Cancer
Cancer , medically known as metastasis , is a wide range of diseases
involving unregulated cell growth . In cancer , cells divide and grow
uncontrollably , forming malignant tumors , and invade nearby parts of the body
. Cancer has also spread to more distant parts of the body through the blood or
lymphatic system . Not all tumors are cancerous ; benign tumors do not invade
nearby tissues or spread throughout the body.
There are more than 200 different types of cancer
known that affect humans.
Causes of cancer are varied and complex , and
only partially understood . It is known that a lot
of things that increase the risk of cancer ,
including tobacco use, dietary factors , and some
infectious diseases , exposure to radiation , and
physical inactivity , obesity, and environmental
pollutants . These factors can directly damage the
genes or combine with existing errors can cause
the cells to cancerous mutations . be attributed to about 5-10 % of cancer cases
directly to the inherited genetic defects . can prevent many of the diseases of
cancer by not smoking, eating more fruits and vegetables and whole grains , and
eat less meat and refined carbohydrates , and maintain a healthy weight ,
exercising, and reducing exposure to sunlight , and being vaccinated against
some infectious diseases .
The cancer can be detected in a number of ways , including the presence of
some of the signs and symptoms , tests , or medical imaging . Once the cancer
has been detected possible is diagnosed by microscopic examination of the
tissue sample . Is usually treated with cancer chemotherapy , radiation therapy
and surgery. The chances of survival of the disease vary greatly depending on
the type and location of the cancer and the extent of the disease at the beginning
of treatment. While cancer can affect people of all ages , and a few types of
cancer are more common in children , the risk of cancer generally increases with
age . In 2007, cancer caused about 13 % of all human deaths worldwide ( 7.9
million ) . Prices go up as more people live to old age and lifestyle changes
occur as comprehensive in the developing world .
How cancer spreads - scientists
reported in Nature
Communications (October 2012
issue) that they have. It has
something to do with their adhesion
(stickiness) properties. Certain
molecular interactions between
cells and the scaffolding that holds
them in place (extracellular matrix)
cause them to become unstuck at
the original tumor site, they
become dislodged, move on and
then reattach themselves at a new site.
The researchers say this discovery is important because cancer mortality is
mainly due to metastatic tumors, those that grow from cells that have traveled
from their original site to another part of the body. Only 10% of cancer deaths
are caused by the primary tumors.
The scientists, from the Massachusetts Institute of Technology, say that finding
a way to stop cancer cells from sticking to new sites could interfere with
metastatic disease, and halt the growth of secondary tumors.
In 2007, cancer claimed the lives of about 7.6 million people in the world.
Physicians and researchers who specialize in the study, diagnosis, treatment, and
prevention of cancer are called oncologists.
Malignant cells are more agile than non-malignant ones –
scientists from the Physical Sciences-Oncology Centers, USA, reported in the
journal Scientific Reports (April 2013 issue). Malignant cells can pass more
easily through smaller gaps, as well as applying a much greater force on their
environment compared to other cells.
Professor Robert Austin and team created a new catalogue of the physical and
chemical features of cancerous cells with over 100 scientists from 20 different
centers across the United States.
The authors believe their catalogue will help oncologists detect cancerous cells
in patients early on, thus preventing the spread of the disease to other parts of
the body.
Prof. Austin said "By bringing together different types of experimental expertise
to systematically compare metastatic and non-metastatic cells, we have
advanced our knowledge of how metastasis occurs."
Cancer can be detected in a number of ways, including the presence of certain
Definitions
There is no one definition that describes all cancers. They are a large family of
diseases which form a subset of neoplasms, which show some features that
suggest of malignancy. 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.
Six characteristics of malignancies have been proposed: sustaining proliferative
signaling, evading growth suppressors, resisting cell death, enabling replicative
immortality, inducing angiogenesis, and activating invasion and metastasis. The
progression from normal cells to cells that can form a discernible mass to
outright cancer involves multiple steps.
Signs and symptoms
Symptoms of cancer metastasis depend on the location of the tumor.
When cancer begins it invariably produces no symptoms with signs and
symptoms only appearing as the mass continues to grow or ulcerates. The
findings that result depend on the type and location of the cancer. Few
symptoms are specific, with many of them also frequently occurring in
individuals who have other conditions. Cancer is the new "great imitator". Thus
it is not uncommon for people diagnosed with cancer to have been treated for
other diseases to which it was assumed their symptoms were due.
Local effects
Local symptoms may occur due to the mass of the tumor or its ulceration. For
example, mass effects from lung cancer can cause blockage of 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, resulting in changes in bowel
habits. Masses in breasts or testicles may be easily felt. Ulceration can cause
bleeding which, 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 build up
of fluid within the chest or abdomen.
Systemic symptoms
General symptoms occur due to distant effects of the cancer that are not related
to direct or metastatic spread. These may include: unintentional weight loss,
fever, being excessively tired, and changes to the skin. Hodgkin disease,
leukemias, and cancers of the liver or kidney can cause a persistent fever of
unknown origin.
Specific constellations of systemic symptoms, termed paraneoplastic
phenomena, may occur with some cancers. Examples include the appearance of
myasthenia gravis in thymoma and clubbing in lung cancer.
Metastasis
Symptoms of metastasis are due to the
spread of cancer to other locations in the
body. They can include enlarged lymph
nodes (which can be felt or sometimes seen
under the skin and are typically hard),
hepatomegaly (enlarged liver) or
splenomegaly (enlarged spleen) which can
be felt in the abdomen, pain or fracture of
affected bones, and neurological
symptoms.Most cancer deaths are due to cancer that has spread from its primary
site to other organs (metastasized).
