Friday, January 14, 2011

cancer


Cancer


Cancer  (medical term: malignant neoplasm) is a class of disease in which a group of cells
display uncontrolled growth through division beyond normal limits, invasion that intrudes upon
and destroys adjacent tissues, and sometimes metastasis, in which cancer cells spread to o-
ther locations in the body vialymph or blood. These three malignant properties of cancers differ-
entiate  them from benign tumors, which are self-limited, and do not invade or metastasize.
Cancers are primarily an environmental disease with 90-95% of cases due environmental factors
such as lifestyle, and 5-10% directly due to heredity.[1] Common environmental factors leading
to cancer include: tobacco (25-30%), diet and obesity (30-35%), infections (15-20%), radiation,
stress, lack of physical activity, and environmental pollutants.[1] These environmental factors ca-
use or enhance abnormalities in the genetic material of cells.[2] Cell reproduction is an extremely
complex process, which is normally tightly regulated by several classes of genes including onco-
genes and tumor suppressor genes. Hereditary or acquired abnormalities in these regulatory ge-
nes can lead to uncontrolled cell growth, and the development of cancer.
The presence of cancer can be suspected on the basis of symptoms, or findings on radiology. De-
finitive diagnosis of cancer, however, requires the microscopic examination of a biopsy specimen.
Most cancers can be treated. Possible treatments include chemotherapyradiotherapy and sur-
gery. The prognosis is influenced by the type of cancer and the extent of disease. While cancer 
can affect people of all ages the risk typically increases with age.[3] In 2007 cancer caused about 
13% of all human deaths worldwide (7.9 million) and it is projected to be 12 million deaths per
 year by 2030.

Cancer
Classification and external resources
A coronal CT scan showing a cancer of rightpleural membranes, the outer surface of the lung and inner surface of the chest wall,malignant mesothelioma.
Legend: → tumor ←, ★ central pleural effusion, 1 & 3 lungs, 2 spine, 4 ribs, 5 aorta, 6 spleen, 7 & 8 kidneys, 9 liver.


Classification

Cancers are classified by the type of cell that the tumor resembles 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, a cancer of the liver is calledhepatocarcin-
oma; a cancer of 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 the cancer under the microscope, which suggests tha-
t 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 also use the
-oma suffix, examples including melanoma and seminoma.

Signs and symptoms

Local symptoms are lead to the growth ofhemorrhage (bleeding from the skin, mouth or anus)
,ulceration andpain. Although local pain commonly occurs in advanced cancer, the initial swelling
is often painless.None of these are diagnostic, as many of these symptoms commonly occur 
in patients who do not have cancer.

Pathophysiology

The affected genes are divided into two broad categories. Oncogenes are genes which promote cell
 growthCancer is fundamentally a disease of failure of regulation of tissue growth. In order for a normal cell to
 transform into a cancer cell, the genes which regulate cell growth and differentiation must be altered.[5]
transformation can occur through the formation of novel oncogenes, the inappropriate over-expression of 
 and reproduction. Tumor suppressor genes are genes which inhibit cell division and survival. Malignant 
normal oncogenes, or by the under-expression or disabling of tumor suppressor genes. Typically, changes
 in many genes are required to transform a normal cell into a cancer cell.[6]
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 aremutations - 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 many 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.
Small-scale mutations include point mutations, deletions, and insertions, which may occur in the promoter
 region of a gene and affect its expression, or may occur in the gene'scoding sequence and alter the function
 or stability of its protein product. Disruption of a single gene may also result from integration of genomic 
material from a DNA virus orretrovirus, and resulting in the expression of viral oncogenes in the affected 
cell and its descendants.
Replication of the enormous amount of 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 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 pres-
ence of disruptive substances called carcinogens, repeated physical injury, heat, ionising radiation, or hypoxia[7]
 (see causes, below).
The errors which cause cancer are self-amplifying and compounding, For example:
1.>A mutation in the error-correcting machinery of a cell might cause that cell and its children to accumulate
 errors more rapidly.
2.>A further mutation in an oncogene might cause the cell to reproduce more rapidly and more frequently than 
its normal counterparts.
3.>A further mutation may cause loss of a tumour suppressor gene, disrupting the apoptosis signalling pathway
 and resulting in the cell becoming immortal.
4.>A further mutation in signaling machinery of the cell might send error-causing signals to nearby cells
The transformation of 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 the controls that limit normal tissue growth.
This rebellion-like scenario becomes 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 
ognoing process, termed clonal evolution drives progression towards more invasive stages.[8]

