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Other names Malignant tumor, malignant neoplasm
Tumor Mesothelioma2 legend.jpg
A coronal CT scan showing a malignant mesothelioma
Legend: →  tumor  ←, ✱ central pleural effusion, 1 & 3  lungs, 2  spine, 4  ribs, 5  aorta, 6  spleen, 7 & 8  kidneys, 9  liver
Specialty Oncology
SymptomsLump, abnormal bleeding, prolonged cough, unexplained weight loss, change in bowel movements [1]
Risk factors Tobacco, obesity, poor diet, lack of physical activity, excessive alcohol, certain infections [2] [3]
Treatment Radiation therapy, surgery, chemotherapy, and targeted therapy. [2] [4]
PrognosisAverage five year survival 66% (USA) [5]
Frequency90.5 million (2015) [6]
Deaths8.8 million (2015) [7]


The term cell growth is used in the contexts of biological cell development and cell division (reproduction). When used in the context of cell development, the term refers to increase in cytoplasmic and organelle volume, as well as increase in genetic material following the replication during S phase. This is not to be confused with growth in the context of cell division, referred to as proliferation, where a cell, known as the "mother cell", grows and divides to produce two "daughter cells".

Benign tumor disease of cellular proliferation that results in abnormal growths in the body which lack the ability to metastasize

A benign tumor is a mass of cells (tumor) that lacks the ability to invade neighboring tissue or metastasize. These do not spread into, or invade, nearby tissues; however, they can sometimes be quite large. When removed, benign tumors usually do not grow back, whereas malignant tumors sometimes do. Unlike most benign tumors elsewhere in the body, benign brain tumors can be life threatening. Benign tumors generally have a slower growth rate than malignant tumors and the tumor cells are usually more differentiated. They are typically surrounded by an outer surface or remain with the epithelium. Common examples of benign tumors include moles and uterine fibroids.

Cancer signs and symptoms

Cancer symptoms are changes in the body caused by the presence of cancer. They are usually caused by the effect of a cancer on the part of the body where it is growing, although the disease can cause more general symptoms such as weight loss or tiredness. There are more than 100 different types of cancer with a wide range of different signs and symptoms which can manifest in different ways.


Tobacco use is the cause of about 22% of cancer deaths. [2] Another 10% are due to obesity, poor diet, lack of physical activity or excessive drinking of alcohol. [2] [9] [10] Other factors include certain infections, exposure to ionizing radiation and environmental pollutants. [3] In the developing world, 15% of cancers are due to infections such as Helicobacter pylori , hepatitis B, hepatitis C, human papillomavirus infection, Epstein–Barr virus and human immunodeficiency virus (HIV). [2] These factors act, at least partly, by changing the genes of a cell. [11] Typically, many genetic changes are required before cancer develops. [11] Approximately 5–10% of cancers are due to inherited genetic defects from a person's parents. [12] Cancer can be detected by certain signs and symptoms or screening tests. [2] It is then typically further investigated by medical imaging and confirmed by biopsy. [13]

Obesity medical condition in which excess body fat harms health

Obesity is a medical condition in which excess body fat has accumulated to an extent that it may have a negative effect on health. People are generally considered obese when their body mass index (BMI), a measurement obtained by dividing a person's weight by the square of the person's height, is over 30 kg/m2; the range 25–30 kg/m2 is defined as overweight. Some East Asian countries use lower values. Obesity increases the likelihood of various diseases and conditions, particularly cardiovascular diseases, type 2 diabetes, obstructive sleep apnea, certain types of cancer, osteoarthritis, and depression.

Diet (nutrition) the sum of food consumed by an organism

In nutrition, diet is the sum of food consumed by a person or other organism. The word diet often implies the use of specific intake of nutrition for health or weight-management reasons. Although humans are omnivores, each culture and each person holds some food preferences or some food taboos. This may be due to personal tastes or ethical reasons. Individual dietary choices may be more or less healthy.

Sedentary lifestyle

A sedentary lifestyle is a type of lifestyle involving little or no physical activity. A person living a sedentary lifestyle is often sitting or lying down while engaged in an activity like reading, socializing, watching television, playing video games, or using a mobile phone/computer for much of the day. A sedentary lifestyle can potentially contribute to ill health and many preventable causes of death.

Many cancers can be prevented by not smoking, maintaining a healthy weight, not drinking too much alcohol, eating plenty of vegetables, fruits and whole grains, vaccination against certain infectious diseases, not eating too much processed and red meat and avoiding too much sunlight exposure. [14] [15] Early detection through screening is useful for cervical and colorectal cancer. [16] The benefits of screening in breast cancer are controversial. [16] [17] Cancer is often treated with some combination of radiation therapy, surgery, chemotherapy and targeted therapy. [2] [4] Pain and symptom management are an important part of care. [2] Palliative care is particularly important in people with advanced disease. [2] The chance of survival depends on the type of cancer and extent of disease at the start of treatment. [11] In children under 15 at diagnosis, the five-year survival rate in the developed world is on average 80%. [18] For cancer in the United States, the average five-year survival rate is 66%. [5]

Alcohol (drug) active ingredient in alcoholic beverages

Alcohol, also known by its chemical name ethanol, is a psychoactive substance that is the active ingredient in drinks such as beer, wine, and distilled spirits. It is one of the oldest and most common recreational substances, causing the characteristic effects of alcohol intoxication ("drunkenness"). Among other effects, alcohol produces a mood lift and euphoria, decreased anxiety, increased sociability, sedation, impairment of cognitive, memory, motor, and sensory function, and generalized depression of central nervous system function. Ethanol is a type of chemical compound known as an alcohol, and is the only type of alcohol that is found in alcoholic beverages or is commonly used for recreational purposes; other alcohols such as methanol and isopropyl alcohol are toxic.

Vaccination administration of a vaccine to protect against disease

Vaccination is the administration of a vaccine to help the immune system develop protection from a disease. Vaccines contain a microorganism in a weakened or killed state, or proteins or toxins from the organism. In stimulating the body's adaptive immunity, they help prevent sickness from an infectious disease. When a sufficiently large percentage of a population has been vaccinated, herd immunity results. The effectiveness of vaccination has been widely studied and verified. Vaccination is the most effective method of preventing infectious diseases; widespread immunity due to vaccination is largely responsible for the worldwide eradication of smallpox and the elimination of diseases such as polio and tetanus from much of the world.

Processed meat

Processed meat is considered to be any meat which has been modified in order either to improve its taste or to extend its shelf life. Methods of meat processing include salting, curing, fermentation, and smoking. Processed meat is usually composed of pork or beef, but also poultry, while it can also contain offal or meat by-products such as blood. Processed meat products include bacon, ham, sausages, salami, corned beef, jerky, canned meat and meat-based sauces. Meat processing includes all the processes that change fresh meat with the exception of simple mechanical processes such as cutting, grinding or mixing.

In 2015, about 90.5 million people had cancer. [6] About 14.1 million new cases occur a year (not including skin cancer other than melanoma). [11] It caused about 8.8 million deaths (15.7% of deaths). [7] The most common types of cancer in males are lung cancer, prostate cancer, colorectal cancer and stomach cancer. [19] In females, the most common types are breast cancer, colorectal cancer, lung cancer and cervical cancer. [11] If skin cancer other than melanoma were included in total new cancer cases each year, it would account for around 40% of cases. [20] [21] In children, acute lymphoblastic leukemia and brain tumors are most common, except in Africa where non-Hodgkin lymphoma occurs more often. [18] In 2012, about 165,000 children under 15 years of age were diagnosed with cancer. [19] The risk of cancer increases significantly with age, and many cancers occur more commonly in developed countries. [11] Rates are increasing as more people live to an old age and as lifestyle changes occur in the developing world. [22] The financial costs of cancer were estimated at $1.16 trillion USD per year as of 2010. [23]

Skin cancer class of skin illnesses, tumor or cancer of the skin

Skin cancers are cancers that arise from the skin. They are due to the development of abnormal cells that have the ability to invade or spread to other parts of the body. There are three main types of skin cancers: basal-cell skin cancer (BCC), squamous-cell skin cancer (SCC) and melanoma. The first two, along with a number of less common skin cancers, are known as nonmelanoma skin cancer (NMSC). Basal-cell cancer grows slowly and can damage the tissue around it but is unlikely to spread to distant areas or result in death. It often appears as a painless raised area of skin, that may be shiny with small blood vessels running over it or may present as a raised area with an ulcer. Squamous-cell skin cancer is more likely to spread. It usually presents as a hard lump with a scaly top but may also form an ulcer. Melanomas are the most aggressive. Signs include a mole that has changed in size, shape, color, has irregular edges, has more than one color, is itchy or bleeds.

Lung cancer cancer in the lung

Lung cancer, also known as lung carcinoma, is a malignant lung tumor characterized by uncontrolled cell growth in tissues of the lung. This growth can spread beyond the lung by the process of metastasis into nearby tissue or other parts of the body. Most cancers that start in the lung, known as primary lung cancers, are carcinomas. The two main types are small-cell lung carcinoma (SCLC) and non-small-cell lung carcinoma (NSCLC). The most common symptoms are coughing, weight loss, shortness of breath, and chest pains.

Prostate cancer male reproductive cancer

Prostate cancer is the development of cancer in the prostate, a gland in the male reproductive system. Most prostate cancers are slow growing; however, some grow relatively quickly. The cancer cells may spread from the prostate to other areas of the body, particularly the bones and lymph nodes. It may initially cause no symptoms. In later stages, it can lead to difficulty urinating, blood in the urine or pain in the pelvis, back, or when urinating. A disease known as benign prostatic hyperplasia may produce similar symptoms. Other late symptoms may include feeling tired due to low levels of red blood cells.

Video summary (script)


Cancers are a large family of diseases that involve abnormal cell growth with the potential to invade or spread to other parts of the body. [2] [8] They form a subset of neoplasms. A neoplasm or tumor is a group of cells that have undergone unregulated growth and will often form a mass or lump, but may be distributed diffusely. [24] [25]

Neoplasm Abnormal mass of tissue as a result of abnormal growth or division of cells

A neoplasm is a type of abnormal and excessive growth, called neoplasia, of tissue. The growth of a neoplasm is uncoordinated with that of the normal surrounding tissue, and it persists growing abnormally, even if the original trigger is removed. This abnormal growth usually forms a mass. When it forms a mass, it may be called a tumor.

All tumor cells show the six hallmarks of cancer. These characteristics are required to produce a malignant tumor. They include: [26]

The Hallmarks of Cancer 2000 paper by Hanahan and Weinberg

"The Hallmarks of Cancer" is a seminal peer-reviewed article published in the journal Cell in January 2000 by the cancer researchers Douglas Hanahan and Robert Weinberg.

The progression from normal cells to cells that can form a detectable mass to outright cancer involves multiple steps known as malignant progression. [26] [27]

Signs and symptoms

Symptoms of cancer metastasis depend on the location of the tumor. Symptoms of cancer metastasis.svg
Symptoms of cancer metastasis depend on the location of the tumor.

When cancer begins, it produces no symptoms. Signs and symptoms appear as the mass grows or ulcerates. The findings that result depend on the cancer's type and location. Few symptoms are specific. Many frequently occur in individuals who have other conditions. Cancer is a "great imitator". Thus, it is common for people diagnosed with cancer to have been treated for other diseases, which were hypothesized to be causing their symptoms. [28]

People may become anxious or depressed post-diagnosis. The risk of suicide in people with cancer is approximately double. [29]

Local symptoms

Local symptoms may occur due to the mass of the tumor or its ulceration. For example, mass effects from lung cancer can block the bronchus resulting in cough or pneumonia; esophageal cancer can cause narrowing of the esophagus, making it difficult or painful to swallow; and colorectal cancer may lead to narrowing or blockages in the bowel, affecting bowel habits. Masses in breasts or testicles may produce observable lumps. Ulceration can cause bleeding that, if it occurs in the lung, will lead to coughing up blood, in the bowels to anemia or rectal bleeding, in the bladder to blood in the urine and in the uterus to vaginal bleeding. Although localized pain may occur in advanced cancer, the initial swelling is usually painless. Some cancers can cause a buildup of fluid within the chest or abdomen. [28]

Systemic symptoms

General symptoms occur due to effects that are not related to direct or metastatic spread. These may include: unintentional weight loss, fever, excessive fatigue and changes to the skin. [30] Hodgkin disease, leukemias and cancers of the liver or kidney can cause a persistent fever. [28]

Some cancers may cause specific groups of systemic symptoms, termed paraneoplastic syndrome. Examples include the appearance of myasthenia gravis in thymoma and clubbing in lung cancer. [28]


Cancer can spread from its original site by local spread, lymphatic spread to regional lymph nodes or by hematogenous spread via the blood to distant sites, known as metastasis. When cancer spreads by a hematogenous route, it usually spreads all over the body. However, cancer 'seeds' grow in certain selected site only ('soil') as hypothesized in the soil and seed hypothesis of cancer metastasis. The symptoms of metastatic cancers depend on the tumor location and can include enlarged lymph nodes (which can be felt or sometimes seen under the skin and are typically hard), enlarged liver or enlarged spleen, which can be felt in the abdomen, pain or fracture of affected bones and neurological symptoms. [28]


The majority of cancers, some 90–95% of cases, are due to genetic mutations from environmental and lifestyle factors. [3] The remaining 5–10% are due to inherited genetics. [3] Environmental , as used by cancer researchers, means any cause that is not inherited genetically, such as lifestyle, economic, and behavioral factors and not merely pollution. [31] Common environmental factors that contribute to cancer death include tobacco (25–30%), diet and obesity (30–35%), infections (15–20%), radiation (both ionizing and non-ionizing, up to 10%), stress, lack of physical activity and pollution. [3] [32]

It is not generally possible to prove what caused a particular cancer because the various causes do not have specific fingerprints. For example, if a person who uses tobacco heavily develops lung cancer, then it was probably caused by the tobacco use, but since everyone has a small chance of developing lung cancer as a result of air pollution or radiation, the cancer may have developed for one of those reasons. Excepting the rare transmissions that occur with pregnancies and occasional organ donors, cancer is generally not a transmissible disease. [33]


The incidence of lung cancer is highly correlated with smoking. Cancer smoking lung cancer correlation from NIH.svg
The incidence of lung cancer is highly correlated with smoking.