Causes
Cancers are primarily an environmental disease with 90–95% of cases attributed
to environmental factors and 5–10% due to genetics. Environmental, as used by
cancer researchers, means any cause that is not inherited genetically, not merely
pollution. 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 environmental pollutants.
It is nearly impossible to prove what caused a cancer in any individual, because
most cancers have multiple possible causes. 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, then there is a small chance that the cancer
developed because of air pollution or radiation.
Further information :
Alcohol and cancer and Smoking and cancer
The incidence of lung cancer is highly
correlated with smoking.
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, and causes 90% of lung
cancer.
Many mutagens are also carcinogens, but some carcinogens are not mutagens.
Alcohol is an example of a chemical carcinogen that is not a mutagen. In
Western Europe 10% of cancers in males and 3% of cancers in females are
attributed to alcohol.
Decades of research has demonstrated the link between tobacco use and cancer
in the lung, larynx, head, neck, stomach, bladder, kidney, esophagus and
pancreas. Tobacco smoke contains over fifty known carcinogens, including
nitrosamines and polycyclic aromatic hydrocarbons. Tobacco is responsible for
about one in three of all cancer deaths in the developed world, and about one in
five worldwide. 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.
However, the numbers of smokers worldwide is still rising, leading to what
some organizations have described as the tobacco epidemic.
Cancer related to one's occupation is believed to represent between 2–20% of all
cases. Every year, at least 200,000 people die worldwide from cancer related to
their workplace.Most cancer deaths caused by occupational risk factors occur in
the developed world.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.Millions of workers run the risk of developing cancers such as lung
cancer and mesothelioma from inhaling asbestos fibers and tobacco smoke, or
leukemia from exposure to benzene at their workplaces
Diet and exercise
Diet, physical inactivity, and obesity
are related to approximately 30–35%
of cancer deaths. 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
all cancer deaths. Physical inactivity
is believed to contribute to cancer risk
not only through its effect on body
weight but also through negative effects on immune system and endocrine
system. More than half of the effect from diet is due to overnutrition rather than
from eating too little healthy foods.
Diets that are low in vegetables, fruits and whole grains, and high in processed
or red meats are linked with a number of cancers. A high-salt diet is linked to
gastric cancer, aflatoxin B1, a frequent food contaminate, with liver cancer, and
Betel nut chewing with oral cancer.This may partly explain differences in cancer
incidence in different countries. For example, gastric cancer is more common in
Japan due to its high-salt diet and colon cancer is more common in the United
States. Immigrants develop the risk of their new country, often within one
generation, suggesting a substantial link between diet and cancer.
Infection
Worldwide approximately 18% of cancer deaths are related to infectious
diseases. This proportion varies in different regions of the world from a high of
25% in Africa to less than 10% in the developed world. Viruses are the usual
infectious agents that cause cancer but bacteria and parasites may also have an
effect.
A virus that can cause cancer is called an oncovirus. These include human
papillomavirus (cervical carcinoma), 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. Parasitic
infections strongly associated with cancer include Schistosoma haematobium
(squamous cell carcinoma of the bladder) and the liver flukes, Opisthorchis
viverrini and Clonorchis sinensis
(cholangiocarcinoma).
Radiation
Up to 10% of invasive cancers are
related to radiation exposure,
including both ionizing radiation
and non-ionizing ultraviolet
radiation. Additionally, the vast
majority of non-invasive cancers are
non-melanoma skin cancers caused
by non-ionizing ultraviolet radiation.
Sources of ionizing radiation include medical imaging, and radon gas. Radiation
can cause cancer in most parts of the body, in all animals, and at any age,
although radiation-induced solid tumors usually take 10–15 years, and can take
up to 40 years, to become clinically manifest, and radiation-induced leukemias
typically require 2–10 years to appear. Some people, such as those with nevoid
basal cell carcinoma syndrome or retinoblastoma, are more susceptible than
average to developing cancer from radiation exposure. Children and adolescents
are twice as likely to develop radiation-induced leukemia as adults; radiation
exposure before birth has ten times the effect. Ionizing radiation is not a
particularly strong mutagen. Residential exposure to radon gas, for example, has
similar cancer risks as passive smoking. Low-dose exposures, such as living
near a nuclear power plant, are generally believed to have no or very little effect
on cancer development. Radiation is a more potent source of cancer when it is
combined with other cancer-causing agents, such as radon gas exposure plus
smoking tobacco.
Unlike chemical or physical triggers for cancer, ionizing radiation hits
molecules within cells randomly. If it happens to strike a chromosome, it can
break the chromosome, result in an abnormal number of chromosomes,
inactivate one or more genes in the part of the chromosome that it hit, delete
parts of the DNA sequence, cause chromosome translocations, or cause other
types of chromosome abnormalities. Major damage normally results in the cell
dying, but smaller damage may leave a stable, partly functional cell that may be
capable of proliferating and developing into cancer, especially if tumor
suppressor genes were damaged by the radiation. Three independent stages
appear to be involved in the creation of cancer with ionizing radiation:
morphological changes to the cell, acquiring cellular immortality (losing
normal, life-limiting cell regulatory processes), and adaptations that favor
formation of a tumor. Even if the radiation particle does not strike the DNA
directly, it triggers responses from cells that indirectly increase the likelihood of
mutations.
Medical use of ionizing radiation is a 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. It is also used in some kinds of
medical imaging. 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. It is estimated that 0.4% of cancers in 2007 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 rates of CT usage during this same time period.