Causes

Cancers are primarily an environmental disease with 90-95% of cases due to environmental factors and 5-10% due
 to genetics.[1] "Environmental", as used by cancer researchers, means any cause that is not genetic, and inclu-
des everything from natural sunlight to industrial pollution to viruses to behavioral choices to old age. Most environ-
mental causes, such as naturally occurringbackground radiation, are not modifiable or controllable. Common env-
ironmental factors that lead to cancer death include: tobacco (25-30% of deaths), diet and obesity (30-35%), infec-
tions (15-20%), radiation, stress, lack of physical activity, and environmental pollutants.[1]

Chemicals


Many mutagens are also carcinogens, but some carcinogens are not mutagens. Alcohol is an example of a Cancer
pathogenesis is traceable back to DNA mutations that impact cell growth and metastasis. Substances
that cause DNA mutations are known as mutagens, and mutagens that cause cancers are known as carcinogens
Particular substances have been linked to specific types of cancer. Tobacco smoking is associated with many
forms of cancer,[9] and causes 90% of lung cancer.[10] Prolonged exposure to asbestos fibers is associated with
chemical carcinogen that is not a mutagen.[13] Such chemicals may promote cancers through stimulating the
 rate of cell division. Faster rates of replication leaves less time for repair enzymes to repair damaged DNA 
duringDNA replication, increasing the likelihood of a mutation.
Decades of research has demonstrated the link between tobacco use and cancer in the lunglarynx, head,
 neck, stomach, bladder, kidney, oesophagus and pancreas.[14]Tobacco smoke contains over fifty known
 carcinogens, including nitrosamines and polycyclic aromatic hydrocarbons.[15] Tobacco is responsible for
 about one in three of all cancer deaths in the developed world,[9] and about one in five worldwide.[15] Indeed,
 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[when?], decreases in smoking
 followed by decreases in lung cancer death rates in men. However, the numbers of smokers worldwide is 
still rising, leading to what some organizations have described as the tobacco epidemic.[16]
Cancer related to ones occupation is believed to represent between 2-20% of all cases.[17] Every year, at
 least 200,000 people die worldwide from cancer related to their workplace.[18] Millions of workers run the
 risk of developing cancers such as lung cancer and mesothelioma from inhaling asbestos fibers and tobacco
 smoke, or leukemiafrom exposure to benzene at their workplaces.[18] Currently, most cancer deaths caused
 by occupational risk factors occur in the developed world.[18] It is estimated that approximately 20,000
 cancer deaths and 40,000 new cases of cancer each year in the U.S. are attributable to occupation.[19]

Radiation

Sources of ionizing radiation, such as radon gas, can cause cancer. Prolonged exposure to ultraviolet 
radiation from the sun can lead to melanoma and other skin malignancies.[20] One report estimates that
approximately 29 000 future cancers could be related to the approximately 70 million CT scans performed
in the US in 2007.[21] It is estimated that 0.4% of current cancers in the United States are due to CTs
performed in the past and that this may increase to as high as 1.5-2% with 2007 rates of CT usage.[22]
Non-ionizing radio frequency radiation from mobile phones and other similar RF sources has also been
proposed as a cause of cancer, but there is currently little established evidence of such a link.[23]