Exposure to particular substances have been linked to specific types of cancer. These substances are called carcinogens .

Tobacco smoke, for example, causes 90% of lung cancer. [34] It also causes cancer in the larynx, head, neck, stomach, bladder, kidney, esophagus and pancreas. [35] Tobacco smoke contains over fifty known carcinogens, including nitrosamines and polycyclic aromatic hydrocarbons. [36]

Tobacco is responsible for about one in five cancer deaths worldwide [36] and about one in three in the developed world. [37] Lung cancer death rates in the United States have mirrored smoking patterns, with increases in smoking followed by dramatic increases in lung cancer death rates and, more recently, decreases in smoking rates since the 1950s followed by decreases in lung cancer death rates in men since 1990. [38] [39]

In Western Europe, 10% of cancers in males and 3% of cancers in females are attributed to alcohol exposure, especially liver and digestive tract cancers. [40] Cancer from work-related substance exposures may cause between 2 and 20% of cases, [41] causing at least 200,000 deaths. [42] Cancers such as lung cancer and mesothelioma can come from inhaling tobacco smoke or asbestos fibers, or leukemia from exposure to benzene. [42]

Diet and exercise

Diet, physical inactivity and obesity are related to up to 30–35% of cancer deaths. [3] [43] In the United States, excess body weight is associated with the development of many types of cancer and is a factor in 14–20% of cancer deaths. [43] A UK study including data on over 5 million people showed higher body mass index to be related to at least 10 types of cancer and responsible for around 12,000 cases each year in that country. [44] Physical inactivity is believed to contribute to cancer risk, not only through its effect on body weight but also through negative effects on the immune system and endocrine system. [43] More than half of the effect from diet is due to overnutrition (eating too much), rather than from eating too few vegetables or other healthful foods.

Some specific foods are linked to specific cancers. A high-salt diet is linked to gastric cancer. [45] Aflatoxin B1, a frequent food contaminant, causes liver cancer. [45] Betel nut chewing can cause oral cancer. [45] National differences in dietary practices may partly explain differences in cancer incidence. For example, gastric cancer is more common in Japan due to its high-salt diet [46] while colon cancer is more common in the United States. Immigrant cancer profiles mirror those of their new country, often within one generation. [47]


Worldwide approximately 18% of cancer deaths are related to infectious diseases. [3] This proportion ranges from a high of 25% in Africa to less than 10% in the developed world. [3] Viruses are the usual infectious agents that cause cancer but cancer bacteria and parasites may also play a role.

Oncoviruses (viruses that can cause cancer) include human papillomavirus (cervical cancer), Epstein–Barr virus (B-cell lymphoproliferative disease and nasopharyngeal carcinoma), Kaposi's sarcoma herpesvirus (Kaposi's sarcoma and primary effusion lymphomas), hepatitis B and hepatitis C viruses (hepatocellular carcinoma) and human T-cell leukemia virus-1 (T-cell leukemias). Bacterial infection may also increase the risk of cancer, as seen in Helicobacter pylori -induced gastric carcinoma. [48] [49] Parasitic infections associated with cancer include Schistosoma haematobium (squamous cell carcinoma of the bladder) and the liver flukes, Opisthorchis viverrini and Clonorchis sinensis (cholangiocarcinoma). [50]


Up to 10% of invasive cancers are related to radiation exposure, including both ionizing radiation and non-ionizing ultraviolet radiation. [3] Additionally, the majority of non-invasive cancers are non-melanoma skin cancers caused by non-ionizing ultraviolet radiation, mostly from sunlight. Sources of ionizing radiation include medical imaging and radon gas.

Ionizing radiation is not a particularly strong mutagen. [51] Residential exposure to radon gas, for example, has similar cancer risks as passive smoking. [51] Radiation is a more potent source of cancer when combined with other cancer-causing agents, such as radon plus tobacco smoke. [51] Radiation can cause cancer in most parts of the body, in all animals and at any age. Children and adolescents are twice as likely to develop radiation-induced leukemia as adults; radiation exposure before birth has ten times the effect. [51]

Medical use of ionizing radiation is a small but growing source of radiation-induced cancers. Ionizing radiation may be used to treat other cancers, but this may, in some cases, induce a second form of cancer. [51] It is also used in some kinds of medical imaging. [52]

Prolonged exposure to ultraviolet radiation from the sun can lead to melanoma and other skin malignancies. [53] Clear evidence establishes ultraviolet radiation, especially the non-ionizing medium wave UVB, as the cause of most non-melanoma skin cancers, which are the most common forms of cancer in the world. [53]

Non-ionizing radio frequency radiation from mobile phones, electric power transmission and other similar sources has been described as a possible carcinogen by the World Health Organization's International Agency for Research on Cancer. [54] However, studies have not found a consistent link between mobile phone radiation and cancer risk. [55]


The vast majority of cancers are non-hereditary (sporadic). Hereditary cancers are primarily caused by an inherited genetic defect. Less than 0.3% of the population are carriers of a genetic mutation that has a large effect on cancer risk and these cause less than 3–10% of cancer. [56] Some of these syndromes include: certain inherited mutations in the genes BRCA1 and BRCA2 with a more than 75% risk of breast cancer and ovarian cancer, [56] and hereditary nonpolyposis colorectal cancer (HNPCC or Lynch syndrome), which is present in about 3% of people with colorectal cancer, [57] among others.

Statistically for cancers causing most mortality, the relative risk of developing colorectal cancer when a first-degree relative (parent, sibling or child) has been diagnosed with it is about 2. [58] The corresponding relative risk is 1.5 for lung cancer, [59] and 1.9 for prostate cancer. [60] For breast cancer, the relative risk is 1.8 with a first-degree relative having developed it at 50 years of age or older, and 3.3 when the relative developed it when being younger than 50 years of age. [61]

Taller people have an increased risk of cancer because they have more cells than shorter people. Since height is genetically determined to a large extent, taller people have a heritable increase of cancer risk. [62]

Physical agents

Some substances cause cancer primarily through their physical, rather than chemical, effects. [63] A prominent example of this is prolonged exposure to asbestos, naturally occurring mineral fibers that are a major cause of mesothelioma (cancer of the serous membrane) usually the serous membrane surrounding the lungs. [63] Other substances in this category, including both naturally occurring and synthetic asbestos-like fibers, such as wollastonite, attapulgite, glass wool and rock wool, are believed to have similar effects. [63] Non-fibrous particulate materials that cause cancer include powdered metallic cobalt and nickel and crystalline silica (quartz, cristobalite and tridymite). [63] Usually, physical carcinogens must get inside the body (such as through inhalation) and require years of exposure to produce cancer. [63]

Physical trauma resulting in cancer is relatively rare. [64] Claims that breaking bones resulted in bone cancer, for example, have not been proven. [64] Similarly, physical trauma is not accepted as a cause for cervical cancer, breast cancer or brain cancer. [64] One accepted source is frequent, long-term application of hot objects to the body. It is possible that repeated burns on the same part of the body, such as those produced by kanger and kairo heaters (charcoal hand warmers), may produce skin cancer, especially if carcinogenic chemicals are also present. [64] Frequent consumption of scalding hot tea may produce esophageal cancer. [64] Generally, it is believed that cancer arises, or a pre-existing cancer is encouraged, during the process of healing, rather than directly by the trauma. [64] However, repeated injuries to the same tissues might promote excessive cell proliferation, which could then increase the odds of a cancerous mutation.

Chronic inflammation has been hypothesized to directly cause mutation. [64] [65] Inflammation can contribute to proliferation, survival, angiogenesis and migration of cancer cells by influencing the tumor microenvironment. [66] [67] Oncogenes build up an inflammatory pro-tumorigenic microenvironment. [68]


Some hormones play a role in the development of cancer by promoting cell proliferation. [69] Insulin-like growth factors and their binding proteins play a key role in cancer cell proliferation, differentiation and apoptosis, suggesting possible involvement in carcinogenesis. [70]

Hormones are important agents in sex-related cancers, such as cancer of the breast, endometrium, prostate, ovary and testis and also of thyroid cancer and bone cancer. [69] For example, the daughters of women who have breast cancer have significantly higher levels of estrogen and progesterone than the daughters of women without breast cancer. These higher hormone levels may explain their higher risk of breast cancer, even in the absence of a breast-cancer gene. [69] Similarly, men of African ancestry have significantly higher levels of testosterone than men of European ancestry and have a correspondingly higher level of prostate cancer. [69] Men of Asian ancestry, with the lowest levels of testosterone-activating androstanediol glucuronide, have the lowest levels of prostate cancer. [69]

Other factors are relevant: obese people have higher levels of some hormones associated with cancer and a higher rate of those cancers. [69] Women who take hormone replacement therapy have a higher risk of developing cancers associated with those hormones. [69] On the other hand, people who exercise far more than average have lower levels of these hormones and lower risk of cancer. [69] Osteosarcoma may be promoted by growth hormones. [69] Some treatments and prevention approaches leverage this cause by artificially reducing hormone levels and thus discouraging hormone-sensitive cancers. [69]

Autoimmune diseases

There is an association between celiac disease and an increased risk of all cancers. People with untreated celiac disease have a higher risk, but this risk decreases with time after diagnosis and strict treatment, probably due to the adoption of a gluten-free diet, which seems to have a protective role against development of malignancy in people with celiac disease. However, the delay in diagnosis and initiation of a gluten-free diet seems to increase the risk of malignancies. [71] Rates of gastrointestinal cancers are increased in people with Crohn's disease and ulcerative colitis, due to chronic inflammation. Also, immunomodulators and biologic agents used to treat these diseases may promote developing extra-intestinal malignancies. [72]


Cancers are caused by a series of mutations. Each mutation alters the behavior of the cell somewhat. Cancer requires multiple mutations from NIHen.png


Cancer is fundamentally a disease of tissue growth regulation. In order for a normal cell to transform into a cancer cell, the genes that regulate cell growth and differentiation must be altered. [73]

The affected genes are divided into two broad categories. Oncogenes are genes that promote cell growth and reproduction. Tumor suppressor genes are genes that inhibit cell division and survival. Malignant transformation can occur through the formation of novel oncogenes, the inappropriate over-expression of normal oncogenes, or by the under-expression or disabling of tumor suppressor genes. Typically, changes in multiple genes are required to transform a normal cell into a cancer cell. [74]

Genetic changes can occur at different levels and by different mechanisms. The gain or loss of an entire chromosome can occur through errors in mitosis. More common are mutations, which are changes in the nucleotide sequence of genomic DNA.

Large-scale mutations involve the deletion or gain of a portion of a chromosome. Genomic amplification occurs when a cell gains copies (often 20 or more) of a small chromosomal locus, usually containing one or more oncogenes and adjacent genetic material. Translocation occurs when two separate chromosomal regions become abnormally fused, often at a characteristic location. A well-known example of this is the Philadelphia chromosome, or translocation of chromosomes 9 and 22, which occurs in chronic myelogenous leukemia and results in production of the BCR-abl fusion protein, an oncogenic tyrosine kinase.


Replication of the data contained within the DNA of living cells will probabilistically result in some errors (mutations). Complex error correction and prevention is built into the process and safeguards the cell against cancer. If a significant error occurs, the damaged cell can self-destruct through programmed cell death, termed apoptosis. If the error control processes fail, then the mutations will survive and be passed along to daughter cells.

Some environments make errors more likely to arise and propagate. Such environments can include the presence of disruptive substances called carcinogens, repeated physical injury, heat, ionising radiation or hypoxia. [75]

The errors that cause cancer are self-amplifying and compounding, for example:

The transformation of a normal cell into cancer is akin to a chain reaction caused by initial errors, which compound into more severe errors, each progressively allowing the cell to escape more controls that limit normal tissue growth. This rebellion-like scenario is an undesirable survival of the fittest, where the driving forces of evolution work against the body's design and enforcement of order. Once cancer has begun to develop, this ongoing process, termed clonal evolution , drives progression towards more invasive stages. [76] Clonal evolution leads to intra-tumour heterogeneity (cancer cells with heterogeneous mutations) that complicates designing effective treatment strategies.

Characteristic abilities developed by cancers are divided into categories, specifically evasion of apoptosis, self-sufficiency in growth signals, insensitivity to anti-growth signals, sustained angiogenesis, limitless replicative potential, metastasis, reprogramming of energy metabolism and evasion of immune destruction. [26] [27]


The central role of DNA damage and epigenetic defects in DNA repair genes in carcinogenesis Diagram Damage to Cancer Wiki 300dpi.svg

The classical view of cancer is a set of diseases that are driven by progressive genetic abnormalities that include mutations in tumor-suppressor genes and oncogenes and chromosomal abnormalities. Later epigenetic alterations' role was identified. [77]

Epigenetic alterations are functionally relevant modifications to the genome that do not change the nucleotide sequence. Examples of such modifications are changes in DNA methylation (hypermethylation and hypomethylation), histone modification [78] and changes in chromosomal architecture (caused by inappropriate expression of proteins such as HMGA2 or HMGA1). [79] Each of these alterations regulates gene expression without altering the underlying DNA sequence. These changes may remain through cell divisions, last for multiple generations and can be considered to be epimutations (equivalent to mutations).