Prolonged exposure to ultraviolet radiation from the sun can lead to melanoma
and other skin malignancies. Clear evidence establishes ultraviolet radiation,
especially the non-ionizing medium wave UVB, as the cause of most nonmelanoma skin cancers, which are the most common forms of cancer in the
world.
Non-ionizing radio frequency radiation from mobile phones, electric power
transmission, and other similar sources have been described as a possible
carcinogen by the World Health Organization's International Agency for
Research on Cancer. However, studies have not found a consistent link between
cell phone radiation and cancer risk.
Heredity
The vast majority of cancers are nonhereditary ("sporadic cancers").
Hereditary cancers are primarily caused
by an inherited genetic defect. Less than
0.3% of the population are carriers of a
genetic mutation which has a large effect
on cancer risk and these cause less than
3–10% of all cancer. 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, and
hereditary nonpolyposis colorectal cancer (HNPCC or Lynch syndrome) which
is present in about 3% of people with colorectal cancer, among others.
Physical agents
Some substances cause cancer primarily
through their physical, rather than chemical,
effects on cells.
A prominent example of this is prolonged
exposure to asbestos, naturally occurring
mineral fibers which are a major cause of
mesothelioma, which is a cancer of the
serous membrane, usually the serous
membrane surrounding the lungs. 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.
Non-fibrous particulate materials that cause cancer include powdered metallic
cobalt and nickel, and crystalline silica (quartz, cristobalite, and tridymite).
Usually, physical carcinogens must get inside the body (such as through
inhaling tiny pieces) and require years of exposure to develop cancer.
Physical trauma resulting in cancer is relatively rare. Claims that breaking bones
resulted in bone cancer, for example, have never been proven. Similarly,
physical trauma is not accepted as a cause for cervical cancer, breast cancer, or
brain cancer.
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.
Frequently drinking scalding hot tea may produce esophageal cancer.
Generally, it is believed that the cancer arises, or a pre-existing cancer is
encouraged, during the process of repairing the trauma, rather than the cancer
being caused directly by the trauma. However, repeated injuries to the same
tissues might promote excessive cell proliferation, which could then increase the
odds of a cancerous mutation. There is no evidence that inflammation itself
causes cancer.
Hormones
Some hormones play a role in
the development of cancer by
promoting cell proliferation.
Insulin-like growth factors and
their binding proteins play a key
role in cancer cell proliferation,
differentiation and apoptosis,
suggesting possible
involvement in carcinogenesis.
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.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 why these women have higher risk of
breast cancer, even in the absence of a breast-cancer gene. Similarly, men of
African ancestry have significantly higher levels of testosterone than men of
European ancestry, and have a correspondingly much higher level of prostate
cancer. Men of Asian ancestry, with the lowest levels of testosterone-activating
androstanediol glucuronide, have the lowest levels of prostate cancer.
Other factors are also relevant: obese people have higher levels of some
hormones associated with cancer and a higher rate of those cancers. Women
who take hormone replacement therapy have a higher risk of developing cancers
associated with those hormones. On the other hand, people who exercise far
more than average have lower levels of these hormones, and lower risk of
cancer. Osteosarcoma may be promoted by growth hormones. Some treatments
and prevention approaches leverage this cause by artificially reducing hormone
levels, and thus discouraging hormone-sensitive cancers.
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 by MHC incompatibility. In
humans and other vertebrates, the immune system uses MHC antigens to
differentiate between "self" and "non-self" cells because these antigens are
different from person to person. When non-self antigens are encountered, the
immune system reacts against the appropriate cell. Such reactions may protect
against 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 leukemia, lymphoma, melanoma and
carcinoma from mother to fetus has been observed. The development of donorderived 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. Job stress does not appear to be a
significant factor at least in lung, colorectal, breast and prostate cancers.
Pathophysiology
Cancers are caused by a series of
mutations. Each mutation alters the
behavior of the cell somewhat.
Genetic alterations
Cancer is fundamentally a disease of
tissue growth regulation failure. In
order for a normal cell to transform into
a cancer cell, the genes which regulate
cell growth and differentiation must be
altered.
The affected genes are divided into two
broad categories. Oncogenes are genes
which promote cell growth and
reproduction. Tumor suppressor genes are genes which 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
many genes are required to transform a normal cell into a cancer cell.
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 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's coding 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 or retrovirus, 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 presence of disruptive substances called
carcinogens, repeated physical injury, heat, ionising radiation, or hypoxia.
The errors which cause cancer are self-amplifying and compounding, for
example:
A mutation in the error-correcting machinery of a cell might cause that cell and
its children to accumulate errors more rapidly.
A further mutation in an oncogene might cause the cell to reproduce more
rapidly and more frequently than its normal counterparts.
A further mutation may cause loss of a tumour suppressor gene, disrupting the
apoptosis signalling pathway and resulting in the cell becoming immortal.
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 ongoing
process, termed clonal evolution drives progression towards more invasive
stages.
Epigenetic alterations
The central role of DNA damage
and epigenetic defects in DNA
repair genes in carcinogenesis
Classically, cancer has been
viewed as a set of diseases that are
driven by progressive genetic
abnormalities that include
mutations in tumour-suppressor
genes and oncogenes, and
chromosomal abnormalities.
However, it has become apparent that cancer is also driven by epigenetic
alterations.
Epigenetic alterations refer to functionally relevant modifications to the genome
that do not involve a change in the nucleotide sequence. Examples of such
modifications are changes in DNA methylation (hypermethylation and
hypomethylation) and histone modification and changes in chromosomal
architecture (caused by inappropriate expression of proteins such as HMGA2 or
HMGA1). Each of these epigenetic alterations serves to regulate 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,
Schnekenburger and Diederich 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.
