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Cancer (medicine), any oI more than 100 diseases characterized by excessive, uncontrolled

growth oI abnormal cells, which invade and destroy other tissues. Cancer develops in almost any
organ or tissue oI the body, but certain types oI cancer are more liIe-threatening than others. In
the United States and Canada cancer ranks as the second leading cause oI death, exceeded only
by heart disease. Each year, about 1.7 million Americans and more than 150,000 Canadians are
diagnosed with cancer, and more than halI a million Americans and about 70,000 Canadians die
oI the disease.
For reasons not well understood, cancer rates vary by gender, race, and geographic region. For
instance, more men than women develop cancer, and AIrican Americans are more likely to
develop cancer than people oI any other racial group in North America. The Irequency oI certain
cancers also varies globally. For example, breast cancer is more common in wealthy countries,
and cervical cancer is more common in poor countries.
Although people oI all ages develop cancer, most types oI cancer are more common in people
over the age oI 50. Cancer usually develops gradually over many years, the result oI a complex
mix oI environmental, nutritional, behavioral, and hereditary Iactors. Scientists do not
completely understand the causes oI cancer, but they know that certain liIestyle choices can
reduce the risk oI developing many types oI cancer. Not smoking, eating a healthy diet, and
exercising moderately Ior at least 30 minutes each day can lower the likelihood oI developing

Estimated Cancer Incidence by Site and Sex

Just 60 years ago a cancer diagnosis carried little hope Ior survival because doctors understood
little about the disease and how to control it. Today about two-thirds oI all Americans diagnosed
with cancer live longer than Iive years. While it is diIIicult to claim that a cancer patient is
disease Iree, long-term survival signiIicantly improves iI the patient has had no recurrence oI the
cancer Ior Iive years aIter the initial diagnosis. For years, death rates Irom cancer were rising in
developing countries. In 2006 the American Cancer Society reported that the number oI cancer
deaths in the United States dropped Ior two years in a row. The decrease was attributed to a
decline in smoking, earlier detection, and improved treatment.
The National Cancer Institute oI the United States (NCI) estimates that more than 10 million
Americans are living with cancer or have been cured oI the disease thanks largely to advances in
detecting cancers earlier. The sooner cancer is Iound and treated, the better a person`s chance Ior
survival. In addition, advances in the Iundamental understanding oI how cancer develops have
reduced deaths caused by certain cancers and hold promise Ior new and better treatments.

Conditions Men Get, Too
Osteoporosis, breast cancer, and eating disorders are sometimes considered women's diseases,
but doctors have Iound that men may also suIIer Irom these same medical problems. Because
men have these conditions so rarely, detection and treatment are oIten quite slow. To help with
early diagnosis, this article Irom FDA Consumer describes some oI the symptoms and possible
causes oI these serious diseases.
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A healthy human body is composed oI 30 trillion cells, most oI which are in constant turnover as
cells die and others reproduce to replace them in an orderly Iashion. Healthy cells oI the skin,
hair, lining oI the stomach, and blood, Ior example, regularly reproduce by dividing to Iorm two
daughter cells (see Mitosis). This cell division cycle proceeds under the regulation oI the body`s
intricately tuned control system. Among other Iunctions, this control system ensures that cells
only divide when needed, so that organs and tissues maintain their correct shape and size. Should
this system Iail, a variety oI backup saIety mechanisms prevent the cell Irom dividing
uncontrollably. In order Ior a cell to become cancerous, every one oI these saIety mechanisms
must Iail.
Cancer begins in genes, bits oI biochemical instructions composed oI individual segments oI the
long, coiled molecule deoxyribonucleic acid (DNA). Genes contain the instructions to make
proteins, molecular laborers that serve as building blocks oI cells, control chemical reactions, or
transport materials to and Irom cells. The proteins produced in a human cell determine the
Iunction oI each cell, and ultimately, the Iunction oI the entire body.
In a cancerous cell, permanent gene alterations, or mutations, cause the cell to malIunction. For a
cell to become cancerous, usually three to seven diIIerent mutations must occur in a single cell.
These genetic mutations may take many years to accumulate, but the convergence oI mutations
enables the cell to become cancerous.