Infection

Some cancers can be caused by infection.[24] This is especially true in animals such as birds, but also
in humans, with oncoviruses responsible for up to 20% of human cancers worldwide.[25] These include
(T-cell leukemias). Bacterial infection may also increase the risk of cancer, as seen in Helicobacter pylori 
inducedgastric carcinoma.[25] Parasitic infections strongly associated with cancer include Schistosoma
Experimental and epidemiological data imply a causative role for viruses and they appear to be the second
most important risk factor for cancer development in humans, exceeded only by tobacco usage.[27] The 
mode of virally induced tumors can be divided into two, acutely transforming or slowly transforming. In acutely
transforming viruses, the virus carries an overactive oncogene called viral-oncogene (v-onc), and the infected
cell is transformed as soon as v-onc is expressed. In contrast, in slowly transforming viruses, the virus 
genome is inserted near a proto-oncogene in the host genome. The viral promoter or other transcription 
regulation elements then cause overexpression of that proto-oncogene. This induces uncontrolled cell division.
Because the site of insertion is not specific to proto-oncogenes and the chance of insertion near any proto
-oncogene is low, slowly transforming viruses will cause tumors much longer after infection than the acutely
transforming viruses.
Hepatitis viruses, including hepatitis B and hepatitis C, can induce a chronic viral infection that leads to live-
r cancer in 0.47% of hepatitis B patients per year (especially in Asia, less so in North America), and in 1.4%
 of hepatitis C carriers per year. Liver cirrhosis, whether from chronic viral hepatitis infection or alcoholism, is
 associated with the development of liver cancer, and the combination of cirrhosis and viral hepatitis presents
 the highest risk of liver cancer development. Worldwide, liver cancer is one of the most common, and most 
deadly, cancers due to a huge burden of viral hepatitis transmission and disease.
Advances in cancer research have made a vaccine designed to prevent cancers available. In 2006, the U.S.
 Food and Drug Administration approved a human papilloma virus vaccine, called Gardasil. The vaccine protects
 against 6,11,16,18 strains of HPV, which together cause 70% of cervical cancers and 90% of genital warts
. It also lists vaginal and vulvar cancers as being protected. In March 2007, the US Centers for Disease Control
 and Prevention (CDC) Advisory Committee on Immunization Practices (ACIP) officially recommended that fem-
ales aged 11–12 receive the vaccine, and indicated that females as young as age 9 and as old as age 26 are
 also candidates for immunization. There is a second vaccine from Cervarix which protects against the more 
dangerous HPV 16,18 strains only. In 2009, Gardasil was approved for protection against genital warts. In 2010
, the Gardasil vaccine was approved for protection against anal cancer for males and reviewers stated there was
 no anatomical, histological or physiological anal differences between the genders so females would also be
 protected.
In addition to viruses, researchers have noted a connection between bacteria and certain cancers. The most
prominent example is the link between chronic infection of the wall of the stomach with Helicobacter pylori 
and gastric cancer.[28][29] Although only a minority of those infected with Helicobacter go on to develop cancer,
 since this pathogen is quite common it is probably responsible for most of these cancers.[30]
HIV is associated with a number of malignancies, including Kaposi's sarcomanon-Hodgkin's lymphoma, and
 HPV-associated malignancies such as anal cancer and cervical cancerAIDS-defining illnesses have long incl-
uded these diagnoses. The increased incidence of malignancies in HIV patients points to the breakdown of imm-
une surveillance as a possible etiology of cancer.[31] Certain other immune deficiency states (e.g. common varia-
ble immunodeficiency and IgA deficiency) are also associated with increased risk of malignancy.[32]

Heredity

Most forms of cancer are sporadic, meaning that there is no inherited cause of the cancer. There are, however, a
 number of recognised syndromes where there is an inherited predisposition to cancer, often due to a defect in a 
gene that protects against tumor formation. Famous examples are:
1.>certain inherited mutations in the genes BRCA1 and BRCA2 are associated with an elevated risk of breast
 cancer and ovarian cancer

3.>tumors of various endocrine organs in multiple endocrine neoplasia (MEN types 1, 2a, 2b)
Li-Fraumeni syndrome (various tumors such as osteosarcoma, breast cancer, soft tissue sarcomabrain
    tumors) due to mutations of p53
    4.>Turcot syndrome (brain tumors and colonic polyposis)
    5.> Familial adenomatous polyposis an inherited mutation of the APC gene that leads to early onset of colon 
    carcinoma.
    6.>Hereditary nonpolyposis colorectal cancer (HNPCC, also known as Lynch syndrome) can include familial 
      cases of colon cancer, uterine cancer, gastric cancer, and ovarian cancer, without a preponderance of
      colon. 
      7.> Retinoblastoma, when occurring in young children, is due to a hereditary mutation in the retinoblastoma
       gene.
      8.> Down syndrome patients, who have an extra chromosome 21, are known to develop malignancies such
       as leukemia and testicular cancer, though the reasons for this difference are not well understood.