Epigenetic alterations occur frequently in cancers. As an example, one study listed protein coding genes that were frequently altered in their methylation in association with colon cancer. These included 147 hypermethylated and 27 hypomethylated genes. Of the hypermethylated genes, 10 were hypermethylated in 100% of colon cancers and many others were hypermethylated in more than 50% of colon cancers. [80]

While epigenetic alterations are found in cancers, the epigenetic alterations in DNA repair genes, causing reduced expression of DNA repair proteins, may be of particular importance. Such alterations are thought to occur early in progression to cancer and to be a likely cause of the genetic instability characteristic of cancers. [81] [82] [83] [84]

Reduced expression of DNA repair genes disrupts DNA repair. This is shown in the figure at the 4th level from the top. (In the figure, red wording indicates the central role of DNA damage and defects in DNA repair in progression to cancer.) When DNA repair is deficient DNA damage remains in cells at a higher than usual level (5th level) and cause increased frequencies of mutation and/or epimutation (6th level). Mutation rates increase substantially in cells defective in DNA mismatch repair [85] [86] or in homologous recombinational repair (HRR). [87] Chromosomal rearrangements and aneuploidy also increase in HRR defective cells. [88]

Higher levels of DNA damage cause increased mutation (right side of figure) and increased epimutation. During repair of DNA double strand breaks, or repair of other DNA damage, incompletely cleared repair sites can cause epigenetic gene silencing. [89] [90]

Deficient expression of DNA repair proteins due to an inherited mutation can increase cancer risks. Individuals with an inherited impairment in any of 34 DNA repair genes (see article DNA repair-deficiency disorder) have increased cancer risk, with some defects ensuring a 100% lifetime chance of cancer (e.g. p53 mutations). [91] Germ line DNA repair mutations are noted on the figure's left side. However, such germline mutations (which cause highly penetrant cancer syndromes) are the cause of only about 1 percent of cancers. [92]

In sporadic cancers, deficiencies in DNA repair are occasionally caused by a mutation in a DNA repair gene but are much more frequently caused by epigenetic alterations that reduce or silence expression of DNA repair genes. This is indicated in the figure at the 3rd level. Many studies of heavy metal-induced carcinogenesis show that such heavy metals cause a reduction in expression of DNA repair enzymes, some through epigenetic mechanisms. DNA repair inhibition is proposed to be a predominant mechanism in heavy metal-induced carcinogenicity. In addition, frequent epigenetic alterations of the DNA sequences code for small RNAs called microRNAs (or miRNAs). miRNAs do not code for proteins, but can "target" protein-coding genes and reduce their expression.

Cancers usually arise from an assemblage of mutations and epimutations that confer a selective advantage leading to clonal expansion (see Field defects in progression to cancer). Mutations, however, may not be as frequent in cancers as epigenetic alterations. An average cancer of the breast or colon can have about 60 to 70 protein-altering mutations, of which about three or four may be "driver" mutations and the remaining ones may be "passenger" mutations. [93]


Metastasis is the spread of cancer to other locations in the body. The dispersed tumors are called metastatic tumors, while the original is called the primary tumor. Almost all cancers can metastasize. [94] Most cancer deaths are due to cancer that has metastasized. [95]

Metastasis is common in the late stages of cancer and it can occur via the blood or the lymphatic system or both. The typical steps in metastasis are local invasion, intravasation into the blood or lymph, circulation through the body, extravasation into the new tissue, proliferation and angiogenesis. Different types of cancers tend to metastasize to particular organs, but overall the most common places for metastases to occur are the lungs, liver, brain and the bones. [94]


Chest x-ray showing lung cancer in the left lung Thorax pa peripheres Bronchialcarcinom li OF markiert.jpg
Chest x-ray showing lung cancer in the left lung

Most cancers are initially recognized either because of the appearance of signs or symptoms or through screening. Neither of these leads to a definitive diagnosis, which requires the examination of a tissue sample by a pathologist. People with suspected cancer are investigated with medical tests. These commonly include blood tests, X-rays, (contrast) CT scans and endoscopy.

The tissue diagnosis from the biopsy indicates the type of cell that is proliferating, its histological grade, genetic abnormalities and other features. Together, this information is useful to evaluate the prognosis and to choose the best treatment.

Cytogenetics and immunohistochemistry are other types of tissue tests. These tests provide information about molecular changes (such as mutations, fusion genes and numerical chromosome changes) and may thus also indicate the prognosis and best treatment.


Cancers are classified by the type of cell that the tumor cells resemble and is therefore presumed to be the origin of the tumor. These types include:

Cancers are usually named using -carcinoma, -sarcoma or -blastoma as a suffix, with the Latin or Greek word for the organ or tissue of origin as the root. For example, cancers of the liver parenchyma arising from malignant epithelial cells is called hepatocarcinoma , while a malignancy arising from primitive liver precursor cells is called a hepatoblastoma and a cancer arising from fat cells is called a liposarcoma . For some common cancers, the English organ name is used. For example, the most common type of breast cancer is called ductal carcinoma of the breast . Here, the adjective ductal refers to the appearance of cancer under the microscope, which suggests that it has originated in the milk ducts.

Benign tumors (which are not cancers) are named using -oma as a suffix with the organ name as the root. For example, a benign tumor of smooth muscle cells is called a leiomyoma (the common name of this frequently occurring benign tumor in the uterus is fibroid ). Confusingly, some types of cancer use the -noma suffix, examples including melanoma and seminoma.

Some types of cancer are named for the size and shape of the cells under a microscope, such as giant cell carcinoma, spindle cell carcinoma and small-cell carcinoma.


Cancer prevention is defined as active measures to decrease cancer risk. [97] The vast majority of cancer cases are due to environmental risk factors. Many of these environmental factors are controllable lifestyle choices. Thus, cancer is generally preventable. [98] Between 70% and 90% of common cancers are due to environmental factors and therefore potentially preventable. [99]

Greater than 30% of cancer deaths could be prevented by avoiding risk factors including: tobacco, excess weight/obesity, poor diet, physical inactivity, alcohol, sexually transmitted infections and air pollution. [100] Not all environmental causes are controllable, such as naturally occurring background radiation and cancers caused through hereditary genetic disorders and thus are not preventable via personal behavior.



Dietary recommendations for cancer prevention typically include an emphasis on vegetables, fruit, whole grains and fish and an avoidance of processed and red meat (beef, pork, lamb), animal fats, pickled foods and refined carbohydrates. [14] [101]


Medications can be used to prevent cancer in a few circumstances. [110] In the general population, NSAIDs reduce the risk of colorectal cancer; however, due to cardiovascular and gastrointestinal side effects, they cause overall harm when used for prevention. [111] Aspirin has been found to reduce the risk of death from cancer by about 7%. [112] COX-2 inhibitors may decrease the rate of polyp formation in people with familial adenomatous polyposis; however, it is associated with the same adverse effects as NSAIDs. [113] Daily use of tamoxifen or raloxifene reduce the risk of breast cancer in high-risk women. [114] The benefit versus harm for 5-alpha-reductase inhibitor such as finasteride is not clear. [115]

Vitamin supplementation does not appear to be effective at preventing cancer. [116] While low blood levels of vitamin D are correlated with increased cancer risk, [117] [118] [119] whether this relationship is causal and vitamin D supplementation is protective is not determined. [120] [121] One 2014 review found that supplements had no significant effect on cancer risk. [121] Another 2014 review concluded that vitamin D3 may decrease the risk of death from cancer (one fewer death in 150 people treated over 5 years), but concerns with the quality of the data were noted. [122]

Beta-carotene supplementation increases lung cancer rates in those who are high risk. [123] Folic acid supplementation is not effective in preventing colon cancer and may increase colon polyps. [124] Selenium supplementation has not been shown to reduce the risk of cancer. [125]


Vaccines have been developed that prevent infection by some carcinogenic viruses. [126] Human papillomavirus vaccine (Gardasil and Cervarix) decrease the risk of developing cervical cancer. [126] The hepatitis B vaccine prevents infection with hepatitis B virus and thus decreases the risk of liver cancer. [126] The administration of human papillomavirus and hepatitis B vaccinations is recommended when resources allow. [127]


Unlike diagnostic efforts prompted by symptoms and medical signs, cancer screening involves efforts to detect cancer after it has formed, but before any noticeable symptoms appear. [128] This may involve physical examination, blood or urine tests or medical imaging. [128]



U.S. Preventive Services Task Force

The U.S. Preventive Services Task Force (USPSTF) issues recommendations for various cancers:


Screens for gastric cancer using photofluorography due to the high incidence there. [22]

Genetic testing

GeneCancer types
BRCA1, BRCA2 Breast, ovarian, pancreatic
HNPCC, MLH1, MSH2, MSH6, PMS1, PMS2 Colon, uterine, small bowel, stomach, urinary tract

Genetic testing for individuals at high-risk of certain cancers is recommended by unofficial groups. [127] [143] Carriers of these mutations may then undergo enhanced surveillance, chemoprevention, or preventative surgery to reduce their subsequent risk. [143]


Many treatment options for cancer exist. The primary ones include surgery, chemotherapy, radiation therapy, hormonal therapy, targeted therapy and palliative care. Which treatments are used depends on the type, location and grade of the cancer as well as the patient's health and preferences. The treatment intent may or may not be curative.


Chemotherapy is the treatment of cancer with one or more cytotoxic anti-neoplastic drugs (chemotherapeutic agents) as part of a standardized regimen. The term encompasses a variety of drugs, which are divided into broad categories such as alkylating agents and antimetabolites. [144] Traditional chemotherapeutic agents act by killing cells that divide rapidly, a critical property of most cancer cells.

Targeted therapy is a form of chemotherapy that targets specific molecular differences between cancer and normal cells. The first targeted therapies blocked the estrogen receptor molecule, inhibiting the growth of breast cancer. Another common example is the class of Bcr-Abl inhibitors, which are used to treat chronic myelogenous leukemia (CML). [4] Currently, targeted therapies exist for many of the most common cancer types, including bladder cancer, breast cancer, colorectal cancer, kidney cancer, leukemia, liver cancer, lung cancer, lymphoma, pancreatic cancer, prostate cancer, skin cancer, and thyroid cancer as well as other cancer types. [145]

The efficacy of chemotherapy depends on the type of cancer and the stage. In combination with surgery, chemotherapy has proven useful in cancer types including breast cancer, colorectal cancer, pancreatic cancer, osteogenic sarcoma, testicular cancer, ovarian cancer and certain lung cancers. [146] Chemotherapy is curative for some cancers, such as some leukemias, [147] [148] ineffective in some brain tumors, [149] and needless in others, such as most non-melanoma skin cancers. [150] The effectiveness of chemotherapy is often limited by its toxicity to other tissues in the body. Even when chemotherapy does not provide a permanent cure, it may be useful to reduce symptoms such as pain or to reduce the size of an inoperable tumor in the hope that surgery will become possible in the future.


Radiation therapy involves the use of ionizing radiation in an attempt to either cure or improve symptoms. It works by damaging the DNA of cancerous tissue, killing it. To spare normal tissues (such as skin or organs, which radiation must pass through to treat the tumor), shaped radiation beams are aimed from multiple exposure angles to intersect at the tumor, providing a much larger dose there than in the surrounding, healthy tissue. As with chemotherapy, cancers vary in their response to radiation therapy. [151] [152] [153]

Radiation therapy is used in about half of cases. The radiation can be either from internal sources (brachytherapy) or external sources. The radiation is most commonly low energy x-rays for treating skin cancers, while higher energy x-rays are used for cancers within the body. [154] Radiation is typically used in addition to surgery and or chemotherapy. For certain types of cancer, such as early head and neck cancer, it may be used alone. [155] For painful bone metastasis, it has been found to be effective in about 70% of patients. [155]


Surgery is the primary method of treatment for most isolated, solid cancers and may play a role in palliation and prolongation of survival. It is typically an important part of definitive diagnosis and staging of tumors, as biopsies are usually required. In localized cancer, surgery typically attempts to remove the entire mass along with, in certain cases, the lymph nodes in the area. For some types of cancer this is sufficient to eliminate the cancer. [146]

Palliative care

Palliative care is treatment that attempts to help the patient feel better and may be combined with an attempt to treat the cancer. Palliative care includes action to reduce physical, emotional, spiritual and psycho-social distress. Unlike treatment that is aimed at directly killing cancer cells, the primary goal of palliative care is to improve quality of life.

People at all stages of cancer treatment typically receive some kind of palliative care. In some cases, medical specialty professional organizations recommend that patients and physicians respond to cancer only with palliative care. [156] This applies to patients who: [157]

  1. display low performance status, implying limited ability to care for themselves [156]
  2. received no benefit from prior evidence-based treatments [156]
  3. are not eligible to participate in any appropriate clinical trial [156]
  4. no strong evidence implies that treatment would be effective [156]

Palliative care may be confused with hospice and therefore only indicated when people approach end of life. Like hospice care, palliative care attempts to help the patient cope with their immediate needs and to increase comfort. Unlike hospice care, palliative care does not require people to stop treatment aimed at the cancer.

Multiple national medical guidelines recommend early palliative care for patients whose cancer has produced distressing symptoms or who need help coping with their illness. In patients first diagnosed with metastatic disease, palliative care may be immediately indicated. Palliative care is indicated for patients with a prognosis of less than 12 months of life even given aggressive treatment. [158] [159] [160]


A variety of therapies using immunotherapy, stimulating or helping the immune system to fight cancer, have come into use since 1997. Approaches include antibodies, checkpoint therapy and adoptive cell transfer. [161]

Laser therapy

Laser therapy uses high-intensity light to treat cancer by shrinking or destroying tumors or precancerous growths. Lasers are most commonly used to treat superficial cancers that are on the surface of the body or the lining of internal organs. It is used to treat basal cell skin cancer and the very early stages of others like cervical, penile, vaginal, vulvar, and non-small cell lung cancer. It is often combined with other treatments, such as surgery, chemotherapy, or radiation therapy. Laser-induced interstitial thermotherapy (LITT), or interstitial laser photocoagulation, uses lasers to treat some cancers using hyperthermia, which uses heat to shrink tumors by damaging or killing cancer cells. Laser are more precise than surgery and cause less damage, pain, bleeding, swelling, and scarring. A disadvantage is surgeons must have specialized training. It may be more expensive than other treatments. [162]

Alternative medicine

Complementary and alternative cancer treatments are a diverse group of therapies, practices and products that are not part of conventional medicine. [163] "Complementary medicine" refers to methods and substances used along with conventional medicine, while "alternative medicine" refers to compounds used instead of conventional medicine. [164] Most complementary and alternative medicines for cancer have not been studied or tested using conventional techniques such as clinical trials. Some alternative treatments have been investigated and shown to be ineffective but still continue to be marketed and promoted. Cancer researcher Andrew J. Vickers stated, "The label 'unproven' is inappropriate for such therapies; it is time to assert that many alternative cancer therapies have been 'disproven'." [165]


Survival rates vary by cancer type and by the stage at which it is diagnosed, ranging from majority survival to complete mortality five years after diagnosis. Once a cancer has metastasized, prognosis normally becomes much worse. About half of patients receiving treatment for invasive cancer (excluding carcinoma in situ and non-melanoma skin cancers) die from that cancer or its treatment. [22]

Survival is worse in the developing world, [22] partly because the types of cancer that are most common there are harder to treat than those associated with developed countries. [166]

Those who survive cancer develop a second primary cancer at about twice the rate of those never diagnosed. [167] The increased risk is believed to be due to the random chance of developing any cancer, the likelihood of surviving the first cancer, the same risk factors that produced the first cancer, unwanted side effects of treating the first cancer (particularly radiation therapy), and to better compliance with screening. [167]

Predicting short- or long-term survival depends on many factors. The most important are the cancer type and the patient's age and overall health. Those who are frail with other health problems have lower survival rates than otherwise healthy people. Centenarians are unlikely to survive for five years even if treatment is successful. People who report a higher quality of life tend to survive longer. [168] People with lower quality of life may be affected by depression and other complications and/or disease progression that both impairs quality and quantity of life. Additionally, patients with worse prognoses may be depressed or report poorer quality of life because they perceive that their condition is likely to be fatal.