While large numbers of 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.
Reduced expression of DNA repair genes causes deficient 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 damages remain in
cells at a higher than usual level (5th level from the top in figure), and these
excess damages cause increased frequencies of mutation and/or epimutation (6th
level from top of figure). Mutation rates increase substantially in cells defective
in DNA mismatch repair or in homologous recombinational repair (HRR).
Chromosomal rearrangements and aneuploidy also increase in HRR defective
cells.
Higher levels of DNA damage not only cause increased mutation (right side of
figure), but also cause increased epimutation. During repair of DNA double
strand breaks, or repair of other DNA damages, incompletely cleared sites of
repair can cause epigenetic gene silencing.
Deficient expression of DNA repair proteins due to an inherited mutation can
cause increased risk of cancer. Individuals with an inherited impairment in any
of 34 DNA repair genes (see article DNA repair-deficiency disorder) have an
increased risk of cancer, with some defects causing up to a 100% lifetime
chance of cancer (e.g. p53 mutations). Germ line DNA repair mutations are
noted in a box on the left side of the figure, with an arrow indicating their
contribution to DNA repair deficiency. However, such germline mutations
(which cause highly penetrant cancer syndromes) are the cause of only about 1
percent of cancers.
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 from the top. For example, when
113 colorectal cancers were examined in sequence, only four had a missense
mutation in the DNA repair gene MGMT, while the majority had reduced
MGMT expression due to methylation of the MGMT promoter region (an
epigenetic alteration). Five different studies found that between 40% and 90% of
colorectal cancers have reduced MGMT expression due to methylation of the
MGMT promoter region.
Similarly, out of 119 cases of mismatch repair-deficient colorectal cancers that
lacked DNA repair gene PMS2 expression, PMS2 was deficient in 6 due to
mutations in the PMS2 gene, while in 103 cases PMS2 expression was deficient
because its pairing partner MLH1 was repressed due to promoter methylation
(PMS2 protein is unstable in the absence of MLH1). In the other 10 cases, loss
of PMS2 expression was likely due to epigenetic overexpression of the
microRNA, miR-155, which down-regulates MLH1.
In further examples, tabulated in the article Epigenetics, epigenetic defects were
found at frequencies of between 13%-100% for the DNA repair genes BRCA1,
WRN, FANCB, FANCF, MGMT, MLH1, MSH2, MSH4, ERCC1, XPF, NEIL1
and ATM in cancers including those in breast, ovarian, colorectal, and head and
neck. In particular, two or more epigenetic deficiencies in expression of ERCC1,
XPF and/or PMS2 occurred simultaneously in the majority of the 49 colon
cancers evaluated by Facista et al.
Many studies of heavy metal-induced carcinogenesis show that such heavy
metals cause reduction in expression of DNA repair enzymes, some through
epigenetic mechanisms. In some cases, DNA repair inhibition is proposed to be
a predominant mechanism in heavy metal-induced carcinogenicity. For
example, one group of studies shows that arsenic inhibits the DNA repair genes
PARP, XRCC1, Ligase III, Ligase IV, DNA POLB, XRCC4, DNA PKCS,
TOPO2B, OGG1, ERCC1, XPF, XPB, XPC, XPE and P53. Another group of
studies shows that cadmium inhibits the DNA repair genes MSH2, ERCC1,
XRCC1, OGG1, MSH6, DNA-PK, XPD and XPC.
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 3 or 4 may be “driver”
mutations, and the remaining ones may be “passenger” mutations. Colon
cancers were also found to have an average of 17 duplicated segments of
chromosomes, 28 deleted segments of chromosomes and up to 10 translocations.
However, by comparison, epigenetic alterations appear to be more frequent in
colon cancers. There are large numbers of hypermethylated genes in colon
cancer, as discussed above.
In addition, there are frequent epigenetic alterations of the DNA sequences
coding for small RNAs called microRNAs (or miRNAs). MiRNAs do not code
for proteins, but can “target” protein-coding genes and reduce their expression.
For instance, epigenetic increase in CpG island methylation of the DNA
sequence encoding miR-137 reduces its expression and is a frequent early
epigenetic event in colorectal carcinogenesis, occurring in 81% of colon cancers
and in 14% of the normal appearing colonic mucosa adjacent to the cancers.
Silencing of miR-137 can affect expression of over 400 genes, the targets of this
miRNA. Changes in the level of miR-137 expression cause altered mRNA
expression of the target genes by 2 to 20-fold and corresponding, though often
smaller, changes in expression of the protein products of the genes. Other
microRNAs, with likely comparable numbers of target genes, are even more
frequently epigenetically altered in colonic field defects and in the colon cancers
that arise from them. These include miR-124a, miR-34b/c and miR-342 which
are silenced by CpG island methylation of their encoding DNA sequences in
primary tumors at rates of 99%, 93% and 86%, respectively, and in the adjacent
normal appearing mucosa at rates of 59%, 26% and 56%, respectively. Thus,
epigenetic alterations are a major source of changes in gene expression,
important in cancer.
As pointed out above under genetic alterations, cancer is caused by failure to
regulate tissue growth, when the genes which regulate cell growth and
differentiation are altered. It has become clear that these alterations are caused
by both DNA sequence mutation in oncogenes and tumor suppressor genes as
well as by epigenetic alterations. The epigenetic deficiencies in expression of
DNA repair genes, in particular, likely cause an increased frequency of
mutations, some of which then occur in oncogenes and tumor suppressor genes.