SaIety Systems

DNA and Cancer

DNA and Cancer
Cancer begins in the genes, segments oI the long, coiled molecule known as
deoxyribonucleic acid (DNA). Genes govern the body`s development and speciIic
characteristics by providing critical instructions that trigger the production oI proteins
within the body. In cancer, certain genes Iail to perIorm their jobs correctly. This
computer-generated model shows two strands oI deoxyribonucleic acid (DNA) and its
double-helical structure.
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While each human cell perIorms its own specialized Iunction, it also exerts inIluence on the cells
around it. Cells communicate with one another via receptors, protein molecules on the cell
surIace. A cell releases chemical messages, which Iit into the surIace receptors oI cells nearby,
much as a key Iits into a lock. A cell may instruct other cells in its neighborhood to divide, Ior
example, by releasing a growth-promoting signal, or rowth factor. The growth Iactor binds to
receptors on adjacent cells, activating a message within each individual cell. This message
travels to the nucleus, where a cell`s genes are located.

Proto-Oncogenes Become

Nucleus oI a Cell

Nucleus oI a Cell
The nucleus, present in eukaryotic cells, is a discrete structure containing chromosomes,
which hold the genetic inIormation Ior the cell. Separated Irom the cytoplasm oI the cell by
a double-layered membrane called the nuclear envelope, the nucleus contains a cellular
material called nucleoplasm. Nuclear pores, present around the circumIerence oI the
nuclear membrane, allow the exchange oI cellular materials between the nucleoplasm and
the cytoplasm.
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When the growth Iactor message reaches the cell nucleus, it activates genes called proto-
oncogenes. These genes produce proteins that stimulate the cell to divide. In cancerous cells,
mutations in proto-oncogenes cause these genes to malIunction. When a proto-oncogene
mutates, it becomes an oncoenea gene that instructs the cell to grow and divide repeatedly
without stimulation Irom neighboring cells. Some oncogenes overproduce growth Iactors,
causing the cell to divide too oIten. Other oncogenes stimulate the cell to reproduce even when
no growth Iactor is present. Cancer researchers have identiIied about 100 diIIerent types oI
proto-oncogenes and their cancer-causing oncogene counterparts.

Tumor Suppressor Genes Stop Working
When runaway cell division occurs, it does not necessarily lead to cancer. Neighboring cells
respond by excreting a growth inhibitor. This chemical binds to receptors in the malIunctioning
cell, sending a signal to the nucleus that activates tumor suppressor genes. Tumor suppressor
genes are like brakes Ior cell growth. When activated, these genes halt the cell cycle, preventing
Iurther cell division.
But iI tumor suppressor genes malIunction due to mutations, the rapidly dividing cell ignores
messages Irom its neighbors telling it to stop dividing. MalIunctioning tumor suppressor genes
are not enough to cause cancerthe cell still must overcome a host oI other saIety mechanisms
beIore it can cause truly signiIicant damage.

Cell Cycle Clock MalIunctions
The cell nucleus contains a collection oI interacting proteins that control cell division.
Sometimes called the cell cycle clock, this group oI proteins interprets incoming messages at
several checkpoints in the cell division cycle. At these checkpoints, the clock evaluates the health
oI the cell. II conditions are right, the clock activates certain proto-oncogenes, which produce
proteins that trigger the cell to enter the next stage oI the cell cycle. II conditions are not right,
certain tumor suppressor genes produce proteins that prevent the cell Irom proceeding with cell
II the cell cycle clock detects DNA damage in a cell, a tumor suppressor gene called p53
prevents the cell Irom reproducing until the damage is repaired. II the cell is unable to repair the
DNA damage, p53 instructs the cell to undergo programmed cell death, or apoptosis, putting a
stop to runaway cell division beIore it starts. Programmed cell death is a normal part oI cell liIe
and is tightly controlled by many genes, primarily p53.
In a cancerous cell, one or more mutations prevent these genes Irom doing their jobs. When
mutated, p53 allows a cell to continue to divide, even with damaged DNA. This can lead to
additional mutations in proto-oncogenes or tumor suppressor genes. In some cases, mutations
occur in genes that produce proteins to repair damaged DNA. Such mutations can lead to yet
other mutations because the Iaulty DNA cannot duplicate properly during cell division.

Cells Achieve Immortality
A normal cell has a liIe span oI about 40 cell divisions. This liIe span is controlled in part by
telomeres, protective segments at the ends oI the cell`s DNA. Telomeres shorten with each cell
division until they can no longer protect the DNA. At this point cell division severely damages
the DNA, ultimately killing the cell. This normal process ensures that older cells, which may
have accumulated mutations, no longer reproduce. Cancer cells escape this protective
mechanism by producing a protein called telomerase. Telomerase extends the length oI
telomeres indeIinitely, rendering the cells immortal and capable oI never-ending cell division.