People with cancer have an increased risk of blood clots in their veins which can be life threatening. [169] The use of blood thinners such as heparin decrease the risk of blood clots but have not been shown to increase survival in people with cancer. [169] People who take blood thinners also have an increased risk of bleeding. [169]


Death from cancer per million persons in 2012
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2,568-3,320 Malignant neoplasms world map-Deaths per million persons-WHO2012.svg
Death from cancer per million persons in 2012

Estimates are that in 2018, 18.1 million new cases of cancer and 9.6 million deaths occur globally. [170] About 20% of males and 17% of females will get cancer at some point in time while 13% of males and 9% of females will die from it. [170]

In 2008, approximately 12.7 million cancers were diagnosed (excluding non-melanoma skin cancers and other non-invasive cancers) [22] and in 2010 nearly 7.98 million people died. [171] Cancers account for approximately 16% of deaths. The most common as of 2018 are lung cancer (1.76 million deaths), colorectal cancer (860,000) stomach cancer (780,000), liver cancer (780,000), and breast cancer (620,000). [2] This makes invasive cancer the leading cause of death in the developed world and the second leading in the developing world. [22] Over half of cases occur in the developing world. [22]

Deaths from cancer were 5.8 million in 1990. [171] Deaths have been increasing primarily due to longer lifespans and lifestyle changes in the developing world. [22] The most significant risk factor for developing cancer is age. [172] Although it is possible for cancer to strike at any age, most patients with invasive cancer are over 65. [172] According to cancer researcher Robert A. Weinberg, "If we lived long enough, sooner or later we all would get cancer." [173] Some of the association between aging and cancer is attributed to immunosenescence, [174] errors accumulated in DNA over a lifetime [175] and age-related changes in the endocrine system. [176] Aging's effect on cancer is complicated by factors such as DNA damage and inflammation promoting it and factors such as vascular aging and endocrine changes inhibiting it. [177]

Some slow-growing cancers are particularly common, but often are not fatal. Autopsy studies in Europe and Asia showed that up to 36% of people have undiagnosed and apparently harmless thyroid cancer at the time of their deaths and that 80% of men develop prostate cancer by age 80. [178] [179] As these cancers do not cause the patient's death, identifying them would have represented overdiagnosis rather than useful medical care.

The three most common childhood cancers are leukemia (34%), brain tumors (23%) and lymphomas (12%). [180] In the United States cancer affects about 1 in 285 children. [181] Rates of childhood cancer increased by 0.6% per year between 1975 and 2002 in the United States [182] and by 1.1% per year between 1978 and 1997 in Europe. [180] Death from childhood cancer decreased by half between 1975 and 2010 in the United States. [181]


Engraving with two views of a Dutch woman who had a tumor removed from her neck in 1689 Clara Jacobi-Tumor.jpg

Cancer has existed for all of human history. [183] The earliest written record regarding cancer is from circa 1600 BC in the Egyptian Edwin Smith Papyrus and describes breast cancer. [183] Hippocrates (c. 460 BC – c. 370 BC) described several kinds of cancer, referring to them with the Greek word καρκίνος karkinos (crab or crayfish). [183] This name comes from the appearance of the cut surface of a solid malignant tumor, with "the veins stretched on all sides as the animal the crab has its feet, whence it derives its name". [184] Galen stated that "cancer of the breast is so called because of the fancied resemblance to a crab given by the lateral prolongations of the tumor and the adjacent distended veins". [185] :738 Celsus (c. 25 BC – 50 AD) translated karkinos into the Latin cancer, also meaning crab and recommended surgery as treatment. [183] Galen (2nd century AD) disagreed with the use of surgery and recommended purgatives instead. [183] These recommendations largely stood for 1000 years. [183]

In the 15th, 16th and 17th centuries, it became acceptable for doctors to dissect bodies to discover the cause of death. [186] The German professor Wilhelm Fabry believed that breast cancer was caused by a milk clot in a mammary duct. The Dutch professor Francois de la Boe Sylvius, a follower of Descartes, believed that all disease was the outcome of chemical processes and that acidic lymph fluid was the cause of cancer. His contemporary Nicolaes Tulp believed that cancer was a poison that slowly spreads and concluded that it was contagious. [187]

The physician John Hill described tobacco snuff as the cause of nose cancer in 1761. [186] This was followed by the report in 1775 by British surgeon Percivall Pott that chimney sweeps' carcinoma, a cancer of the scrotum, was a common disease among chimney sweeps. [188] With the widespread use of the microscope in the 18th century, it was discovered that the 'cancer poison' spread from the primary tumor through the lymph nodes to other sites ("metastasis"). This view of the disease was first formulated by the English surgeon Campbell De Morgan between 1871 and 1874. [189]

Society and culture

Although many diseases (such as heart failure) may have a worse prognosis than most cases of cancer, cancer is the subject of widespread fear and taboos. The euphemism of "a long illness" to describe cancers leading to death is still commonly used in obituaries, rather than naming the disease explicitly, reflecting an apparent stigma. [190] In Nigeria, one local name for cancer translates into English as "the disease that cannot be cured". [191] This deep belief that cancer is necessarily a difficult and usually deadly disease is reflected in the systems chosen by society to compile cancer statistics: the most common form of cancer—non-melanoma skin cancers, accounting for about one-third of cancer cases worldwide, but very few deaths [192] [193] —are excluded from cancer statistics specifically because they are easily treated and almost always cured, often in a single, short, outpatient procedure. [194]


In the United States and some other cultures, cancer is regarded as a disease that must be "fought" to end the "civil insurrection"; a War on Cancer was declared in the US. Military metaphors are particularly common in descriptions of cancer's human effects, and they emphasize both the state of the patient's health and the need to take immediate, decisive actions himself rather than to delay, to ignore or to rely entirely on others. The military metaphors also help rationalize radical, destructive treatments. [195] [196]

In the 1970s, a relatively popular alternative cancer treatment in the US was a specialized form of talk therapy, based on the idea that cancer was caused by a bad attitude. [197] People with a "cancer personality"—depressed, repressed, self-loathing and afraid to express their emotions—were believed to have manifested cancer through subconscious desire. Some psychotherapists said that treatment to change the patient's outlook on life would cure the cancer. [197] Among other effects, this belief allowed society to blame the victim for having caused the cancer (by "wanting" it) or having prevented its cure (by not becoming a sufficiently happy, fearless and loving person). [198] It also increased patients' anxiety, as they incorrectly believed that natural emotions of sadness, anger or fear shorten their lives. [198] The idea was ridiculed by Susan Sontag, who published Illness as Metaphor while recovering from treatment for breast cancer in 1978. [197] Although the original idea is now generally regarded as nonsense, the idea partly persists in a reduced form with a widespread, but incorrect, belief that deliberately cultivating a habit of positive thinking will increase survival. [198] This notion is particularly strong in breast cancer culture. [198]

One idea about why people with cancer are blamed or stigmatized, called the just-world hypothesis, is that blaming cancer on the patient's actions or attitudes allows the blamers to regain a sense of control. This is based upon the blamers' belief that the world is fundamentally just and so any dangerous illness, like cancer, must be a type of punishment for bad choices, because in a just world, bad things would not happen to good people. [199]

Economic effect

The total health care expenditure on cancer in the US was estimated to be $80.2 billion in 2015. [200] Even though cancer-related health care expenditure have increased in absolute terms during recent decades, the share of health expenditure devoted to cancer treatment has remained close to 5% between the 1960s and 2004. [201] [202] A similar pattern has been observed in Europe where about 6% of all health care expenditure are spent on cancer treatment. [203] In addition to health care expenditure, cancer causes indirect costs in terms of productivity losses due to lost work days and premature death, as well as informal care. Indirect costs are typically estimated to exceed the health care costs of cancer. [204]


In the United States, cancer is included as a protected condition by the Equal Employment Opportunity Commission (EEOC), mainly due to the potential for cancer having discriminating effects on workers. [205] Discrimination in the workplace could occur if an employer holds a false belief that a person with cancer is not capable of doing a job properly, and may ask for more sick leave than other employees. Employers may also make hiring or firing decisions based on misconceptions about cancer disabilities, if present. The EEOC provides interview guidelines for employers, as well as lists of possible solutions for assessing and accommodating employees with cancer. [205]


University of Florida Cancer Hospital UF CancerHospital.JPG
University of Florida Cancer Hospital

Because cancer is a class of diseases, [206] [207] it is unlikely that there will ever be a single "cure for cancer" any more than there will be a single treatment for all infectious diseases. [208] Angiogenesis inhibitors were once incorrectly thought to have potential as a "silver bullet" treatment applicable to many types of cancer. [209] Angiogenesis inhibitors and other cancer therapeutics are used in combination to reduce cancer morbidity and mortality. [210]

Experimental cancer treatments are studied in clinical trials to compare the proposed treatment to the best existing treatment. Treatments that succeeded in one cancer type can be tested against other types. [211] Diagnostic tests are under development to better target the right therapies to the right patients, based on their individual biology. [212]

Cancer research focuses on the following issues:

The improved understanding of molecular biology and cellular biology due to cancer research has led to new treatments for cancer since US President Richard Nixon declared the "War on Cancer" in 1971. Since then, the country has spent over $200 billion on cancer research, including resources from public and private sectors. [213] The cancer death rate (adjusting for size and age of the population) declined by five percent between 1950 and 2005. [214]

Competition for financial resources appears to have suppressed the creativity, cooperation, risk-taking and original thinking required to make fundamental discoveries, unduly favoring low-risk research into small incremental advancements over riskier, more innovative research. Other consequences of competition appear to be many studies with dramatic claims whose results cannot be replicated and perverse incentives that encourage grantee institutions to grow without making sufficient investments in their own faculty and facilities. [215] [216] [217] [218]

Virotherapy, which uses convert viruses, is being studied.


Cancer affects approximately 1 in 1,000 pregnant women. The most common cancers found during pregnancy are the same as the most common cancers found in non-pregnant women during childbearing ages: breast cancer, cervical cancer, leukemia, lymphoma, melanoma, ovarian cancer and colorectal cancer. [219]

Diagnosing a new cancer in a pregnant woman is difficult, in part because any symptoms are commonly assumed to be a normal discomfort associated with pregnancy. As a result, cancer is typically discovered at a somewhat later stage than average. Some imaging procedures, such as MRIs (magnetic resonance imaging), CT scans, ultrasounds and mammograms with fetal shielding are considered safe during pregnancy; some others, such as PET scans, are not. [219]

Treatment is generally the same as for non-pregnant women. However, radiation and radioactive drugs are normally avoided during pregnancy, especially if the fetal dose might exceed 100 cGy. In some cases, some or all treatments are postponed until after birth if the cancer is diagnosed late in the pregnancy. Early deliveries are often used to advance the start of treatment. Surgery is generally safe, but pelvic surgeries during the first trimester may cause miscarriage. Some treatments, especially certain chemotherapy drugs given during the first trimester, increase the risk of birth defects and pregnancy loss (spontaneous abortions and stillbirths). [219]

Elective abortions are not required and, for the most common forms and stages of cancer, do not improve the mother's survival. In a few instances, such as advanced uterine cancer, the pregnancy cannot be continued and in others, the patient may end the pregnancy so that she can begin aggressive chemotherapy. [219]

Some treatments can interfere with the mother's ability to give birth vaginally or to breastfeed. [219] Cervical cancer may require birth by Caesarean section. Radiation to the breast reduces the ability of that breast to produce milk and increases the risk of mastitis. Also, when chemotherapy is given after birth, many of the drugs appear in breast milk, which could harm the baby. [219]

Other animals

Veterinary oncology, concentrating mainly on cats and dogs, is a growing specialty in wealthy countries and the major forms of human treatment such as surgery and radiotherapy may be offered. The most common types of cancer differ, but the cancer burden seems at least as high in pets as in humans. Animals, typically rodents, are often used in cancer research and studies of natural cancers in larger animals may benefit research into human cancer. [220]

In non-humans, a few types of transmissible cancer have been described, wherein the cancer spreads between animals by transmission of the tumor cells themselves. This phenomenon is seen in dogs with Sticker's sarcoma (also known as canine transmissible venereal tumor), and in Tasmanian devils with devil facial tumour disease (DFTD). [221]