Diagnosis
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 lead 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, CT scans and endoscopy.
Most people are distressed to learn that they have cancer. They may become
extremely anxious and depressed. The risk of suicide in people with cancer is
approximately double the normal risk.
Classification
Further information: List of cancer types and List of oncology-related terms
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:
Carcinoma: Cancers derived from epithelial cells. This group includes many of
the most common cancers, particularly in the aged, and include nearly all those
developing in the breast, prostate, lung, pancreas, and colon.
Sarcoma: Cancers arising from connective tissue (i.e. bone, cartilage, fat, nerve),
each of which develop from cells originating in mesenchymal cells outside the
bone marrow.
Lymphoma and leukemia: These two classes of cancer arise from hematopoietic
(blood-forming) cells that leave the marrow and tend to mature in the lymph
nodes and blood, respectively. Leukemia is the most common type of cancer in
children accounting for about 30%.
Germ cell tumor: Cancers derived from pluripotent cells, most often presenting
in the testicle or the ovary (seminoma and dysgerminoma, respectively).
Blastoma: Cancers derived from immature "precursor" cells or embryonic
tissue. Blastomas are more common in children than in older adults.
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
the 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.
Pathology
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 other types of testing that the pathologist may
perform on the tissue specimen. These tests may provide information about the
molecular changes (such as mutations, fusion 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.
An invasive ductal carcinoma of the breast (pale area at the center) surrounded
by spikes of whitish scar tissue and yellow fatty tissue.
An invasive colorectal carcinoma (top center) in a colectomy specimen.
A squamous-cell carcinoma (the whitish tumor) near the bronchi in a lung
specimen.
A large invasive ductal carcinoma in a mastectomy specimen.
Prevention
Cancer prevention is defined as active measures to decrease the risk of cancer.
The vast majority of cancer cases are due to environmental risk factors, and
many, but not all, of these environmental factors are controllable lifestyle
choices. Thus, cancer is considered a largely preventable disease. Greater than
30% of cancer deaths could be prevented by avoiding risk factors including:
tobacco, overweight / obesity, an insufficient diet, physical inactivity, alcohol,
sexually transmitted infections, and air pollution. Not all environmental causes
are controllable, such as naturally occurring background radiation, and other
cases of cancer are caused through hereditary genetic disorders, and thus it is not
possible to prevent all cases of cancer.
Dietary
While many dietary recommendations have been proposed to reduce the risk of
cancer, the evidence to support them is not definitive. The primary dietary
factors that increase risk are obesity and alcohol consumption; with a diet low in
fruits and vegetables and high in red meat being implicated but not confirmed.
Consumption of coffee is associated with a reduced risk of liver cancer. Studies
have linked consumption of red or processed meat to an increased risk of breast
cancer, colon cancer, and pancreatic cancer, a phenomenon which could be due
to the presence of carcinogens in meats cooked at high temperatures. 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, and refined carbohydrates.
Medication
The concept that medications can be used to prevent cancer is attractive, and
evidence supports their use in a few defined circumstances. In the general
population NSAIDs reduce the risk of colorectal cancer however due to the
cardiovascular and gastrointestinal side effects they cause overall harm when
used for prevention. Aspirin has been found to reduce the risk of death from
cancer by about 7%. COX-2 inhibitor may decrease the rate of polyp formation
in people with familial adenomatous polyposis however are associated with the
same adverse effects as NSAIDs. Daily use of tamoxifen or raloxifene has been
demonstrated to reduce the risk of developing breast cancer in high-risk women.
The benefit verses harm for 5-alpha-reductase inhibitor such as finasteride is not
clear.
Vitamins have not been found to be effective at preventing cancer, although low
blood levels of vitamin D are correlated with increased cancer risk. Whether this
relationship is causal and vitamin D supplementation is protective is not
determined. Beta-Carotene supplementation has been found to increase lung
cancer rates in those who are high risk. Folic acid supplementation has not been
found effective in preventing colon cancer and may increase colon polyps.
Vaccination
Vaccines have been developed that prevent some infection by some viruses.
Human papillomavirus vaccine (Gardasil and Cervarix) decreases the risk of
developing cervical cancer. The hepatitis B vaccine prevents infection with
hepatitis B virus and thus decreases the risk of liver cancer.
Screening
Unlike diagnosis efforts prompted by
symptoms and medical signs, cancer
screening involves efforts to detect cancer
after it has formed, but before any
noticeable symptoms appear.This may
involve physical examination, blood or
urine tests, or medical imaging.
Cancer screening is currently not possible
for many types of cancers, and even when tests are available, they may not be
recommended for everyone. Universal screening or mass screening involves
screening everyone. Selective screening identifies people who are known to be
at higher risk of developing cancer, such as people with a family history of
cancer.Several factors are considered to determine whether the benefits of
screening outweigh the risks and the costs of screening. These factors include:
Possible harms from the screening test: for example, X-ray images involve
exposure to potentially harmful ionizing radiation.
The likelihood of the test correctly identifying cancer.
The likelihood of cancer being present: Screening is not normally useful for rare
cancers.
Possible harms from follow-up procedures.
Whether suitable treatment is available.
Whether early detection improves treatment outcomes.
Whether the cancer will ever need treatment.
Whether the test is acceptable to the people: If a screening test is too
burdensome (for example, being extremely painful), then people will refuse to
participate.