Cells Break Free and Spread
Evading the many obstacles that guard against runaway cell division is still not enough Ior
cancer to develop. A malIunctioning cell must also skirt a number oI saIety mechanisms
designed to prevent cells Irom growing where they are not supposed to in the body.
Normal cells adhere to each other and to a Iibrous meshwork called an extracellular matrix. This
matrix exists throughout all tissues and provides the structural support on which cells grow and
Iorm organs and other complex tissues. While a normal cell will oIten die iI it cannot adhere to
an extracellular matrix, cancer cells survive without this matrix.

Tumor Forms

Abnormal Cells and Cancer

Abnormal Cells and Cancer
Cancerous cells usually become much diIIerent Irom the tissue Irom which they arise. The
ovarian tumor pictured here bears no resemblance to the normal tissue oI the ovary.
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A tumor is a mass oI cells not dependent upon an extracellular matrix. These cells can grow on
top oI each other, creating a mass oI abnormal cells. OIten a tumor develops its own network oI
tiny blood vessels to supply itselI with nutrient-rich blood, a process called anioenesis.
There are two general types oI tumors. Benign tumors do not invade other tissues and are limited
to one site, making surgical removal possible and the odds Ior a Iull recovery excellent. Some
benign tumors are quite harmless and are not surgically removed unless they are unsightly or
uncomIortable. For example, warts are benign tumors oI the outer layer oI the skin. Although
they are usually not dangerous, warts may cause discomIort. Other benign tumors are thought to
be precursors to cancerous, or malignant, tumors.

Tumors Spread

The Development and Spread oI


The Development and Spread oI Tumors
Lung cancer begins when epithelial cells lining the respiratory tract start to reproduce in an
uncontrolled Iashion. These cells invade surrounding tissue, Iorming a mass called a tumor
and, when hardened, a carcinoma. Cancerous cells may penetrate blood and lymph vessels,
to be carried through the body until they reach a juncture through which they cannot pass.
At this point, they lodge and new tumors Iorm. Metastasis, the spreading oI cancer Irom its
original location to other parts oI the body, is the disease`s most destructive characteristic.
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Tumors are malignant only iI they can invade other parts oI the body. Malignant tumors extend
into neighboring tissue or travel to distant sites, Iorming secondary growths known as
metastases. To metastasize, tumor cells break through a nearby blood vessel to enter the
circulatory system or through a lymphatic vessel wall to enter the lymphatic system. Most
metastases occur in organs that are the next site downstream in the circulatory system or the
lymphatic system and contain a network oI capillaries, or small blood vessels. For example,
cancer oI the large intestine oIten travels through the bloodstream to the liver, the organ
immediately downstream Irom the intestines. In the lymphatic system, tumor cells can spread to
surrounding lymph nodes, or lymph glands. Normally, lymph nodes Iilter out and destroy
inIectious materials circulating in the lymphatic system.
The unique receptors on the surIace oI a cell may also play a role in where tumors metastasize.
Specialized molecules on a cell`s surIace identiIy where in the body the cell belongs. Similar
cells adhere to one another when their surIace receptors are compatible. Most oIten cells Irom
diIIerent tissues and organs have incompatible surIace receptors. However, some tissue types
share similar surIace receptors, enabling cancerous cells to move between them and proliIerate.
Prostate cells and bone cells, Ior example, have similar surIace receptors. This gives prostate
cancer cells a natural aIIinity Ior bone tissue, where they can settle to Iorm a new tumor.
Many cancers shed cells into the bloodstream early in their growth. Most oI these cells die in the
bloodstream, but some lodge against the surIace oI the blood vessel walls, eventually breaking
through them and into adjacent tissue. In some cases, these cells survive and grow into a tumor.
Others may divide only a Iew times, Iorming a small nest oI cells that remain dormant as a
micrometastasis. They may remain dormant Ior many years, only to grow again Ior reasons not
yet known.