  1. 1 2 3 "Cancer – Signs and symptoms". NHS Choices. Archived from the original on 8 June 2014. Retrieved 10 June 2014.
  2. 1 2 3 4 5 6 7 8 9 10 11 12 "Cancer". World Health Organization. 12 September 2018. Retrieved 19 December 2018.
  3. 1 2 3 4 5 6 7 8 9 Anand P, Kunnumakkara AB, Sundaram C, Harikumar KB, Tharakan ST, Lai OS, Sung B, Aggarwal BB (September 2008). "Cancer is a preventable disease that requires major lifestyle changes". Pharmaceutical Research. 25 (9): 2097–116. doi:10.1007/s11095-008-9661-9. PMC   2515569 . PMID   18626751.
  4. 1 2 3 National Cancer Institute (26 February 2018). "Targeted Cancer Therapies". Retrieved 28 March 2018.
  5. 1 2 "SEER Stat Fact Sheets: All Cancer Sites". National Cancer Institute. Archived from the original on 26 September 2010. Retrieved 18 June 2014.
  6. 1 2 GBD 2015 Disease and Injury Incidence and Prevalence, Collaborators. (8 October 2016). "Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015". Lancet. 388 (10053): 1545–1602. doi:10.1016/S0140-6736(16)31678-6. PMC   5055577 . PMID   27733282.
  7. 1 2 GBD 2015 Mortality and Causes of Death, Collaborators. (8 October 2016). "Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980–2015: a systematic analysis for the Global Burden of Disease Study 2015". Lancet. 388 (10053): 1459–1544. doi:10.1016/s0140-6736(16)31012-1. PMC   5388903 . PMID   27733281.
  8. 1 2 3 4 "Defining Cancer". National Cancer Institute. 17 September 2007. Retrieved 28 March 2018.
  9. "Obesity and Cancer Risk". National Cancer Institute. 3 January 2012. Archived from the original on 4 July 2015. Retrieved 4 July 2015.
  10. Jayasekara H, MacInnis RJ, Room R, English DR (May 2016). "Long-Term Alcohol Consumption and Breast, Upper Aero-Digestive Tract and Colorectal Cancer Risk: A Systematic Review and Meta-Analysis". Alcohol and Alcoholism. 51 (3): 315–30. doi:10.1093/alcalc/agv110. PMID   26400678.
  11. 1 2 3 4 5 6 World Cancer Report 2014. World Health Organization. 2014. pp. Chapter 1.1. ISBN   978-92-832-0429-9. Archived from the original on 12 July 2017.
  12. "Heredity and Cancer". American Cancer Society. Archived from the original on 2 August 2013. Retrieved 22 July 2013.
  13. "How is cancer diagnosed?". American Cancer Society. 29 January 2013. Archived from the original on 14 July 2014. Retrieved 10 June 2014.
  14. 1 2 3 Kushi LH, Doyle C, McCullough M, Rock CL, Demark-Wahnefried W, Bandera EV, Gapstur S, Patel AV, Andrews K, Gansler T (2012). "American Cancer Society Guidelines on nutrition and physical activity for cancer prevention: reducing the risk of cancer with healthy food choices and physical activity". CA Cancer J Clin. 62 (1): 30–67. doi:10.3322/caac.20140. PMID   22237782.
  15. Parkin DM, Boyd L, Walker LC (December 2011). "16. The fraction of cancer attributable to lifestyle and environmental factors in the UK in 2010". British Journal of Cancer. 105 Suppl 2: S77–81. doi:10.1038/bjc.2011.489. PMC   3252065 . PMID   22158327.
  16. 1 2 World Cancer Report 2014. World Health Organization. 2014. pp. Chapter 4.7. ISBN   978-92-832-0429-9. Archived from the original on 12 July 2017.
  17. Gøtzsche PC, Jørgensen KJ (June 2013). "Screening for breast cancer with mammography". The Cochrane Database of Systematic Reviews. 6 (6): CD001877. doi:10.1002/14651858.CD001877.pub5. PMID   23737396.
  18. 1 2 World Cancer Report 2014. World Health Organization. 2014. pp. Chapter 1.3. ISBN   978-92-832-0429-9. Archived from the original on 12 July 2017.
  20. Dubas LE, Ingraffea A (February 2013). "Nonmelanoma skin cancer". Facial Plastic Surgery Clinics of North America. 21 (1): 43–53. doi:10.1016/j.fsc.2012.10.003. PMID   23369588.
  21. Cakir BÖ, Adamson P, Cingi C (November 2012). "Epidemiology and economic burden of nonmelanoma skin cancer". Facial Plastic Surgery Clinics of North America. 20 (4): 419–22. doi:10.1016/j.fsc.2012.07.004. PMID   23084294.
  22. 1 2 3 4 5 6 7 8 Jemal A, Bray F, Center MM, Ferlay J, Ward E, Forman D (February 2011). "Global cancer statistics". Ca. 61 (2): 69–90. doi:10.3322/caac.20107. PMID   21296855.
  23. World Cancer Report 2014. World Health Organization. 2014. pp. Chapter 6.7. ISBN   978-92-832-0429-9. Archived from the original on 12 July 2017.
  24. "Cancer Glossary". American Cancer Society. Archived from the original on 1 September 2013. Retrieved 11 September 2013.
  25. "What is cancer?". National Cancer Institute. 17 September 2007. Retrieved 28 March 2018.
  26. 1 2 3 4 Hanahan D, Weinberg RA (January 2000). "The hallmarks of cancer". Cell. 100 (1): 57–70. doi:10.1016/S0092-8674(00)81683-9. PMID   10647931.
  27. 1 2 Hanahan D, Weinberg RA (March 2011). "Hallmarks of cancer: the next generation". Cell. 144 (5): 646–74. doi:10.1016/j.cell.2011.02.013. PMID   21376230.
  28. 1 2 3 4 5 Holland Chp. 1
  29. Anguiano L, Mayer DK, Piven ML, Rosenstein D (July – August 2012). "A literature review of suicide in cancer patients". Cancer Nursing. 35 (4): E14–26. doi:10.1097/NCC.0b013e31822fc76c. PMID   21946906.
  30. O'Dell, edited by Michael D. Stubblefield, Michael W. (2009). Cancer rehabilitation principles and practice. New York: Demos Medical. p. 983. ISBN   978-1-933864-33-4.CS1 maint: Extra text: authors list (link)
  31. Manton K, Akushevich I, Kravchenko J (28 December 2008). Cancer Mortality and Morbidity Patterns in the U.S. Population: An Interdisciplinary Approach. Springer Science & Business Media. ISBN   978-0-387-78193-8. The term environment refers not only to air, water, and soil but also to substances and conditions at home and at the workplace, including diet, smoking, alcohol, drugs, exposure to chemicals, sunlight, ionizing radiation, electromagnetic fields, infectious agents, etc. Lifestyle, economic and behavioral factors are all aspects of our environment.
  32. Islami F, Goding Sauer A, Miller KD, Siegel RL, Fedewa SA, Jacobs EJ, McCullough ML, Patel AV, Ma J, Soerjomataram I, Flanders WD, Brawley OW, Gapstur SM, Jemal A (January 2018). "Proportion and number of cancer cases and deaths attributable to potentially modifiable risk factors in the United States". Ca. 68 (1): 31–54. doi:10.3322/caac.21440. PMID   29160902.
  33. Tolar J, Neglia JP (June 2003). "Transplacental and other routes of cancer transmission between individuals". Journal of Pediatric Hematology/Oncology. 25 (6): 430–4. doi:10.1097/00043426-200306000-00002. PMID   12794519.
  34. Biesalski HK, Bueno de Mesquita B, Chesson A, Chytil F, Grimble R, Hermus RJ, Köhrle J, Lotan R, Norpoth K, Pastorino U, Thurnham D (1998). "European Consensus Statement on Lung Cancer: risk factors and prevention. Lung Cancer Panel". Ca. 48 (3): 167–76, discussion 164–66. doi:10.3322/canjclin.48.3.167. PMID   9594919.
  35. Kuper H, Boffetta P, Adami HO (September 2002). "Tobacco use and cancer causation: association by tumour type". Journal of Internal Medicine. 252 (3): 206–24. doi:10.1046/j.1365-2796.2002.01022.x. PMID   12270001.
  36. 1 2 Kuper H, Adami HO, Boffetta P (June 2002). "Tobacco use, cancer causation and public health impact". Journal of Internal Medicine. 251 (6): 455–66. doi:10.1046/j.1365-2796.2002.00993.x. PMID   12028500.
  37. Sasco AJ, Secretan MB, Straif K (August 2004). "Tobacco smoking and cancer: a brief review of recent epidemiological evidence". Lung Cancer. 45 Suppl 2: S3–9. doi:10.1016/j.lungcan.2004.07.998. PMID   15552776.
  38. Thun MJ, Jemal A (October 2006). "How much of the decrease in cancer death rates in the United States is attributable to reductions in tobacco smoking?". Tobacco Control. 15 (5): 345–47. doi:10.1136/tc.2006.017749. PMC   2563648 . PMID   16998161.
  39. Dubey S, Powell CA (May 2008). "Update in lung cancer 2007". American Journal of Respiratory and Critical Care Medicine. 177 (9): 941–46. doi:10.1164/rccm.200801-107UP. PMC   2720127 . PMID   18434333.
  40. Schütze M, Boeing H, Pischon T, Rehm J, Kehoe T, Gmel G, Olsen A, Tjønneland AM, Dahm CC, Overvad K, Clavel-Chapelon F, Boutron-Ruault MC, Trichopoulou A, Benetou V, Zylis D, Kaaks R, Rohrmann S, Palli D, Berrino F, Tumino R, Vineis P, Rodríguez L, Agudo A, Sánchez MJ, Dorronsoro M, Chirlaque MD, Barricarte A, Peeters PH, van Gils CH, Khaw KT, Wareham N, Allen NE, Key TJ, Boffetta P, Slimani N, Jenab M, Romaguera D, Wark PA, Riboli E, Bergmann MM (April 2011). "Alcohol attributable burden of incidence of cancer in eight European countries based on results from prospective cohort study". BMJ. 342: d1584. doi:10.1136/bmj.d1584. PMC   3072472 . PMID   21474525.
  41. Irigaray P, Newby JA, Clapp R, Hardell L, Howard V, Montagnier L, Epstein S, Belpomme D (December 2007). "Lifestyle-related factors and environmental agents causing cancer: an overview". Biomedicine & Pharmacotherapy. 61 (10): 640–58. doi:10.1016/j.biopha.2007.10.006. PMID   18055160.
  42. 1 2 "WHO calls for prevention of cancer through healthy workplaces" (Press release). World Health Organization. 27 April 2007. Archived from the original on 12 October 2007. Retrieved 13 October 2007.
  43. 1 2 3 Kushi LH, Byers T, Doyle C, Bandera EV, McCullough M, McTiernan A, Gansler T, Andrews KS, Thun MJ (2006). "American Cancer Society Guidelines on Nutrition and Physical Activity for cancer prevention: reducing the risk of cancer with healthy food choices and physical activity". Ca. 56 (5): 254–81, quiz 313–14. doi:10.3322/canjclin.56.5.254. PMID   17005596.
  44. Bhaskaran K, Douglas I, Forbes H, dos-Santos-Silva I, Leon DA, Smeeth L (August 2014). "Body-mass index and risk of 22 specific cancers: a population-based cohort study of 5·24 million UK adults". Lancet. 384 (9945): 755–65. doi:10.1016/S0140-6736(14)60892-8. PMC   4151483 . PMID   25129328.
  45. 1 2 3 Park S, Bae J, Nam BH, Yoo KY (2008). "Aetiology of cancer in Asia". Asian Pacific Journal of Cancer Prevention. 9 (3): 371–80. PMID   18990005. Archived from the original (PDF) on 4 September 2011.
  46. Brenner H, Rothenbacher D, Arndt V (2009). Epidemiology of stomach cancer. Methods in Molecular Biology (Clifton, NJ). Methods in Molecular Biology. 472. pp. 467–77. doi:10.1007/978-1-60327-492-0_23. ISBN   978-1-60327-491-3. PMC   2166976 . PMID   19107449.
  47. Buell P, Dunn JE (May 1965). "Cancer Mortality Among Japanese Issei and Nisei of California". Cancer. 18 (5): 656–64. doi:10.1002/1097-0142(196505)18:5<656::AID-CNCR2820180515>3.0.CO;2-3. PMID   14278899.
  48. Pagano JS, Blaser M, Buendia MA, Damania B, Khalili K, Raab-Traub N, Roizman B (December 2004). "Infectious agents and cancer: criteria for a causal relation". Seminars in Cancer Biology. 14 (6): 453–71. Bibcode:2004SCB....16...13G. doi:10.1016/j.semcancer.2004.06.009. PMID   15489139.
  49. Ljubojevic S, Skerlev M (2014). "HPV-associated diseases". Clinics in Dermatology. 32 (2): 227–34. doi:10.1016/j.clindermatol.2013.08.007. PMID   24559558.
  50. Samaras V, Rafailidis PI, Mourtzoukou EG, Peppas G, Falagas ME (June 2010). "Chronic bacterial and parasitic infections and cancer: a review" (PDF). Journal of Infection in Developing Countries. 4 (5): 267–81. doi:10.3855/jidc.819. PMID   20539059. Archived from the original on 4 October 2011.
  51. 1 2 3 4 5 Little JB (2000). "Chapter 14: Ionizing Radiation". In Kufe DW, Pollock RE, Weichselbaum RR, Bast RC, Gansler TS, Holland JF, Frei E (eds.). Cancer medicine (6th ed.). Hamilton, Ont: B.C. Decker. ISBN   978-1-55009-113-7. Archived from the original on 2 January 2016.
  52. Brenner DJ, Hall EJ (November 2007). "Computed tomography—an increasing source of radiation exposure". The New England Journal of Medicine. 357 (22): 2277–84. doi:10.1056/NEJMra072149. PMID   18046031.
  53. 1 2 Cleaver JE, Mitchell DL (2000). "15. Ultraviolet Radiation Carcinogenesis". In Bast RC, Kufe DW, Pollock RE, et al. (eds.). Holland-Frei Cancer Medicine (5th ed.). Hamilton, Ontario: B.C. Decker. ISBN   978-1-55009-113-7. Archived from the original on 4 September 2015. Retrieved 31 January 2011.
  54. "IARC classifies radiofrequency electromagnetic fields as possibly carcinogenic to humans" (PDF). World Health Organization. Archived (PDF) from the original on 1 June 2011.
  55. "Cell Phones and Cancer Risk – National Cancer Institute". 8 May 2013. Retrieved 28 March 2018.
