your exercise-induced hematuria lasts more than one week, you are an adult over the age of 40, or you have risk factors for urinary tract cancer, like a history of smoking.

Injury to any organ in the urinary tract system can cause hematuria, although the kidneys are the most vulnerable, involved in a little over 3% of all trauma cases.

Examples of such forms of trauma include:

• Blunt trauma like from a motor vehicle accident, fall, pedestrian accident, motorcycling, and playground accidents (in children)
• Penetrating trauma from a firearm or stab wound

Symptoms of trauma to a urinary tract organ like the kidney can cause gross or microscopic hematuria.

Depending on the extent of the injury, the hematuria may be painless or associated with other symptoms like tenderness and swelling of the flank (the area in your lower back just below your lower ribs), bruising, and rib fractures.

Urinary Tract Infection (UTI)

Urinary tract infections are usually caused by bacteria. Hematuria is a common symptom of a UTI, although other urinary symptoms, namely discomfort or pain, are also typically present.

Two types of UTIs include:

• Cystitis occurs when bacteria travel to and infect the bladder. Symptoms may include burning pain when urinating, frequent and strong urges to urinate, tenderness in the lower abdomen, and visible blood in the urine.
• Pyelonephritis occurs when bacteria travel to and infect one or both kidneys. Symptoms may include fever, chills, flank pain, nausea and vomiting, and sometimes symptoms of cystitis.

Kidney or Bladder Stones

Kidney stones are hard lumps of minerals that anchor themselves within the kidney.

Most people with kidney stones—what's known as nephrolithiasis —have gross or microscopic hematuria.

Depending on factors like the size of the stone and whether it's blocking the flow of urine from the kidney to the bladder, other symptoms may be present, such as:

• Waves of pain, often severe, occurring in the flank or lower abdomen and traveling to the groin area
• Nausea or vomiting
• Strong urge to urinate
• Pain when urinating

Like kidney stones, bladder stones are hardened mineral deposits anchored in the bladder. However, they often originate in the kidney, and their symptoms are similar to those of kidney stones.

Kidney Diseases

Certain kidney diseases can cause hematuria. A common cause is glomerulonephritis , a disease affecting the part of the kidney responsible for filtering blood.

There are several types of glomerulonephritis, with unique causes (e.g., lupus , diabetes, or viral infection) and varying degrees of severity.

In addition to hematuria, other symptoms include proteinuria (protein in the urine), which causes foamy urine, and swelling in the ankles, hands, and around the eyes.

Bladder or kidney cancer can cause painless hematuria.

Bladder Cancer

Blood in the urine is the predominant initial symptom of bladder cancer. It's typically painless, gross (but can be microscopic), and intermittent, appearing one day and disappearing the next.

Other potential symptoms of bladder cancer , especially in the early stages, are similar to those seen with a urinary tract infection, like burning during urination and having a frequent and strong urge to urinate.

Overall, females have a 3 to 4 times lower risk of developing bladder cancer compared to males. Still, females are more likely to have advanced disease upon diagnosis.

Kidney Cancer

Globally, kidney cancer is the 10th most common type of cancer in females.

Most cases are diagnosed between the ages of 60 and 70 years. Like bladder cancer, kidney cancer is more common in males.

Gross or microscopic hematuria without pain is a possible sign of kidney cancer, along with fever and symptoms of cystitis with no infection. Flank or lower back pain on one side that feels deep and may be located beneath the rib cage may also occur.

Angiomyolipomas

Angiomyolipoma , while rare, is the most common benign (noncancerous) kidney tumor, and it usually develops in females.

Angiomyolipomas are composed of blood vessels, muscle, and fat cells. They are associated with the genetic condition tuberous sclerosis but can also develop randomly.

Symptoms are often absent, but if they are present, they can include painless hematuria and flank pain. If they enlarge and rupture (break open), they can cause life-threatening bleeding, requiring immediate treatment.

While not an exhaustive list, other possible causes of hematuria include:

• Adverse effects from a urinary tract-related procedure, like placing or removing a Foley catheter or a kidney biopsy
• Radiation-induced bladder inflammation (radiation cystitis)
• Blood vessel problems—for example, blockage of the main artery feeding the kidney

Side effects from medications or various inherited diseases may also cause hematuria.

 Medication Side Effects

Compared to other drugs, blood thinners are the most frequent cause of hematuria.

Of blood thinners, research suggests that Jantoven (warfarin) and Xarelto (rivaroxaban) perhaps present the most risk of triggering hematuria, while Eliquis (apixaban) is the safest.

Other drugs linked to serious hematuria episodes, specifically hemorrhagic cystitis , include the chemotherapy drug cyclophosphamide .

Inherited Diseases

A few diseases that run in families may cause hematuria. Examples include:

• Polycystic kidney disease is characterized by cysts (fluid-filled punches) that grow within the kidneys, potentially affecting their function.
• Alport syndrome is associated with kidney disease, hearing loss, and eye problems.
• Sickle cell disease is associated with abnormally shaped red blood cells that can block blood flow in blood vessels, causing severe pain episodes. Hematuria may develop if the kidneys' internal blood vessels are affected.

What Are the Risk Factors for Hematuria?

Risk factors for hematuria depend on the underlying cause.

For example, factors that increase a person's risk for bladder cancer include:

• Smoking and tobacco use
• Increased body mass index (BMI)
• Workplace exposure to certain chemicals like hair dyes and diesel fumes
• Exposure to certain drugs, like the diabetes drug Actos ( pioglitazone ) or cyclophosphamide
• Infection with a parasitic worm, schistosomiasis (very rare in the United States)

Likewise, risk factors for kidney cancer include:

• High blood pressure
• Tobacco use, including smoking
• Having obesity
• Workplace exposure to trichloroethylene
• Family history of certain genetic syndromes, especially von Hippel-Lindau disease

When to Contact a Healthcare Provider

All cases of hematuria require investigation, with gross hematuria often requiring a more extensive workup. If you are experiencing blood in your urine, contact a healthcare provider.

All said, it's important to note that blood in the urine, whether pink, red, or tea-colored, is not always due to red blood cells. Notably, uterine or vaginal bleeding may be mistaken for hematuria.

Moreover, dehydration can cause the urine to turn a dark yellow, sometimes mistaken for blood.

Other causes in people of any sex include:

• Myoglobin (a protein found in muscle) in urine may occur from rhabdomyolysis (when muscle tissue becomes severely injured, leading to the release of myoglobin)
• Most types of porphyria , a rare group of inherited disorders associated with problems making heme, are an important component of hemoglobin.
• Certain medications, like rifampin (a tuberculosis drug) and Pyridium ( phenazopyridine ), a drug that relieves symptoms of a UTI
• Certain foods, namely beets and rhubarb

Hematuria is red blood cells in the urine. It can be associated with or without pain and be gross (visible) or microscopic (only visible under a microscope).

Multiple potential causes of painless hematuria exist, including strenuous or prolonged exercise, kidney disease, and, most seriously, bladder or kidney cancer.

Bladder or kidney infections and stones can also cause hematuria, although they are generally associated with discomfort when urinating and lower abdominal/flank pain, respectively.

If you are experiencing hematuria, see a healthcare provider for further evaluation. While it may be a transient (passing) or benign finding, you will want to get to the root cause so you can be treated, if necessary.

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By Colleen Doherty, MD Dr. Doherty is a board-certified internist and writer living with multiple sclerosis. She is based in Chicago.