Factors that AIIect the
Development oI Cancer

Scientists do not Iully understand the causes oI cancer, but studies show that some people are
more likely to develop the disease than others. Scientists called epidemiologists study particular
populations to identiIy why cancer rates vary (see Epidemiology). One method they use is to
compare cancer patients with healthy people in terms oI behavior such as diet, exercise, and
smoking and traits such as gender, age, and race. Population studies provide useIul inIormation
about risk Iactors that increase the likelihood oI developing cancer.
Study Finds No Link Between Power Lines, Leukemia
In the late 1970s, a study Iirst touched oII concern that electromagnetic Iields Irom power lines
might be creating an increased cancer risk among children. This article Irom the July 1997
edition oI the Encarta Yearbook reports on the results oI a recent large study on this subject, and
the continued debate over this issue.
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One oI the greatest risk Iactors Ior cancer is prolonged or repeated exposure to carcinogens
chemical, biological, or physical agents that cause the cellular damage that leads to cancer. The
details oI how carcinogens cause cancer remain unclear. One theory is that exposure to
carcinogens, when combined with the eIIects oI aging, causes an increase in chemicals in the
body called Iree radicals. An excessive number oI Iree radicals causes damage by taking
negatively charged particles called electrons Irom key cellular components oI the body, such as
DNA. This may make genes more vulnerable to the mutating eIIects oI carcinogens.

1. Tobacco
Report Calls Smoking Health Peril
The landmark report oI the United States Surgeon General discussed in this 1964 os Aneles
Times article, linked cigarette smoking to cancer. The conclusions, developed by a panel oI
scientists, led to government restrictions on tobaco products and contributed to a general decline
in smoking. Some oI the statistics and conclusions cited may have been revised or updated since
the report was published.
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Smoking causes up to 30 percent oI cancer deaths in the United States and Canada, making
tobacco smoke the most lethal carcinogen in North America. Smoking is associated with cancer
in the lungs, esophagus, respiratory tract, bladder, pancreas, and probably cancers oI the
stomach, liver, and kidneys. The risk oI cancer increases depending on the number oI cigarettes
smoked per day, the cigarette`s tar content, and how many years a person smokes. Starting to
smoke while young signiIicantly increases the risk oI developing cancer.
Each year in the United States, several thousand nonsmoking adults die oI lung cancer caused by
exposure to the smoke oI others` cigarettes, called secondhand smoke or environmental tobacco
smoke. Nonsmoking spouses oI smokers are 30 percent more likely to develop lung cancer than
those married to nonsmokers. Breathing secondhand smoke also increases the risk oI cancer in
the children oI smokers and in nonsmokers who work in smoky places. For this reason smoking
has been banned in many places such as restaurants and bars.
Cigars, pipes, and smokeless tobacco have also been implicated in increased risk Ior cancer.
Cigars contain most oI the same cancer-producing chemicals as cigarettes, and people who
smoke cigars have a 30 percent higher risk oI developing cancer than nonsmokers. Oral cancers
occur more Irequently in people who use smokeless tobacco, or snuff. SnuII users, Ior example,
are 50 times more likely to develop cancers oI the cheek or gum than nonusers.


Hamburger and Fries

Hamburger and Fries
A diet high in Iatty Ioods, such as what some consider to be the quintessential American
meala hamburger and Iriescan contribute to many cancers.
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Diet can also contribute to cancer. Saturated Iats Irom red meats, such as hamburger or steak,
and high-Iat dairy products are linked with several cancers. High salt intake increases the risk oI
stomach cancer. Adult obesity increases the risk Ior cancer oI the uterus in women and also
appears to increase the risk Ior cancers in the breast, colon, kidney, and gallbladder. Alcohol
consumption increases the risk oI cancer oI the esophagus and stomach, especially when
combined with smoking.


Hepatitis B Virus

Hepatitis B Virus
The hepatitis B virus (HBV), recognizable under magniIication by the round, inIectious
'Dane particles accompanied by tube-shaped, empty viral envelopes, causes nearly 80
percent oI liver cancers worldwide.
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Some carcinogens are living organisms. Certain viruses, bacteria, and parasites account Ior about
15 percent oI all cancer deaths in the United States. Cancer-causing viruses include the human
papillomavirus (HPV), a sexually transmitted virus responsible Ior 70 to 80 percent oI all cases
oI cancer oI the cervix. Hepatitis B and C viruses cause almost 80 percent oI all liver cancer in
the world. Epstein-Barr virus can also be carcinogenic, causing cancer oI the lymphatic system.
Human immunodeIiciency virus (HIV) or a type oI herpesvirus can lead to rare cancers oI the
lymphatic and circulatory systems. elicobacter pylori, a bacterium associated with stomach
ulcers, likely causes cancer oI the stomach. Researchers have linked a polyomavirus to a rare,
aggressive Iorm oI skin cancer called Merkel cell carcinoma.
In developing countries, parasitic organisms are major carcinogens. In parts oI AIrica, China,
and southern Asia, inIestation with the liver Iluke Clonorchis sinensis causes a Iorm oI liver
cancer. In North AIrica, inIection with the parasite Schistosoma haematobium causes cancer oI
the bladder.