  56. 1 2 Roukos DH (April 2009). "Genome-wide association studies: how predictable is a person's cancer risk?". Expert Review of Anticancer Therapy. 9 (4): 389–92. doi:10.1586/era.09.12. PMID   19374592.
  57. Cunningham D, Atkin W, Lenz HJ, Lynch HT, Minsky B, Nordlinger B, Starling N (March 2010). "Colorectal cancer". Lancet. 375 (9719): 1030–47. doi:10.1016/S0140-6736(10)60353-4. PMID   20304247.
  58. Kampman, E. (2007). "A First-Degree Relative with Colorectal Cancer: What Are We Missing?". Cancer Epidemiology, Biomarkers & Prevention. 16 (1): 1–3. doi:10.1158/1055-9965.EPI-06-0984. ISSN   1055-9965. PMID   17220324.
  59. Coté ML, Liu M, Bonassi S, Neri M, Schwartz AG, Christiani DC, et al. (September 2012). "Increased risk of lung cancer in individuals with a family history of the disease: a pooled analysis from the International Lung Cancer Consortium". European Journal of Cancer. 48 (13): 1957–68. doi:10.1016/j.ejca.2012.01.038. PMC   3445438 . PMID   22436981.
  60. Bruner DW, Moore D, Parlanti A, Dorgan J, Engstrom P (December 2003). "Relative risk of prostate cancer for men with affected relatives: systematic review and meta-analysis". International Journal of Cancer. 107 (5): 797–803. doi:10.1002/ijc.11466. PMID   14566830.
  61. Singletary, S. Eva (2003). "Rating the Risk Factors for Breast Cancer". Annals of Surgery. 237 (4): 474–82. doi:10.1097/01.SLA.0000059969.64262.87. ISSN   0003-4932. PMC   1514477 . PMID   12677142.
  62. Green J, Cairns BJ, Casabonne D, Wright FL, Reeves G, Beral V (August 2011). "Height and cancer incidence in the Million Women Study: prospective cohort, and meta-analysis of prospective studies of height and total cancer risk". The Lancet. Oncology. 12 (8): 785–94. doi:10.1016/S1470-2045(11)70154-1. PMC   3148429 . PMID   21782509.
  63. 1 2 3 4 5 Maltoni CF, Holland JF (2000). "Chapter 16: Physical Carcinogens". In Bast RC, Kufe DW, Pollock RE, et al. (eds.). Holland-Frei Cancer Medicine (5th ed.). Hamilton, Ontario: B.C. Decker. ISBN   978-1-55009-113-7. Archived from the original on 4 September 2015. Retrieved 31 January 2011.
  64. 1 2 3 4 5 6 7 Gaeta JF (2000). "Chapter 17: Trauma and Inflammation". In Bast RC, Kufe DW, Pollock RE, et al. (eds.). Holland-Frei Cancer Medicine (5th ed.). Hamilton, Ontario: B.C. Decker. ISBN   978-1-55009-113-7. Archived from the original on 4 September 2015. Retrieved 27 January 2011.
  65. Colotta F, Allavena P, Sica A, Garlanda C, Mantovani A (July 2009). "Cancer-related inflammation, the seventh hallmark of cancer: links to genetic instability". Carcinogenesis (review). 30 (7): 1073–81. doi:10.1093/carcin/bgp127. PMID   19468060.
  66. Ungefroren H, Sebens S, Seidl D, Lehnert H, Hass R (September 2011). "Interaction of tumor cells with the microenvironment". Cell Communication and Signaling. 9 (18): 18. doi:10.1186/1478-811X-9-18. PMC   3180438 . PMID   21914164. Archived from the original on 22 February 2014.
  67. Mantovani A (June 2010). "Molecular pathways linking inflammation and cancer". Current Molecular Medicine (review). 10 (4): 369–73. doi:10.2174/156652410791316968. PMID   20455855.
  68. Borrello MG, Degl'Innocenti D, Pierotti MA (August 2008). "Inflammation and cancer: the oncogene-driven connection". Cancer Letters (review). 267 (2): 262–70. doi:10.1016/j.canlet.2008.03.060. PMID   18502035.
  69. 1 2 3 4 5 6 7 8 9 10 Henderson BE, Bernstein L, Ross RK (2000). "Chapter 13: Hormones and the Etiology of Cancer". In Bast RC, Kufe DW, Pollock RE, et al. (eds.). Holland-Frei Cancer Medicine (5th ed.). Hamilton, Ontario: B.C. Decker. ISBN   978-1-55009-113-7. Archived from the original on 10 September 2017. Retrieved 27 January 2011.
  70. Rowlands MA, Gunnell D, Harris R, Vatten LJ, Holly JM, Martin RM (May 2009). "Circulating insulin-like growth factor peptides and prostate cancer risk: a systematic review and meta-analysis". International Journal of Cancer. 124 (10): 2416–29. doi:10.1002/ijc.24202. PMC   2743036 . PMID   19142965.
  71. Han Y, Chen W, Li P, Ye J (September 2015). "Association Between Coeliac Disease and Risk of Any Malignancy and Gastrointestinal Malignancy: A Meta-Analysis". Medicine. 94 (38): e1612. doi:10.1097/MD.0000000000001612. PMC   4635766 . PMID   26402826.
  72. Axelrad JE, Lichtiger S, Yajnik V (May 2016). "Inflammatory bowel disease and cancer: The role of inflammation, immunosuppression, and cancer treatment". World Journal of Gastroenterology. 22 (20): 4794–801. doi:10.3748/wjg.v22.i20.4794. PMC   4873872 . PMID   27239106.
  73. Croce CM (January 2008). "Oncogenes and cancer". The New England Journal of Medicine. 358 (5): 502–11. doi:10.1056/NEJMra072367. PMID   18234754.
  74. Knudson AG (November 2001). "Two genetic hits (more or less) to cancer". Nature Reviews. Cancer. 1 (2): 157–62. doi:10.1038/35101031. PMID   11905807.
  75. Nelson DA, Tan TT, Rabson AB, Anderson D, Degenhardt K, White E (September 2004). "Hypoxia and defective apoptosis drive genomic instability and tumorigenesis". Genes & Development. 18 (17): 2095–107. doi:10.1101/gad.1204904. PMC   515288 . PMID   15314031.
  76. Merlo LM, Pepper JW, Reid BJ, Maley CC (December 2006). "Cancer as an evolutionary and ecological process". Nature Reviews. Cancer. 6 (12): 924–35. doi:10.1038/nrc2013. PMID   17109012.
  77. Baylin SB, Ohm JE (February 2006). "Epigenetic gene silencing in cancer – a mechanism for early oncogenic pathway addiction?". Nature Reviews. Cancer. 6 (2): 107–16. doi:10.1038/nrc1799. PMID   16491070.
  78. Kanwal R, Gupta S (April 2012). "Epigenetic modifications in cancer". Clinical Genetics. 81 (4): 303–11. doi:10.1111/j.1399-0004.2011.01809.x. PMC   3590802 . PMID   22082348.
  79. Baldassarre G, Battista S, Belletti B, Thakur S, Pentimalli F, Trapasso F, Fedele M, Pierantoni G, Croce CM, Fusco A (April 2003). "Negative regulation of BRCA1 gene expression by HMGA1 proteins accounts for the reduced BRCA1 protein levels in sporadic breast carcinoma". Molecular and Cellular Biology. 23 (7): 2225–38. doi:10.1128/MCB.23.7.2225-2238.2003. PMC   150734 . PMID   12640109./
  80. Schnekenburger M, Diederich M (March 2012). "Epigenetics Offer New Horizons for Colorectal Cancer Prevention". Current Colorectal Cancer Reports. 8 (1): 66–81. doi:10.1007/s11888-011-0116-z. PMC   3277709 . PMID   22389639.
  81. Jacinto FV, Esteller M (July 2007). "Mutator pathways unleashed by epigenetic silencing in human cancer". Mutagenesis. 22 (4): 247–53. doi:10.1093/mutage/gem009. PMID   17412712. Archived from the original on 4 September 2015.
  82. Lahtz C, Pfeifer GP (February 2011). "Epigenetic changes of DNA repair genes in cancer". Journal of Molecular Cell Biology. 3 (1): 51–8. doi:10.1093/jmcb/mjq053. PMC   3030973 . PMID   21278452. Archived from the original on 16 October 2015.
  83. Bernstein C, Nfonsam V, Prasad AR, Bernstein H (March 2013). "Epigenetic field defects in progression to cancer". World Journal of Gastrointestinal Oncology. 5 (3): 43–49. doi:10.4251/wjgo.v5.i3.43. PMC   3648662 . PMID   23671730. Archived from the original on 15 December 2013.
  84. Bernstein C, Prasad AR, Nfonsam V, Bernstein H (2013). "DNA Damage, DNA Repair and Cancer". In Chen C (ed.). New Research Directions in DNA Repair. InTech. doi:10.5772/53919. ISBN   978-953-51-1114-6. Archived from the original on 24 September 2015.
  85. Narayanan L, Fritzell JA, Baker SM, Liskay RM, Glazer PM (April 1997). "Elevated levels of mutation in multiple tissues of mice deficient in the DNA mismatch repair gene Pms2". Proceedings of the National Academy of Sciences of the United States of America. 94 (7): 3122–27. Bibcode:1997PNAS...94.3122N. doi:10.1073/pnas.94.7.3122. PMC   20332 . PMID   9096356.
  86. Hegan DC, Narayanan L, Jirik FR, Edelmann W, Liskay RM, Glazer PM (December 2006). "Differing patterns of genetic instability in mice deficient in the mismatch repair genes Pms2, Mlh1, Msh2, Msh3 and Msh6". Carcinogenesis. 27 (12): 2402–08. doi:10.1093/carcin/bgl079. PMC   2612936 . PMID   16728433.
  87. Tutt AN, van Oostrom CT, Ross GM, van Steeg H, Ashworth A (March 2002). "Disruption of Brca2 increases the spontaneous mutation rate in vivo: synergism with ionizing radiation". EMBO Reports. 3 (3): 255–60. doi:10.1093/embo-reports/kvf037. PMC   1084010 . PMID   11850397.
  88. German J (March 1969). "Bloom's syndrome. I. Genetical and clinical observations in the first twenty-seven patients". American Journal of Human Genetics. 21 (2): 196–227. PMC   1706430 . PMID   5770175.
  89. O'Hagan HM, Mohammad HP, Baylin SB (August 2008). Lee JT (ed.). "Double strand breaks can initiate gene silencing and SIRT1-dependent onset of DNA methylation in an exogenous promoter CpG island". PLoS Genetics. 4 (8): e1000155. doi:10.1371/journal.pgen.1000155. PMC   2491723 . PMID   18704159.
  90. Cuozzo C, Porcellini A, Angrisano T, Morano A, Lee B, Di Pardo A, Messina S, Iuliano R, Fusco A, Santillo MR, Muller MT, Chiariotti L, Gottesman ME, Avvedimento EV (July 2007). "DNA damage, homology-directed repair, and DNA methylation". PLoS Genetics. 3 (7): e110. doi:10.1371/journal.pgen.0030110. PMC   1913100 . PMID   17616978.
  91. Malkin D (April 2011). "Li-fraumeni syndrome". Genes & Cancer. 2 (4): 475–84. doi:10.1177/1947601911413466. PMC   3135649 . PMID   21779515.
  92. Fearon ER (November 1997). "Human cancer syndromes: clues to the origin and nature of cancer". Science. 278 (5340): 1043–50. Bibcode:1997Sci...278.1043F. doi:10.1126/science.278.5340.1043. PMID   9353177.
  93. Vogelstein B, Papadopoulos N, Velculescu VE, Zhou S, Diaz LA, Kinzler KW (March 2013). "Cancer genome landscapes". Science. 339 (6127): 1546–58. Bibcode:2013Sci...339.1546V. doi:10.1126/science.1235122. PMC   3749880 . PMID   23539594.
  94. 1 2 "Metastatic Cancer: Questions and Answers". National Cancer Institute. 12 May 2015. Retrieved 28 March 2018.
  95. "What is Metastasized Cancer?". National Comprehensive Cancer Network. Archived from the original on 7 July 2013. Retrieved 18 July 2013.
  96. Varricchio CG (2004). A cancer source book for nurses. Boston: Jones and Bartlett Publishers. p. 229. ISBN   978-0-7637-3276-9.
  97. "Cancer prevention: 7 steps to reduce your risk". Mayo Clinic. 27 September 2008. Archived from the original on 8 February 2010. Retrieved 30 January 2010.
  98. Danaei G, Vander Hoorn S, Lopez AD, Murray CJ, Ezzati M (November 2005). "Causes of cancer in the world: comparative risk assessment of nine behavioural and environmental risk factors". Lancet. 366 (9499): 1784–93. doi:10.1016/S0140-6736(05)67725-2. PMID   16298215.
  99. Wu S, Powers S, Zhu W, Hannun YA (January 2016). "Substantial contribution of extrinsic risk factors to cancer development". Nature. 529 (7584): 43–7. Bibcode:2016Natur.529...43W. doi:10.1038/nature16166. PMC   4836858 . PMID   26675728.
  100. "Cancer". World Health Organization. Archived from the original on 29 December 2010. Retrieved 9 January 2011.
  101. 1 2 Wicki A, Hagmann J (September 2011). "Diet and cancer". Swiss Medical Weekly. 141: w13250. doi:10.4414/smw.2011.13250. PMID   21904992.
  102. Cappellani A, Di Vita M, Zanghi A, Cavallaro A, Piccolo G, Veroux M, Berretta M, Malaguarnera M, Canzonieri V, Lo Menzo E (January 2012). "Diet, obesity and breast cancer: an update". Frontiers in Bioscience. 4: 90–108. doi:10.2741/253. PMID   22202045.
  103. Key TJ (January 2011). "Fruit and vegetables and cancer risk". British Journal of Cancer. 104 (1): 6–11. doi:10.1038/sj.bjc.6606032. PMC   3039795 . PMID   21119663.
  104. Wang X, Ouyang Y, Liu J, Zhu M, Zhao G, Bao W, Hu FB (July 2014). "Fruit and vegetable consumption and mortality from all causes, cardiovascular disease, and cancer: systematic review and dose-response meta-analysis of prospective cohort studies". BMJ. 349: g4490. doi:10.1136/bmj.g4490. PMC   4115152 . PMID   25073782.
  105. Larsson SC, Wolk A (May 2007). "Coffee consumption and risk of liver cancer: a meta-analysis". Gastroenterology. 132 (5): 1740–5. doi:10.1053/j.gastro.2007.03.044. PMID   17484871.
  106. Zheng W, Lee SA (2009). "Well-done meat intake, heterocyclic amine exposure, and cancer risk". Nutrition and Cancer. 61 (4): 437–46. doi:10.1080/01635580802710741. PMC   2769029 . PMID   19838915.