      Other

      Excepting the rare transmissions that occur with pregnancies and only a marginal few organ donors, cancer
      is generally not a transmissible disease. The main reason for this is tissue graft rejection caused byMHC in-
      compatibility.[33] In humans and other vertebrates, the immune system uses MHC antigens to differentiate bet-
      ween "self" and "non-self" cells because these antigens are different from person to person. When non-self anti-
      gens are encountered, the immune system reacts against the appropriate cell. Such reactions may protect aga-
      inst tumour cell engraftment by eliminating implanted cells. In the United States, approximately 3,500 pregnant
      women have a malignancy annually, and transplacental transmission of acute leukaemialymphomamelanom
      a and carcinoma from mother to fetus has been observed.[33] The development of donor-derived tumors from organ
      transplants is exceedingly rare. The main cause of organ transplant associated tumors seems to be malignant 
      melanoma, that was undetected at the time of organ harvest.[34] though other cases exist[35] In fact, cancer from
      one organism will usually grow in another organism of that species, as long as they share the same histocomp-
      atibility genes,[36] proven using mice; however this would never happen in a real-world setting except as described 
      above.
      In non-humans, a few types of transmissible cancer have been described, wherein the cancer spreads between an-
      imals by transmission of the tumor cells themselves. This phenomenon is seen in dogs withSticker's sarcoma, a-
      lso known as canine transmissible venereal tumor,[37] as well as Devil facial tumour disease in Tasmanian devils.

      Diagnosis

      of these lead to a definitive diagnosis, which usually requires the opinion of a pathologist, a type of physician
      (medical doctor) who specializes in the diagnosis of cancer and other diseases. People with suspected cancer
      are investigated with medical tests. These commonly include blood testsX-raysCT scans and endoscopy.
      Most cancers are initially recognized either because signs or symptoms appear or through screening. Neither

      Pathology

      A cancer may be suspected for a variety of reasons, but the definitive diagnosis of most malignancies must be 
      confirmed by histological examination of the cancerous cells by a pathologist. Tissue can be obtained from a 
      biopsy or surgery. Many biopsies (such as those of the skin, breast or liver) can be done in a doctor's office.
      Biopsies of other organs are performed under anesthesia and require surgery in an operating room.
      The tissue diagnosis given by the pathologist indicates the type of cell that is proliferating, its histological grade,
      genetic abnormalities, and other features of the tumor. Together, this information is useful to evaluate the
      prognosis of the patient and to choose the best treatment. Cytogenetics and immunohistochemistry are othe-
      r types of testing that the pathologist may perform on the tissue specimen. These tests may provide information
      about the molecular changes (such as mutationsfusion genes, and numerical chromosome changes) that has
      happened in the cancer cells, and may thus also indicate the future behavior of the cancer (prognosis) and best
      treatment.


      A large invasive ductal carcinoma in amastectomy specimen.

      Prevention

      Cancer prevention is defined as active measures to decrease the incidence of cancer.[38] The vast majority of
       cancer risk factors are environmental or lifestyle-related, thus cancer is largely a preventable disease.[39]Greate-
      r than 30% of cancer is preventable via avoiding risk factors including: tobaccooverweight or obesity, low fruit and 
      Examples of modifiable cancer risk factors include alcohol consumption (associated with increased risk of oral, 
      esophageal, breast, and other cancers), smoking (80% of women with lung cancer have smoked in the past, and 
      90% of men[41]), physical inactivity (associated with increased risk of colon, breast, and possibly other cancers),
      and being overweight / obese (associated with colon, breast, endometrial, and possibly other cancers). Based on
      epidemiologic evidence, it is now thought that avoiding excessive alcohol consumption may contribute to reduc-
      tions in risk of certain cancers; however, compared with tobacco exposure, the magnitude of effect is modest or
      small and the strength of evidence is often weaker. Other lifestyle and environmental factors known to affect can-
      cer risk (either beneficially or detrimentally) include certain sexually transmitted diseases (such as those conveyed
      by the human papillomavirus), the use of exogenous hormones, exposure to ionizing radiation and ultraviolet radi-
      ation from the sun or from tanning beds, and certain occupational and chemical exposures.