Recommendations
The U.S. Preventive Services Task Force (USPSTF) strongly recommends
cervical cancer screening in women who are sexually active and have a cervix at
least until the age of 65. They recommend that Americans be screened for
colorectal cancer via fecal occult blood testing, sigmoidoscopy, or colonoscopy
starting at age 50 until age 75. There is insufficient evidence to recommend for
or against screening for skin cancer, oral cancer, lung cancer, or prostate cancer
in men under 75. Routine screening is not recommended for bladder cancer,
testicular cancer, ovarian cancer, pancreatic cancer, or prostate cancer.
The USPSTF recommends mammography for breast cancer screening every two
years for those 50–74 years old; however, they do not recommend either breast
self-examination or clinical breast examination. A 2011 Cochrane review came
to slightly different conclusions with respect to breast cancer screening stating
that routine mammography may do more harm than good.
Japan screens for gastric cancer using photofluorography due to the high
incidence there.
Genes - the DNA type
Cells can experience uncontrolled growth if there are damages or mutations to
DNA, and therefore, damage to the genes involved in cell division. Four key
types of gene are responsible for the cell division process: oncogenes tell cells
when to divide, tumor suppressor genes tell cells when not to divide, suicide
genes control apoptosis and tell the cell to kill itself if something goes wrong,
and DNA-repair genes instruct a cell to repair damaged DNA.
Cancer occurs when a cell's gene mutations make the cell unable to correct
DNA damage and unable to commit suicide. Similarly, cancer is a result of
mutations that inhibit oncogene and tumor suppressor gene function, leading to
uncontrollable cell growth.
Carcinogens
Carcinogens are a class of substances that are directly responsible for damaging
DNA, promoting or aiding cancer. Tobacco, asbestos, arsenic, radiation such as
gamma and x-rays, the sun, and compounds in car exhaust fumes are all
examples of carcinogens. When our bodies are exposed to carcinogens, free
radicals are formed that try to steal electrons from other molecules in the body.
Theses free radicals damage cells and affect their ability to function normally.
Genes - the family type
Cancer can be the result of a genetic predisposition that is inherited from family
members. It is possible to be born with certain genetic mutations or a fault in a
gene that makes one statistically more likely to develop cancer later in life.
What are the symptoms of cancer?
Cancer symptoms are quite varied and depend on where the cancer is located,
where it has spread, and how big the tumor is. Some cancers can be felt or seen
through the skin - a lump on the breast or testicle can be an indicator of cancer
in those locations. Skin cancer (melanoma) is often noted by a change in a wart
or mole on the skin. Some oral cancers present white patches inside the mouth
or white spots on the tongue.
Other cancers have symptoms that are less physically apparent. Some brain
tumors tend to present symptoms early in the disease as they affect important
cognitive functions. Pancreas cancers are usually too small to cause symptoms
until they cause pain by pushing against nearby nerves or interfere with liver
function to cause a yellowing of the skin and eyes called jaundice. Symptoms
also can be created as a tumor grows and pushes against organs and blood
vessels. For example, colon cancers lead to symptoms such as constipation,
diarrhea, and changes in stool size. Bladder or prostate cancers cause changes in
bladder function such as more frequent or infrequent urination.
As cancer cells use the body's energy and interfere with normal hormone
function, it is possible to present symptoms such as fever, fatigue, excessive
sweating, anemia, and unexplained weight loss. However, these symptoms are
common in several other maladies as well. For example, coughing and
hoarseness can point to lung or throat cancer as well as several other conditions.
When cancer spreads, or metastasizes, additional symptoms can present
themselves in the newly affected area. Swollen or enlarged lymph nodes are
common and likely to be present early. If cancer spreads to the brain, patients
may experience vertigo, headaches, or seizures. Spreading to the lungs may
cause coughing and shortness of breath. In addition, the liver may become
enlarged and cause jaundice and bones can become painful, brittle, and break
easily. Symptoms of metastasis ultimately depend on the location to which the
cancer has spread.
How is cancer classified?
There are five broad groups that are used to classify cancer.
1. Carcinomas are characterized by cells that cover internal and external parts
of the body such as lung, breast, and colon cancer.
2. Sarcomas are characterized by cells that are located in bone, cartilage, fat,
connective tissue, muscle, and other supportive tissues.
3. Lymphomas are cancers that begin in the lymph nodes and immune system
tissues.
4. Leukemias are cancers that begin in the bone marrow and often
accumulate in the bloodstream.
5. Adenomas are cancers that arise in the thyroid, the pituitary gland, the
adrenal gland, and other glandular tissues.
Cancers are often referred to by terms that contain a prefix related to the cell
type in which the cancer originated and a suffix such as -sarcoma, -carcinoma,
or just -oma. Common prefixes include:

Adeno- = gland

Melano- = pigment cell

Chondro- = cartilage

Myelo- = bone marrow

Erythro- = red blood cell

Myo- = muscle

Hemangio- = blood vessels

Osteo- = bone

Hepato- = liver

Uro- = bladder

Lipo- = fat

Retino- = eye

Lympho- = white blood cell

Neuro- = brain
How is cancer diagnosed and staged?
Early detection of cancer can
greatly improve the odds of
successful treatment and survival.
Physicians use information from
symptoms and several other
procedures to diagnose cancer.
Imaging techniques such as X-rays,
CT scans, MRI scans, PET scans,
and ultrasound scans are used
regularly in order to detect where a
tumor is located and what organs
may be affected by it. Doctors may
also conduct an endoscopy, which
is a procedure that uses a thin tube
with a camera and light at one end, to look for abnormalities inside the body.