  107. Ferguson LR (February 2010). "Meat and cancer". Meat Science. 84 (2): 308–13. doi:10.1016/j.meatsci.2009.06.032. PMID   20374790.
  108. Staff (26 October 2015). "World Health Organization – IARC Monographs evaluate consumption of red meat and processed meat" (PDF). International Agency for Research on Cancer . Archived (PDF) from the original on 26 October 2015. Retrieved 26 October 2015.
  109. Hauser, Christine (26 October 2015). "W.H.O. Report Links Some Cancers With Processed or Red Meat". The New York Times . Archived from the original on 26 October 2015. Retrieved 26 October 2015.
  110. Holland Chp.33
  111. Rostom A, Dubé C, Lewin G, Tsertsvadze A, Barrowman N, Code C, Sampson M, Moher D (March 2007). "Nonsteroidal anti-inflammatory drugs and cyclooxygenase-2 inhibitors for primary prevention of colorectal cancer: a systematic review prepared for the U.S. Preventive Services Task Force". Annals of Internal Medicine. 146 (5): 376–89. doi:10.7326/0003-4819-146-5-200703060-00010. PMID   17339623.
  112. Rothwell PM, Fowkes FG, Belch JF, Ogawa H, Warlow CP, Meade TW (January 2011). "Effect of daily aspirin on long-term risk of death due to cancer: analysis of individual patient data from randomised trials". Lancet. 377 (9759): 31–41. doi:10.1016/S0140-6736(10)62110-1. PMID   21144578.
  113. Cooper K, Squires H, Carroll C, Papaioannou D, Booth A, Logan RF, Maguire C, Hind D, Tappenden P (June 2010). "Chemoprevention of colorectal cancer: systematic review and economic evaluation". Health Technology Assessment. 14 (32): 1–206. doi:10.3310/hta14320. PMID   20594533.
  114. Thomsen A, Kolesar JM (December 2008). "Chemoprevention of breast cancer". American Journal of Health-System Pharmacy. 65 (23): 2221–28. doi:10.2146/ajhp070663. PMID   19020189.
  115. Wilt TJ, MacDonald R, Hagerty K, Schellhammer P, Kramer BS (April 2008). Wilt TJ (ed.). "Five-alpha-reductase Inhibitors for prostate cancer prevention". The Cochrane Database of Systematic Reviews (2): CD007091. doi:10.1002/14651858.CD007091. PMID   18425978.
  116. "Vitamins and minerals: not for cancer or cardiovascular prevention". Prescrire International. 19 (108): 182. August 2010. PMID   20939459. Archived from the original on 25 May 2012.
  117. Giovannucci E, Liu Y, Rimm EB, Hollis BW, Fuchs CS, Stampfer MJ, Willett WC (April 2006). "Prospective study of predictors of vitamin D status and cancer incidence and mortality in men". Journal of the National Cancer Institute. 98 (7): 451–59. doi:10.1093/jnci/djj101. PMID   16595781.
  118. "Vitamin D Has Role in Colon Cancer Prevention". Archived from the original on 4 December 2006. Retrieved 27 July 2007.
  119. Holick MF (January 2013). "Vitamin D, sunlight and cancer connection". Anti-Cancer Agents in Medicinal Chemistry. 13 (1): 70–82. doi:10.2174/187152013804487308. PMID   23094923.
  120. Schwartz GG, Blot WJ (April 2006). "Vitamin D status and cancer incidence and mortality: something new under the sun". Journal of the National Cancer Institute. 98 (7): 428–30. doi:10.1093/jnci/djj127. PMID   16595770.
  121. 1 2 Bolland MJ, Grey A, Gamble GD, Reid IR (April 2014). "The effect of vitamin D supplementation on skeletal, vascular, or cancer outcomes: a trial sequential meta-analysis". The Lancet. Diabetes & Endocrinology. 2 (4): 307–20. doi:10.1016/S2213-8587(13)70212-2. PMID   24703049.
  122. Bjelakovic G, Gluud LL, Nikolova D, Whitfield K, Wetterslev J, Simonetti RG, Bjelakovic M, Gluud C (January 2014). "Vitamin D supplementation for prevention of mortality in adults". The Cochrane Database of Systematic Reviews. 1 (1): CD007470. doi:10.1002/14651858.cd007470.pub3. PMID   24414552.
  123. Fritz H, Kennedy D, Fergusson D, Fernandes R, Doucette S, Cooley K, Seely A, Sagar S, Wong R, Seely D (2011). Minna JD (ed.). "Vitamin A and retinoid derivatives for lung cancer: a systematic review and meta analysis". PLOS ONE. 6 (6): e21107. Bibcode:2011PLoSO...6E1107F. doi:10.1371/journal.pone.0021107. PMC   3124481 . PMID   21738614.
  124. Cole BF, Baron JA, Sandler RS, Haile RW, Ahnen DJ, Bresalier RS, McKeown-Eyssen G, Summers RW, Rothstein RI, Burke CA, Snover DC, Church TR, Allen JI, Robertson DJ, Beck GJ, Bond JH, Byers T, Mandel JS, Mott LA, Pearson LH, Barry EL, Rees JR, Marcon N, Saibil F, Ueland PM, Greenberg ER (June 2007). "Folic acid for the prevention of colorectal adenomas: a randomized clinical trial". JAMA. 297 (21): 2351–59. doi:10.1001/jama.297.21.2351. PMID   17551129.
  125. Vinceti, Marco; Filippini, Tommaso; Del Giovane, Cinzia; Dennert, Gabriele; Zwahlen, Marcel; Brinkman, Maree; Zeegers, Maurice Pa; Horneber, Markus; D'Amico, Roberto (2018). "Selenium for preventing cancer". The Cochrane Database of Systematic Reviews. 1: CD005195. doi:10.1002/14651858.CD005195.pub4. ISSN   1469-493X. PMC   6491296 . PMID   29376219.
  126. 1 2 3 "Cancer Vaccine Fact Sheet". NCI. 8 June 2006. Retrieved 28 March 2018.
  127. 1 2 Lertkhachonsuk AA, Yip CH, Khuhaprema T, Chen DS, Plummer M, Jee SH, Toi M, Wilailak S (November 2013). "Cancer prevention in Asia: resource-stratified guidelines from the Asian Oncology Summit 2013". The Lancet. Oncology. 14 (12): e497–507. arXiv: cond-mat/0606434 . doi:10.1016/S1470-2045(13)70350-4. PMID   24176569.
  128. 1 2 3 "Cancer Screening Overview (PDQ®)–Patient Version". National Cancer Institute. 13 January 2010. Retrieved 28 March 2018.
  129. 1 2 3 Wilson JMG, Jungner G. (1968) Principles and practice of screening for disease. Geneva:World Health Organization. Public Health Papers, #34.
  130. "Screening for Cervical Cancer". U.S. Preventive Services Task Force . 2003. Archived from the original on 23 December 2010.
  131. "Screening for Colorectal Cancer". U.S. Preventive Services Task Force . 2008. Archived from the original on 7 February 2015.
  132. "Screening for Skin Cancer". U.S. Preventive Services Task Force . 2009. Archived from the original on 8 January 2011.
  133. "Screening for Oral Cancer". U.S. Preventive Services Task Force . 2004. Archived from the original on 24 October 2010.
  134. "Lung Cancer Screening". U.S. Preventive Services Task Force . 2004. Archived from the original on 4 November 2010.
  135. "Screening for Prostate Cancer". U.S. Preventive Services Task Force . 2008. Archived from the original on 31 December 2010.
  136. "Screening for Bladder Cancer". U.S. Preventive Services Task Force . 2004. Archived from the original on 23 August 2010.
  137. "Screening for Testicular Cancer". U.S. Preventive Services Task Force . 2004. Archived from the original on 15 May 2016.
  138. "Screening for Ovarian Cancer". U.S. Preventive Services Task Force . 2004. Archived from the original on 23 October 2010.
  139. "Screening for Pancreatic Cancer". U.S. Preventive Services Task Force . 2004. Archived from the original on 21 November 2010.
  140. Chou R, Croswell JM, Dana T, Bougatous C, Blazina I, Fu R, Gleitsmann K, Koenig HC, et al. (7 October 2011). "Screening for Prostate Cancer: A Review of the Evidence for the U.S. Preventive Services Task Force". United States Preventive Services Task Force. Archived from the original on 11 October 2011. Retrieved 8 October 2011.
  141. "Screening for Breast Cancer". U.S. Preventive Services Task Force . 2009. Archived from the original on 2 January 2013.
  142. Gøtzsche PC, Jørgensen KJ (June 2013). "Screening for breast cancer with mammography". The Cochrane Database of Systematic Reviews (6): CD001877. doi:10.1002/14651858.CD001877.pub5. PMID   23737396.
  143. 1 2 Gulati AP, Domchek SM (January 2008). "The clinical management of BRCA1 and BRCA2 mutation carriers". Current Oncology Reports. 10 (1): 47–53. doi:10.1007/s11912-008-0008-9. PMID   18366960.
  144. Lind MJ (2008). "Principles of cytotoxic chemotherapy". Medicine. 36 (1): 19–23. doi:10.1016/j.mpmed.2007.10.003.
  145. "Targeted Cancer Therapies". About Cancer. National Cancer Institute. 26 February 2018. Retrieved 28 March 2018.
  146. 1 2 Holland Chp. 40
  147. Nastoupil LJ, Rose AC, Flowers CR (May 2012). "Diffuse large B-cell lymphoma: current treatment approaches". Oncology. 26 (5): 488–95. PMID   22730604.
  148. Freedman A (October 2012). "Follicular lymphoma: 2012 update on diagnosis and management". American Journal of Hematology. 87 (10): 988–95. doi:10.1002/ajh.23313. PMID   23001911.
  149. Rampling R, James A, Papanastassiou V (June 2004). "The present and future management of malignant brain tumours: surgery, radiotherapy, chemotherapy". Journal of Neurology, Neurosurgery, and Psychiatry. 75 Suppl 2 (Suppl 2): ii24–30. doi:10.1136/jnnp.2004.040535. PMC   1765659 . PMID   15146036.
  150. Madan V, Lear JT, Szeimies RM (February 2010). "Non-melanoma skin cancer". Lancet. 375 (9715): 673–85. doi:10.1016/S0140-6736(09)61196-X. PMC   3339125 . PMID   20171403.
  151. CK Bomford, IH Kunkler, J Walter. Walter and Miller's Textbook of Radiation therapy (6th Ed), p311
  152. Prince, Jim McMorran, Damian Crowther, Stew McMorran, Steve Youngmin, Ian Wacogne, Jon Pleat, Clive. "tumour radiosensitivity – General Practice Notebook". Archived from the original on 24 September 2015.
  153. Tidy C. "Radiotherapy". Patient UK. Archived from the original on 9 July 2017. Last Checked: 23 December 2015
  154. Hill R, Healy B, Holloway L, Kuncic Z, Thwaites D, Baldock C (March 2014). "Advances in kilovoltage x-ray beam dosimetry". Physics in Medicine and Biology. 59 (6): R183–231. Bibcode:2014PMB....59R.183H. doi:10.1088/0031-9155/59/6/r183. PMID   24584183.
  155. 1 2 Holland Chp. 41
  156. 1 2 3 4 5 American Society of Clinical Oncology. "Five Things Physicians and Patients Should Question" (PDF). Choosing Wisely: An Initiative of the ABIM Foundation. Archived from the original (PDF) on 31 July 2012. Retrieved 14 August 2012
    • The American Society of Clinical Oncology made this recommendation based on various cancers. See American Society of Clinical Oncology. "Five Things Physicians and Patients Should Question" (PDF). Choosing Wisely: An Initiative of the ABIM Foundation. Archived from the original (PDF) on 31 July 2012. Retrieved 14 August 2012
    • for lung cancer, see Azzoli CG, Temin S, Aliff T, Baker S, Brahmer J, Johnson DH, Laskin JL, Masters G, Milton D, Nordquist L, Pao W, Pfister DG, Piantadosi S, Schiller JH, Smith R, Smith TJ, Strawn JR, Trent D, Giaccone G (October 2011). "2011 Focused Update of 2009 American Society of Clinical Oncology Clinical Practice Guideline Update on Chemotherapy for Stage IV Non-Small-Cell Lung Cancer". Journal of Clinical Oncology. 29 (28): 3825–31. doi:10.1200/JCO.2010.34.2774. PMC   3675703 . PMID   21900105. and Ettinger DS, Akerley W, Bepler G, Blum MG, Chang A, Cheney RT, et al. (July 2010). "Non-small cell lung cancer". Journal of the National Comprehensive Cancer Network. 8 (7): 740–801. PMID   20679538.
    • for breast cancer, see Carlson RW, Allred DC, Anderson BO, Burstein HJ, Carter WB, Edge SB, et al. (February 2009). "Breast cancer. Clinical practice guidelines in oncology". Journal of the National Comprehensive Cancer Network. 7 (2): 122–92. PMID   19200416.
    • for colon cancer, see Engstrom PF, Arnoletti JP, Benson AB, Chen YJ, Choti MA, Cooper HS, Covey A, Dilawari RA, Early DS, Enzinger PC, Fakih MG, Fleshman J, Fuchs C, Grem JL, Kiel K, Knol JA, Leong LA, Lin E, Mulcahy MF, Rao S, Ryan DP, Saltz L, Shibata D, Skibber JM, Sofocleous C, Thomas J, Venook AP, Willett C (September 2009). "NCCN Clinical Practice Guidelines in Oncology: colon cancer". Journal of the National Comprehensive Cancer Network. 7 (8): 778–831. PMID   19755046.
    • for other general statements see Smith TJ, Hillner BE (May 2011). "Bending the cost curve in cancer care". The New England Journal of Medicine. 364 (21): 2060–5. doi:10.1056/NEJMsb1013826. PMC   4042405 . PMID   21612477. and Peppercorn JM, Smith TJ, Helft PR, Debono DJ, Berry SR, Wollins DS, Hayes DM, Von Roenn JH, Schnipper LE (February 2011). "American society of clinical oncology statement: toward individualized care for patients with advanced cancer". Journal of Clinical Oncology. 29 (6): 755–60. doi:10.1200/JCO.2010.33.1744. PMID   21263086.
  157. "NCCN Guidelines". Archived from the original on 14 May 2008.