      Diet and obesity

      The consensus on diet and cancer is that obesity increases the risk of developing cancer. Particular dietary 
      practices often explain differences in cancer incidence in different countries (e.g. gastric cancer is more 
      common in Japan, while colon cancer is more common in the United States. In this example the preceding
      consideration of Haplogroups are excluded). Studies have shown that immigrants develop the risk of their
      new country, often within one generation, suggesting a substantial link between diet and cancer.[42] Whether
      reducing obesity in a population also reduces cancer incidence is unknown.
      However some studies have found that consuming lots of fruits and vegetables has little if any effect on 
      preventing cancer.[43]
      Proposed dietary interventions for primary cancer risk reduction generally gain support from epidemiological 
      association studies. Examples of such studies include reports that reduced meat consumption is associated
      with decreased risk of colon cancer,[44] and reports that consumption of coffee is associated with a reduced
      risk of liver cancer.[45] Studies have linked consumption of grilled meat to an increased risk ofstomach cancer,[46]
      colon cancer,[47] breast cancer,[48] and pancreatic cancer,[49] a phenomenon which could be due to the presence
      of carcinogens such as benzopyrene in foods cooked at high temperatures.
      A recent study analysed the correlation between many factors and cancer and concluded that the major contrib-
      utory dietary factor was animal protein, whereas plant protein did not have an effect. Animal studies confirmed the
      mechanism by showing that reducing the proportion of animal protein switched off both the initiation and promoti-
      on stages.[50]
      A 2005 secondary prevention study showed that consumption of a plant-based diet and lifestyle changes resulted
      in a reduction in cancer markers in a group of men with prostate cancer who were using no conventional treat-
      ments at the time.[51] These results were amplified by a 2006 study. Over 2,400 women were studied, half rando-
      mly assigned to a normal diet, the other half assigned to a diet containing less than 20% calories from fat. The -
      women on the low fat diet were found to have a markedly lower risk of breast cancer recurrence, in the interim 
      report of December, 2006.[52]
      Recent[when?] studies have also demonstrated potential links between some forms of cancer and high consump-
      tion of refined sugars and other simple carbohydrates.[53][54][55][56][57] Although the degree of correlation and the
      degree of causality is still debated,[58][59][60] some organizations have in fact begun to recommend reducing
      intake of refined sugars and starches as part of their cancer prevention regimens.[61][62][63]
       Recommendations to reduce the risk of developing cancer, including the following dietary guidelines: 
      (1) reducing intake of foods and drinks that promote weight gain, namely energy-dense foods and sugary drinks, 
      (2) eating mostly foods of plant origin,
      (3) limiting intake of red meat and avoiding processed meat,
      (4) limiting consumption of alcoholic beverages, and 
      (5) reducing intake of salt and avoiding mouldy cereals (grains) or pulses (legumes).[64][65]

      Medication

      The concept that medications could be used to prevent cancer is an attractive one, and many
      high-quality clinical trials support the use of such chemoprevention in defined circumstances.
      Aspirin has been found to reduce the risk of death from cancer.[66]
      Daily use of tamoxifen, a selective estrogen receptor modulator (SERM), typically for 5 years, has
      been demonstrated to reduce the risk of developing breast cancer in high-risk women by about 50%
      Raloxifenealso a SERM; has been shown to reduce the risk of breast cancer in high-risk women 
      equally as well as tamoxifen. It had fewer side effects than tamoxifen, though it did permit more DCIS
      to form.[67]
      Finasteride, a 5-alpha-reductase inhibitor, has been shown to lower the risk of prostate cancer, though it
      seems to mostly prevent low-grade tumors.[68] The effect of COX-2 inhibitors such as rofecoxib and cele-
      coxibupon the risk of colon polyps have been studied in familial adenomatous polyposis patients[69] and in
      the general population.[70][71] In both groups, there were significant reductions in colon polyp incidence, but 
      this came at the price of increased cardiovascular toxicity.
      As of 2010 vitamins have not been found to be effective at preventing cancer,[72] while low levels of vitamin D
      is correlated with increased cancer risk.[73][74] Whether this relationship is causal and vitamin D supplemen-
      tation is protective is yet to be determined.[75] Beta-carotene supplementation has been found to increase
      slightly, but not significantly risks of lung cancer.[76] Folic acid supplementation has not been found effective
      in preventing colon cancer and may increase colon polyps.[77]

      Vaccination

      Vaccines have been developed to prevent oncogenic infectious agents and therapeutic vaccines are in
      development to stimulate an immune response against cancer-specific epitopes.[78]
      Human papillomavirus vaccine (Gardasil and Cervarix) decreases the risk of developing cervical cancer.[78]
      The hepatitis B vaccine prevents infection with hepatitis B virus and thus decreases the risk of liver cancer.[78]

      Screening

      Cancer screening involves efforts to detect cancer before symptoms appear.[79] This may involve physical 
      examinationblood or urine tests, or medical imaging.[79] As screening tests may have risks these must
      be weighted against the benefits of early detection and treatment.[79] Especially if they are going to be
      recommended for large segments of the population.