Extracting cancer cells and looking at them under a microscope is the only
absolute way to diagnose cancer. This procedure is called a biopsy. Other types
of molecular diagnostic tests are frequently employed as well. Physicians will
analyze your body's sugars, fats, proteins, and DNA at the molecular level. For
example, cancerous prostate cells release a higher level of a chemical called
PSA (prostate-specific antigen) into the bloodstream that can be detected by a
blood test. Molecular diagnostics, biopsies, and imaging techniques are all used
together to diagnose cancer.
After a diagnosis is made, doctors find out how far the cancer has spread and
determine the stage of the cancer. The stage determines which choices will be
available for treatment and informs prognoses. The most common cancer
staging method is called the TNM system. T (1-4) indicates the size and direct
extent of the primary tumor, N (0-3) indicates the degree to which the cancer
has spread to nearby lymph nodes, and M (0-1) indicates whether the cancer has
metastasized to other organs in the body. A small tumor that has not spread to
lymph nodes or distant organs may be staged as (T1, N0, M0), for example.
TNM descriptions then lead to a simpler categorization of stages, from 0 to 4,
where lower numbers indicate that the cancer has spread less. While most Stage
1 tumors are curable, most Stage 4 tumors are inoperable or untreatable.
How is cancer treated?
Cancer treatment depends on
the type of cancer, the stage
of the cancer (how much it
has spread), age, health
status, and additional
personal characteristics.
There is no single treatment
for cancer, and patients often
receive a combination of
therapies and palliative care.
Treatments usually fall into
one of the following
categories: surgery, radiation,
chemotherapy, immunotherapy, hormone therapy, or gene therapy.
Surgery
Surgery is the oldest known treatment for cancer. If a cancer has not
metastasized, it is possible to completely cure a patient by surgically removing
the cancer from the body. This is often seen in the removal of the prostate or a
breast or testicle. After the disease has spread, however, it is nearly impossible
to remove all of the cancer cells. Surgery may also be instrumental in helping to
control symptoms such as bowel obstruction or spinal cord compression.
Innovations continue to be developed to aid the surgical process, such as the .
Currently, when a tumor is removed surgeons also take out a “margin” of
healthy tissue to make sure no malignant cells are left behind. This usually
means keeping the patients under general anesthetic for an extra 30 minutes
while tissue samples are tested in the lab for “clear margins”. If there are no
clear margins, the surgeon has to go back in and remove more tissue (if
possible). Scientists from Imperial College London say the iKnife may remove
the need for sending samples to the lab.
Radiation
Radiation treatment, also
known as radiotherapy,
destroys cancer by focusing
high-energy rays on the
cancer cells. This causes
damage to the molecules
that make up the cancer
cells and leads them to
commit suicide.
Radiotherapy utilizes highenergy gamma-rays that are
emitted from metals such as
radium or high-energy xrays that are created in a special machine. Early radiation treatments caused
severe side-effects because the energy beams would damage normal, healthy
tissue, but technologies have improved so that beams can be more accurately
targeted. Radiotherapy is used as a standalone treatment to shrink a tumor or
destroy cancer cells (including those associated with leukemia and lymphoma),
and it is also used in combination with other cancer treatments.
Chemotherapy
Chemotherapy utilizes chemicals that interfere with the cell division process damaging proteins or DNA - so that cancer cells will commit suicide. These
treatments target any rapidly dividing cells (not necessarily just cancer cells),
but normal cells usually can recover from any chemical-induced damage while
cancer cells cannot. Chemotherapy is generally used to treat cancer that has
spread or metastasized because the medicines travel throughout the entire body.
It is a necessary treatment for some forms of leukemia and lymphoma.
Chemotherapy treatment occurs in cycles so the body has time to heal between
doses. However, there are still common side effects such as hair loss, nausea,
fatigue, and vomiting. Combination therapies often include multiple types of
chemotherapy or chemotherapy combined with other treatment options.
Immunotherapy
Immunotherapy aims to get the body's immune system to fight the tumor. Local
immunotherapy injects a treatment into an affected area, for example, to cause
inflammation that causes a tumor to shrink. Systemic immunotherapy treats the
whole body by administering an agent such as the protein interferon alpha that
can shrink tumors. Immunotherapy can also be considered non-specific if it
improves cancer-fighting abilities by stimulating the entire immune system, and
it can be considered targeted if the treatment specifically tells the immune
system to destroy cancer cells. These therapies are relatively young, but
researchers have had success with treatments that introduce antibodies to the
body that inhibit the growth of breast cancer cells. Bone marrow transplantation
( hematopoetic stem cell transplantation ) can also be considered
immunotherapy because the donor's immune cells will often attack the tumor or
cancer cells that are present in the host.
Hormone therapy
Several cancers have been linked to some types of hormones, most notably
breast and prostate cancer. Hormone therapy is designed to alter hormone
production in the body so that cancer cells stop growing or are killed
completely. Breast cancer hormone therapies often focus on reducing estrogen
levels (a common drug for this is tamoxifen) and prostate cancer hormone
therapies often focus on reducing testosterone levels. In addition, some leukemia
and lymphoma cases can be treated with the hormone cortisone.
Gene therapy
The goal of gene therapy is to replace damaged genes with ones that work to
address a root cause of cancer: damage to DNA. For example, researchers are
trying to replace the damaged gene that signals cells to stop dividing (the p53
gene) with a copy of a working gene. Other gene-based therapies focus on
further damaging cancer cell DNA to the point where the cell commits suicide.
Gene therapy is a very young field and has not yet resulted in any successful
treatments.