  158. "Clinical Practice Guidelines for Quality Palliative Care" (PDF). The National Consensus Project for Quality Palliative Care (NCP). Archived from the original (PDF) on 16 May 2011.
  159. Levy MH, Back A, Bazargan S, Benedetti C, Billings JA, Block S, Bruera E, Carducci MA, Dy S, Eberle C, Foley KM, Harris JD, Knight SJ, Milch R, Rhiner M, Slatkin NE, Spiegel D, Sutton L, Urba S, Von Roenn JH, Weinstein SM (September 2006). "Palliative care. Clinical practice guidelines in oncology". Journal of the National Comprehensive Cancer Network. 4 (8): 776–818. PMID   16948956.
  160. Waldmann TA (March 2003). "Immunotherapy: past, present and future". Nature Medicine. 9 (3): 269–77. doi:10.1038/nm0303-269. PMID   12612576.
  161. "Lasers in Cancer Treatment". National Institutes of Health, National Cancer Institute. 13 September 2011. Retrieved 15 December 2017.PD-icon.svgThis article incorporates text from this source, which is in the public domain.
  162. Cassileth BR, Deng G (2004). "Complementary and alternative therapies for cancer". The Oncologist. 9 (1): 80–89. doi:10.1634/theoncologist.9-1-80. PMID   14755017.
  163. What Is CAM? Archived 8 December 2005 at WebCite National Center for Complementary and Alternative Medicine. retrieved 3 February 2008.
  164. Vickers A (2004). "Alternative cancer cures: "unproven" or "disproven"?". Ca. 54 (2): 110–18. CiteSeerX . doi:10.3322/canjclin.54.2.110. PMID   15061600.
  165. World Cancer Report 2014. World Health Organization. 2014. p. 22. ISBN   978-92-832-0429-9. Archived from the original on 12 July 2017.
  166. 1 2 Rheingold S, Neugut A, Meadows A (2003). "156: Secondary Cancers: Incidence, Risk Factors, and Management". In Frei E, Kufe DW, Holland JF (eds.). Holland-Frei Cancer Medicine (6th ed.). Hamilton, Ont: BC Decker. p. 2399. ISBN   978-1-55009-213-4.
  167. Montazeri A (December 2009). "Quality of life data as prognostic indicators of survival in cancer patients: an overview of the literature from 1982 to 2008". Health and Quality of Life Outcomes. 7: 102. doi:10.1186/1477-7525-7-102. PMC   2805623 . PMID   20030832.
  168. 1 2 3 Akl, Elie A.; Kahale, Lara A.; Hakoum, Maram B.; Matar, Charbel F.; Sperati, Francesca; Barba, Maddalena; Yosuico, Victor E. D.; Terrenato, Irene; Synnot, Anneliese (2017). "Parenteral anticoagulation in ambulatory patients with cancer". The Cochrane Database of Systematic Reviews. 9: CD006652. doi:10.1002/14651858.CD006652.pub5. ISSN   1469-493X. PMC   6419241 . PMID   28892556.
  169. 1 2 "Latest global cancer data: Cancer burden rises to 18.1 million new cases and 9.6 million cancer deaths in 2018" (PDF). Retrieved 5 December 2018.
  170. 1 2 Lozano R, Naghavi M, Foreman K, Lim S, Shibuya K, Aboyans V, et al. (December 2012). "Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010". Lancet. 380 (9859): 2095–128. doi:10.1016/S0140-6736(12)61728-0. hdl:10536/DRO/DU:30050819. PMID   23245604.
  171. 1 2 Coleman WB, Rubinas TC (2009). "4". In Tsongalis GJ, Coleman WL (eds.). Molecular Pathology: The Molecular Basis of Human Disease. Amsterdam: Elsevier Academic Press. p. 66. ISBN   978-0-12-374419-7.
  172. Johnson G (28 December 2010). "Unearthing Prehistoric Tumors, and Debate". The New York Times . Archived from the original on 24 June 2017.
  173. Pawelec G, Derhovanessian E, Larbi A (August 2010). "Immunosenescence and cancer". Critical Reviews in Oncology/Hematology. 75 (2): 165–72. doi:10.1016/j.critrevonc.2010.06.012. PMID   20656212.
  174. Alberts B, Johnson A, Lewis J, et al. (2002). "The Preventable Causes of Cancer". Molecular biology of the cell (4th ed.). New York: Garland Science. ISBN   978-0-8153-4072-0. Archived from the original on 2 January 2016. A certain irreducible background incidence of cancer is to be expected regardless of circumstances: mutations can never be absolutely avoided, because they are an inescapable consequence of fundamental limitations on the accuracy of DNA replication, as discussed in Chapter 5. If a human could live long enough, it is inevitable that at least one of his or her cells would eventually accumulate a set of mutations sufficient for cancer to develop.
  175. Anisimov VN, Sikora E, Pawelec G (August 2009). "Relationships between cancer and aging: a multilevel approach". Biogerontology. 10 (4): 323–38. doi:10.1007/s10522-008-9209-8. PMID   19156531.
  176. de Magalhães JP (May 2013). "How ageing processes influence cancer". Nature Reviews. Cancer. 13 (5): 357–65. doi:10.1038/nrc3497. PMID   23612461.
  177. Schottenfeld D, Fraumeni JF (24 August 2006). Cancer Epidemiology and Prevention. Oxford University Press. p. 977. ISBN   978-0-19-974797-9.
  178. Bostwick DG, Eble JN (2007). Urological Surgical Pathology. St. Louis: Mosby. p. 468. ISBN   978-0-323-01970-5.
  179. 1 2 Kaatsch P (June 2010). "Epidemiology of childhood cancer". Cancer Treatment Reviews. 36 (4): 277–85. doi:10.1016/j.ctrv.2010.02.003. PMID   20231056.
  180. 1 2 Ward E, DeSantis C, Robbins A, Kohler B, Jemal A (January 2014). "Childhood and adolescent cancer statistics, 2014". Ca. 64 (2): 83–103. doi:10.3322/caac.21219. PMID   24488779.
  181. Ward EM, Thun MJ, Hannan LM, Jemal A (September 2006). "Interpreting cancer trends". Annals of the New York Academy of Sciences. 1076 (1): 29–53. Bibcode:2006NYASA1076...29W. doi:10.1196/annals.1371.048. PMID   17119192.
  182. 1 2 3 4 5 6 Hajdu SI (March 2011). "A note from history: landmarks in history of cancer, part 1". Cancer. 117 (5): 1097–102. doi:10.1002/cncr.25553. PMID   20960499.
  183. Paul of Aegina, 7th Century AD, quoted in Moss, Ralph W. (2004). "Galen on Cancer". CancerDecisions. Archived from the original on 16 July 2011. Referenced from Michael Shimkin, Contrary to Nature, Washington, DC: Superintendent of Document, DHEW Publication No. (NIH) 79–720, p. 35.
  184. Majno G, Joris I (12 August 2004). Cells, Tissues, and Disease : Principles of General Pathology: Principles of General Pathology. Oxford University Press. ISBN   978-0-19-974892-1 . Retrieved 11 September 2013.
  185. 1 2 Hajdu SI (June 2011). "A note from history: landmarks in history of cancer, part 2". Cancer. 117 (12): 2811–20. doi:10.1002/cncr.25825. PMID   21656759.
  186. Yalom, Marilyn (1998). A history of the breast (1 ed.). New York: Ballantine Books. ISBN   978-0-679-43459-7.
  187. Hajdu SI (February 2012). "A note from history: landmarks in history of cancer, part 3". Cancer. 118 (4): 1155–68. doi:10.1002/cncr.26320. PMID   21751192.
  188. Grange JM, Stanford JL, Stanford CA (June 2002). "Campbell De Morgan's 'Observations on cancer', and their relevance today". Journal of the Royal Society of Medicine. 95 (6): 296–99. doi:10.1258/jrsm.95.6.296. PMC   1279913 . PMID   12042378.
  189. Ehrenreich, Barbara (November 2001). "Welcome to Cancerland". Harper's Magazine . ISSN   0017-789X. Archived from the original on 8 November 2013.
  190. 1 2 3 4 Chochinov HM, Breitbart W (2009). Handbook of Psychiatry in Palliative Medicine. Oxford University Press. p. 196. ISBN   978-0-19-530107-6.
  191. Rapini RP, Bolognia JL, Jorizzo JL (2007). Dermatology: 2-Volume Set. St. Louis: Mosby. ISBN   978-1-4160-2999-1.
  192. "Skin cancers". World Health Organization. Archived from the original on 27 September 2010. Retrieved 19 January 2011.
  193. McCulley M, Greenwell P (2007). Molecular therapeutics: 21st-century medicine. London: J. Wiley. p. 207. ISBN   978-0-470-01916-0.
  194. Low G, Cameron L (1999). "10". Researching and Applying Metaphor. Cambridge University Press. ISBN   978-0-521-64964-3.
  195. Sulik, Gayle A. (2010). Pink Ribbon Blues: How Breast Cancer Culture Undermines Women's Health. Oxford University Press. pp. 78–89. ISBN   978-0-19-974993-5.
  196. 1 2 3 Olson JS (2005). Bathsheba's Breast: Women, Cancer, and History. JHU Press. pp. 145–70. ISBN   978-0-8018-8064-3. OCLC   186453370.
  197. 1 2 3 4 Ehrenreich, Barbara (2009). Bright-sided: How the Relentless Promotion of Positive Thinking Has Undermined America. Henry Holt and Company. pp. 15–44. ISBN   978-0-8050-8749-9.
  198. Huff C (24 September 2013). "A Sick Stigma: Why are cancer patients blamed for their illness?". Slate. Archived from the original on 11 October 2013.
  199. "Economic Impact of Cancer". American Cancer Society. 3 January 2018. Retrieved 5 July 2018.
  200. Bosanquet N, Sikora, K (2004). "The economics of cancer care in the UK". Lancet Oncology. 5 (9): 568–74. doi:10.1016/S1470-2045(04)01569-4. PMID   15337487.
  201. Mariotto AB, Yabroff KR, Shao Y, Feuer EJ, Brown ML (2011). "Projections of the cost of cancer care in the United States: 2010-2020". Journal of the National Cancer Institute. 103 (2): 117–28. doi:10.1093/jnci/djq495. PMC   3107566 . PMID   21228314.
  202. Jönsson B, Hofmarcher T, Lindgren P, Wilking N (2016). "The cost and burden of cancer in the European Union 1995-2014". European Journal of Cancer. 66 (Oct): 162–70. doi:10.1016/j.ejca.2016.06.022. PMID   27589247.
  203. Luengo-Fernandez R, Leal J, Gray A, Sullivan R (2013). "Economic burden of cancer across the European Union: a population-based cost analysis". Lancet Oncology. 14 (12): 1165–74. doi:10.1016/S1470-2045(13)70442-X. PMID   24131614.
  204. 1 2 U.S. Equal Employment Opportunity Commission. "Questions & Answers about Cancer in the Workplace and the Americans with Disabilities Act (ADA)."
  205. "What Is Cancer?". National Cancer Institute. 17 September 2007. Retrieved 28 March 2018.
  206. "Cancer Fact Sheet". Agency for Toxic Substances & Disease Registry. 30 August 2002. Archived from the original on 13 August 2009. Retrieved 17 August 2009.
  207. Wanjek C (16 September 2006). "Exciting New Cancer Treatments Emerge Amid Persistent Myths". Archived from the original on 16 May 2008. Retrieved 17 August 2009.
  208. Hayden EC (April 2009). "Cutting off cancer's supply lines". Nature. 458 (7239): 686–87. doi:10.1038/458686b. PMID   19360048.
  209. Bagri A, Kouros-Mehr H, Leong KG, Plowman GD (March 2010). "Use of anti-VEGF adjuvant therapy in cancer: challenges and rationale". Trends in Molecular Medicine. 16 (3): 122–32. doi:10.1016/j.molmed.2010.01.004. PMID   20189876.
  210. Sleigh SH, Barton CL (2010). "Repurposing Strategies for Therapeutics". Pharm Med. 24 (3): 151–59. doi:10.2165/11536770-000000000-00000 (inactive 29 December 2018).
  211. Winther H, Jorgensen JT (2010). "Drug-Diagnostic Co-Development in Cancer". Pharm Med. 24 (6): 363–75. doi:10.2165/11586320-000000000-00000 (inactive 29 December 2018).
  212. Begley S (16 September 2008). "Rethinking the War on Cancer". Newsweek. Archived from the original on 10 September 2008. Retrieved 8 September 2008.
  213. Kolata G (23 April 2009). "Advances Elusive in the Drive to Cure Cancer". The New York Times . Archived from the original on 14 January 2012. Retrieved 5 May 2009.
  214. Bruce Alberts, Marc W. Kirschner, Shirley Tilghman, and Harold Varmus (2014). "Rescuing US biomedical research from its systemic flaws". Proceedings of the National Academy of Sciences of the United States of America. 111 (16): 5773–77. Bibcode:2014PNAS..111.5773A. doi:10.1073/pnas.1404402111. PMC   4000813 . PMID   24733905. Archived from the original on 18 May 2014.CS1 maint: Multiple names: authors list (link)
  216. Kolata G (27 June 2009). "Grant System Leads Cancer Researchers to Play It Safe". The New York Times. Archived from the original on 8 June 2011. Retrieved 29 December 2009.
  217. Powell K (2016). "Young, talented and fed-up: scientists tell their stories". Nature. 538 (7626): 446–49. Bibcode:2016Natur.538..446P. doi:10.1038/538446a. PMID   27786221. Archived from the original on 27 October 2016.
  218. 1 2 3 4 5 6 Yarbro CH, Wujcik D, Gobel BH (2010). Cancer Nursing: Principles and Practice. Jones & Bartlett Learning. pp. 901–05. ISBN   978-0-7637-6357-2.
  219. Thamm, Douglas (March 2009). "How companion animals contribute to the fight against cancer in humans" (PDF). Veterinaria Italiana. 54 (1): 111–20. Archived (PDF) from the original on 23 July 2014. Retrieved 18 July 2014.
  220. Murgia C, Pritchard JK, Kim SY, Fassati A, Weiss RA (August 2006). "Clonal origin and evolution of a transmissible cancer". Cell. 126 (3): 477–87. doi:10.1016/j.cell.2006.05.051. PMC   2593932 . PMID   16901782.

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