      Recommendations

      The U.S. Preventive Services Task Force (USPSTF) strongly recommends cervical cancer screening in those
      who are sexually active and have a cervix at least until the age of 65.[80] They recommendsmammography for
      breast cancer screening every two years for those 50–74 years old, however do not recommend either breast
      blood testing, sigmoidoscopy, or colonoscopy starting at age of 50 until age 75.[82] There is insufficient evide-
      nce to recommend for or against screening for skin cancer,[83] oral cancer,[84] lung cancer,[85] or prostate 
      cancer in men under 75.[86] Routine screening is not recommended for bladder cancer,[87] testicular cancer,[88]
      to slightly different conclusions with respect to breast cancer screening stating that routine mammography 
      may do more harm than good.[91]

      Genetic testing

      Genetic testing for high-risk individuals is already available for certain cancer-related genetic mutations
      Carriers of genetic mutations that increase risk for cancer incidence can undergo enhanced surveillance,
      chemoprevention, or risk-reducing surgery. Early identification of inherited genetic risk for cancer, along
      with cancer-preventing interventions such as surgery or enhanced surveillance, can be lifesaving for high-
      risk individuals.
      Gene
      Cancer types
      Breast, ovarian, pancreatic
      Colon, uterine, small bowel, stomach, urinary tract

      Management

      Many management options for cancer exist including: chemotherapyradiation therapysurgery,
      immunotherapymonoclonal antibody therapy and other methods. Which are used depends upon
      the location and grade of the tumor and the stage of the disease, as well as the general state of a
      person's health. Experimental cancer treatments are also under development.
      Complete removal of the cancer without damage to the rest of the body is the goal of treatment. 
      Sometimes this can be accomplished by surgery, but the propensity of cancers to invade adjacent
      tissue or to spread to distant sites by microscopic metastasis often limits its effectiveness. Surgery
      often required the removal of a wide surgical margin or a free margin. The width of the free margin
      depends on the type of the cancer, the method of removal (CCPDMAMohs surgery, POMA, etc.).
      The margin can be as little as 1 mm for basal cell cancer using CCPDMA or Mohs surgery, to several
      centimeters for aggressive cancers. The effectiveness of chemotherapy is often limited by toxicity to
      other tissues in the body. Radiation can also cause damage to normal tissue.
      Because cancer is a class of diseases,[92][93] 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.[94] Angiogenesis inhibitors were
      once thought to have potential as a "silver bullet" treatment applicable to many types of cancer, but this
      has not been the case in practice.[95]

      Prognosis

      Cancer has a reputation as a deadly disease. While this certainly applies to certain particular types, 
      the truths behind the historical connotations of cancer are increasingly overturned by advances in
      medical care. Some types of cancer have a prognosis that is substantially better than nonmalignant 
      diseases such as heart failure and stroke.
      Progressive and disseminated malignant disease has a substantial impact on a cancer patient's quality
      of life, and many cancer treatments (such as chemotherapy) may have severe side-effects. In the 
      advanced stages of cancer, many patients need extensive care, affecting family members and friends.
      Palliative care solutions may include permanent or "respite" hospice nursing.

      Epidemiology

      As of 2004, worldwide cancer caused 13% of all deaths (7.4 million). The leading causes were:
      lung cancer (1.3 million deaths/year), stomach cancer (803,000 deaths),colorectal cancer
      (639,000 deaths), liver cancer (610,000 deaths), and breast cancer (519,000 deaths).[97] The
      most significant risk factor is age. According to cancer researcher Robert A. Weinberg, "If we
      lived long enough, sooner or later we all would get cancer."[98] Essentially all of the increase in 
      Cancer rates between ancient times and people who died in England during 1901 and 1905 is due
      to increased lifespans.[98] Since then, some other factors, especially the increased use of tobacco,
      have further raised the rates.[98]
      In the United States, cancer is responsible for 25% of all deaths with 30% of these from lung cancer
      The most commonly occurring cancer in men is prostate cancer(about 25% of new cases) and in 
      women is breast cancer (also about 25%). Cancer can occur in children and adolescents, but it is
      uncommon (about 150 cases per million in the U.S.), with leukemia the most common.[99] In the
      first year of life the incidence is about 230 cases per million in the U.S., with the most common being
      In the developed world, one in three people will develop cancer during their lifetimes. If all cancer patients
      survived and cancer occurred randomly, the lifetime odds of developing a second primary cancer would 
      be one in nine.[101] However, cancer survivors have an increased risk of developing a second primary cancer
      and the odds are about two in nine.[101] About half of these second primaries can be attributed to the
      normal one-in-nine risk associated with random chance.[101] The increased risk is believed to be primarily
      due to the same risk factors that produced the first cancer (such as the person's genetic profile, alcohol
      and tobacco use, obesity, and environmental exposures), and partly due to the treatment for the first cancer,
      which typically includes mutagenic chemotherapeutic drugs or radiation.[101] Cancer survivors may also 
      be more likely to comply with recommended screening, and thus may be more likely than average to detect
      cancers.[101]