Using cancer-specific immune system cells to treat cancer
Scientists from the RIKEN Research Centre for Allergy and Immunology in
Yokohama, Japan, explained in the journal Cell Stem Cell (January 2013 issue
The authors added that their study has shown that it is possible to clone versions
of the patients’ own cells to enhance their immune system so that cancer cells
could be destroyed naturally.
Hiroshi Kawamoto and team created cancer-specific killer T-lymphocytes from
iPSCs. They started off with mature T-lymphocytes which were specific for a
type of skin cancer and reprogrammed them into iPSCs with the help of
“Yamanaka factors”. The iPSCs eventually turned into fully active, cancerspecific T-lymphocytes - in other words, cells that target and destroy cancer
cells.
How can cancer be prevented?
Cancers that are closely linked to certain behaviors are the easiest to prevent.
For example, choosing not to smoke tobacco or drink alcohol significantly lower
the risk of several types of cancer - most notably lung, throat, mouth, and liver
cancer. Even if you are a current tobacco user, quitting can still greatly reduce
your chances of getting cancer.
Skin cancer can be prevented by staying in the shade, protecting yourself with a
hat and shirt when in the sun, and using sunscreen. Diet is also an important part
of cancer prevention since what we eat has been linked to the disease.
Physicians recommend diets that are low in fat and rich in fresh fruits and
vegetables and whole grains.
Certain vaccinations have been associated with the prevention of some cancers.
For example, many women receive a vaccination for the human papillomavirus
because of the virus's relationship with cervical cancer. Hepatitis B vaccines
prevent the hepatitis B virus, which can cause liver cancer.
Some cancer prevention is based on systematic screening in order to detect
small irregularities or tumors as early as possible even if there are no clear
symptoms present. Breast self-examination, mammograms, testicular selfexamination, and Pap smears are common screening methods for various
cancers.
Researchers from Northwestern University Feinberg School of Medicine in
Chicago reported in the journal Circulation. They include being physically
active, eating a healthy diet, controlling cholesterol, managing blood pressure,
reducing blood sugar and not smoking.
Targeting cancers for new drug therapies
Researchers at The Institute of Cancer Research reported in the journal Nature
Reviews Drug Discovery (January 2013 issue) that they have found a new way
of rapidly prioritizing the best druggable targets online. They managed to
identify 46 previously overlooked targets.
The researchers used the cancer database together with a tool and were able to
compare up to 500 drug targets in a matter of minutes. .
The scientists analyzed 479 cancer genes to determine which ones were
potential targets for medications. Their approach was effective - they found 46
new potentially “druggable” cancer proteins.
Not only will this approach lead to much more targeted cancer drugs, but also
considerably cheaper ones, the authors added.
Cancer Types
Cancer
Adrenal Cancer
Nasopharyngeal Cancer
Anal Cancer
Neuroblastoma
Aplastic Anemia
Non-Hodgkin Lymphoma
Bile Duct Cancer
Non-Hodgkin Lymphoma In
Children
Bladder Cancer
Oral Cavity and Oropharyngeal
Cancer
Osteosarcoma
Ovarian Cancer
Pancreatic Cancer
Penile Cancer
Bone Cancer
Brain/CNS Tumors In Adults
Brain/CNS Tumors In Children
Breast Cancer
Breast Cancer In Men
Cancer in Children
Cancer of Unknown Primary
Pituitary Tumors
Prostate Cancer
Renal Cancer
Retinoblastoma
Castleman Disease
Cervical Cancer
Colon/Rectum Cancer
Endometrial Cancer
Rhabdomyosarcoma
Esophagus Cancer
Salivary Gland Cancer
Ewing Family Of Tumors
Gestational Trophoblastic
Disease
Sarcoma - Adult Soft Tissue Cancer
Skin Cancer
Hodgkin Disease
Skin Cancer - Basal and Squamous
Cell
Skin Cancer - Melanoma
Small Intestine Cancer
Stomach Cancer
Testicular Cancer
Thymus Cancer
Kaposi Sarcoma
Kidney Cancer
Laryngeal and Hypopharyngeal
Cancer
Leukemia
Thyroid Cancer
Leukemia - Acute Lymphocytic
(ALL) in Adults
Uterine Sarcoma
Leukemia - Acute Myeloid (AML)
Vaginal Cancer
Leukemia - Chronic Lymphocytic
(CLL)
Vulvar Cancer
Waldenstrom Macroglobulinemia
Wilms Tumor
Leukemia - Chronic Myeloid
(CML)
Eye Cancer
Leukemia - Chronic
Myelomonocytic (CMML)
Gallbladder Cancer
Leukemia in Children
Gastric Cancer
Liver Cancer
Gastrointestinal Carcinoid Tumors
Lung Cancer
Gastrointestinal Stromal Tumor
(GIST)
Lung Cancer - Non-Small Cell
Lung Cancer - Small Cell
Lymphoma of the Skin
Lung Carcinoid Tumor
Malignant Mesothelioma
Lymphoma
Multiple Myeloma
Lymphoma - Hodgkin
Nasal Cavity and Paranasal Sinus
Lymphoma - Non-Hodgkin
Myelodysplastic Syndrome
Lymphoma - Non-Hodgkin in
Children
References :medicalnewstoday
American Cancer Society
Cancer Research, UK
Wikipedia
Centers for Disease Control and Prevention: http://www.cdc.gov/nccdphp/dcpc
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Cancer
Names
ID
Bola Tharwat Kodus
1131486
Mina Romany Ratib
1131467
Ramy Edwerd Baselyous
1131738
Ahmed Atef Mohamed
1131636
Under the supervision of :
Dr.
Wegdan Lotfi