      in US females, by mortality[99]
      Death rate from malignant cancer per 100,000 inhabitants in 2004.[96]
        no data
        ≤ 55
        55-80
        80-105
        105-130
        130-155
        155-180
        180-205
        205-230
        230-255
        255-280
        280-305
        ≥ 305

      History

      Hippocrates (ca. 460 BC – ca. 370 BC) described several kinds of cancers, referring to them with the
      Greek word carcinos (crab or crayfish), among others.[102] This name comes from the appearance of the
      cut surface of a solid malignant tumour, with "the veins stretched on all sides as the animal the crab has
      its feet, whence it derives its name".[103] Since it was against Greek tradition to open the body, Hippocra-
      tes only described and made drawings of outwardly visible tumors on the skin, nose, and breasts. Treatm-
      ent was based on the humor theory of four bodily fluids (black and yellow bile, blood, and phlegm). Accord-
      ing to the patient's humor, treatment consisted of diet, blood-letting, and/or laxatives. Through the centuries
      it was discovered that cancer could occur anywhere in the body, but humor-theory based treatment remai-
      ned popular until the 19th century with the discovery of cells.
      Celsus (ca. 25 BC - 50 AD) translated carcinos into the Latin cancer, also meaning crab. Galen (2nd cent-
      ury AD) called benign tumours oncos, Greek for swelling, reserving Hippocrates' carcinos for malignant tu-
      mours. He later added the suffix -oma, Greek for swelling, giving the name carcinoma.
      The oldest known description and surgical treatment of cancer was discovered in Egypt and dates back to
      approximately 1600 BC. The Papyrus describes 8 cases of ulcers of the breast that were treated by cauter-
      ization, with a tool called "the fire drill." The writing says about the disease, "There is no treatment."[104]
      Another very early surgical treatment for cancer was described in the 1020s by Avicenna (Ibn Sina) in The 
      Canon of Medicine. He stated that the excision should be radical and that all diseased tissue should be re-
      moved, which included the use of amputation or the removal of veins running in the direction of the tumor.
      He also recommended the use of cauterization for the area treated if necessary.[105]
      In the 16th and 17th centuries, it became more acceptable for doctors to dissect bodies to discover the
      cause of death. 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 conc-
      luded that it was contagious.[106]
      The first cause of cancer was identified by British surgeon Percivall Pott, who discovered in 1775 that
      cancer of the scrotum was a common disease among chimney sweeps. The work of other individual
      physicians led to various insights, but when physicians started working together they could make firmer
      conclusions.
      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.[107] 
      The use of surgery to treat cancer had poor results due to problems with hygiene. The renowned Scottish
      surgeon Alexander Monro saw only 2 breast tumor patients out of 60 surviving surgery for two years. In the
      19th century, asepsis improved surgical hygiene and as the survival statistics went up, surgical removal 
      of the tumor became the primary treatment for cancer. With the exception of William Coley who in the late
      19th century felt that the rate of cure after surgery had been higher before asepsis (and who injected bact-
      eria into tumors with mixed results), cancer treatment became dependent on the individual art of the surgeon
      at removing a tumor. During the same period, the idea that the body was made up of various tissues, that in
      turn were made up of millions of cells, laid rest the humor-theories about chemical imbalances in the body.
      The age of cellular pathology was born.
      The genetic basis of cancer was recognised in 1902 by the German zoologist Theodor Boveri, professor of 
      zoology at Munich and later in Würzburg.[108] He discovered a method to generate cells with multiple copies
      of the centrosome, a structure he discovered and named. He postulated that chromosomes were distinct 
      and transmitted different inheritance factors. He suggested that mutations of the chromosomes could gene-
      rate a cell with unlimited growth potential which could be passed onto its descendants. He proposed the 
      existence of cell cycle check points, tumour suppressor genes and oncogenes. He speculated that canc-
      ers might be caused or promoted by radiation, physical or chemical insults or by pathogenic microorganisms.
      When Marie Curie and Pierre Curie discovered radiation at the end of the 19th century, they stumbled upon
      the first effective non-surgical cancer treatment. With radiation also came the first signs of multi-disciplinary
      approaches to cancer treatment. The surgeon was no longer operating in isolation, but worked together with
      hospital radiologists to help patients. The complications in communication this brought, along with the nec-
      essity of the patient's treatment in a hospital facility rather than at home, also created a parallel process of
      compiling patient data into hospital files, which in turn led to the first statistical patient studies.
      A founding paper of cancer epidemiology was the work of Janet Lane-Claypon, who published a comparative
      study in 1926 of 500 breast cancer cases and 500 control patients of the same background and lifestyle 
      for the British Ministry of Health. Her ground-breaking work on cancer epidemiology was carried on by Ric-
      hard Doll andAustin Bradford Hill, who published "Lung Cancer and Other Causes of Death In Relation to 
      Smoking. A Second Report on the Mortality of British Doctors" followed in 1956 (otherwise known as the
      British doctors study). Richard Doll left the London Medical Research Center (MRC), to start the Oxford 
      unit for Cancer epidemiology in 1968. With the use of computers, the unit was the first to compile large
      amounts of cancer data. Modern epidemiological methods are closely linked to current concepts of disease 
      and public health policy. Over the past 50 years, great efforts have been spent on gathering data across 
      medical practise, hospital, provincial, state, and even country boundaries to study the interdependence of
      environmental and cultural factors on cancer incidence.
      Cancer patient treatment and studies were restricted to individual physicians' practices until World War II
      ,when medical research centers discovered that there were large international differences in disease inci-
      dence. This insight drove national public health bodies to make it possible to compile health data across 
      practises and hospitals, a process that many countries do today. The Japanese medical community obse-
      rved that the bone marrow of victims of the atomic bombings of Hiroshima and Nagasakiwas completely
      destroyed. They concluded that diseased bone marrow could also be destroyed with radiation, and this
      led to the discovery of bone marrow transplants forleukemia. Since World War II, trends in cancer treatme-
      nt are to improve on a micro-level the existing treatment methods, standardize them, and globalize them to
      find cures through epidemiology and international partnerships.
      Engraving with two views of a Dutch woman who had a tumor removed from her neck in 1689.


      1938 poster identifying surgery, x-rays and radium as the proper treatments for cancer.

      Society and culture

      While some diseases (such as heart failure) may have a worse prognosis than certain types of cancer,
      it is the subject of widespread fear and taboos. For instance, many will avoid using the word directly and
      resort to euphemisms such as "big C".[citation needed]
      In Western culture, cancer is regarded as a disease that must be "fought" (see below on Richard Nixon's
      "War on Cancer", announced in 1971). On an individual level, there is a widespread perception that peop-
      le with cancer who remain optimistic can expect a better prognosis. A 2007 study indicated that this beli-
      ef is probably incorrect.[109]

      Research

      Cancer research is the intense scientific effort to understand disease processes and discover possible
      therapies.
      Research about cancer causes focusses on the following issues:
      1.> Agents (e.g. viruses) and events (e.g. mutations) which cause or facilitate genetic changes in cells
      destined to become cancer.
      2.>The precise nature of the genetic damage, and the genes which are affected by it.
      3.>The consequences of those genetic changes on the biology of the cell, both in generating the defining
      properties of a cancer cell, and in facilitating additional genetic events which lead to further progression of 
      the cancer.
      The improved understanding of molecular biology and cellular biology due to cancer research has led to a
      number of new, effective treatments for cancer since President Nixon declared "War on Cancer" in 1971. 
      Since 1971 the United States has invested over $200 billion on cancer research; that total includes money 
      invested by public and private sectors and foundations.[110] Despite this substantial investment, the country
      has seen a five percent decrease in the cancer death rate (adjusting for size and age of the population)
      between 1950 and 2005.[111]
      Cancer can be devided into three groups:-
      1.>Metastatic symptoms: are due to the spread of cancer to other locations in the body. 
       or metastatic lymph nodes (which can be felt or sometimes seen under the skin), hepatomegaly
       (enlarged liver) or splenomegaly.


      (enlarged spleen) which can be felt in the abdomen, pain or fracture of affected bones, and neurologicalsymptoms.
      spread. Some of these effects can include weight loss (poor appetite and cachexia), fatigue, excessive sweating
      (especially night sweats), anemia (low blood count) and other specific conditions termed paraneoplastic phenom-
      ena. These may be mediated by immunological or hormonal signals from the cancer cells.


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