Thyroid Cancers Linked to Atomic Bomb Tests
During the 1940s and 1950s the United States government conducted above-ground nuclear
bomb tests in Nevada. In 1982 Congress directed the National Cancer Institute (NCI) to
investigate the health eIIects oI radioactive Iallout Irom those tests. The study was the most
comprehensive look ever at radioactive exposure. It took 14 years to complete: 100,000 pages
oI data, statistics, and research were Iinally compiled into a 1000-page report. The results,
which Iocus on the correlation between milk consumption and thyroid cancer, are summarized
in this article Irom the 1997 Encarta Yearbook.
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Exposure to electromagnetic radiation, invisible, high-energy light waves such as sunlight and X
rays, accounts Ior a small percentage oI cancer deaths (see Radiation EIIects, Biological). Most
cancer deaths Irom radiation are Irom skin cancer, which is triggered by too much sun exposure.
Sunlight that reaches the Earth`s surIace contains two kinds oI ultraviolet (UV) radiation. UV-A
and UV-B both contribute to sunburn and skin cancer as well as to conditions such as premature
wrinkling oI the skin. Depletion oI the ozone layer, which absorbs ultraviolet radiation in the
upper atmosphere, will continue to increase skin damage and skin cancer rates in the Iuture.
Radon, a colorless, odorless, radioactive gas, seeps Irom the Earth in some regions oI the United
States. Breathing the gas over a long period has been linked to a small number oI lung cancer
cases. Providing adequate air circulation in a building reduces exposure to radon. InIrequently,
radiation exposure associated with medical treatments, such as therapeutic radiology, leads to

Environmental and Occupational Chemicals

Air Pollution in Cubato, Brazil

Air Pollution in Cubato, Brazil
A thick layer oI Iumes hovers over the city oI Cubato in So Paulo state, Brazil. Pollution
in the air, water, and soil accounts Ior about 2 percent oI all American cancer deaths, and
may be responsible Ior a higher percentage oI cancer deaths in countries with less stringent
pollution control laws. Lung cancer rates tend to be higher in urban and industrial centers,
where air pollution is a constant problem.
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Air pollution, water pollution, and pollutants in the soil contribute particularly to lung and
bladder cancer. Lung cancer rates are generally higher in cities, where increased industry and
automobile traIIic produce air pollution. Some people encounter carcinogenic chemicals in their
working environment. Occupational carcinogens include such industrial chemicals as benzene,
asbestos, vinyl chloride, aniline dyes, arsenic, and certain petroleum products (see Occupational
and Environmental Disease).

Hereditary Factors
Evidence suggests that heredity plays a role in developing cancer. Some gene mutations
associated with cancer are inherited. For example, inheriting mutated tumor suppressor genes
BRCA1 or BRCA2 greatly increases a woman`s chances oI developing breast cancer. About 50
to 60 percent oI women with inherited BRCA1 or BRCA2 mutations will develop breast cancer
by the age oI 70. Inherited mutations in the genes MSH2, MLH1, PMS1, and PMS2, all oI which
repair DNA, are especially prevalent in a rare Iorm oI hereditary colon cancer.
Scientists suspect that many other hereditary Iactors contribute to cancer. In addition to inherited
mutations, other genetic variations, particularly those inIluencing how the body responds to
carcinogens, may create a greater susceptibility to cancer. The identities oI the majority oI these
genetic variations are not yet known.

Steroid Hormones
Medical research suggests that cancers oI the reproductive organs may be aIIected by naturally
occurring steroid hormones produced by the endocrine system. These hormones stimulate
reproductive organ cells to divide and grow. In women, relatively high or long exposure to the
Iemale sex hormone estrogen seems to increase the risk oI breast and uterine cancers. Thus, early
age at Iirst menstruation, late age at menopause, having a Iirst child aIter age 30, and never
having children, all oI which aIIect the duration oI estrogen exposure in the body, increase the
risk Ior these cancers. Studies also indicate that hormone replacement therapy (HRT), in which
women take estrogen to oIIset the unpleasant eIIects oI menopause, increases the risk oI breast
cancer. Male sex hormones, particularly testosterone, appear to play a role in cancers oI the male
reproductive organs, but this role is not yet well understood.

Population Demographics
Population studies show that a person`s age, race, and gender aIIect the probability that he or she
will develop cancer. Most cancers occur in adults middle-aged or older. The risk oI cancer
increases as individuals age because genetic mutations accumulate slowly over many years, and
the older a person is, the more likely that he or she will have accumulated the collection oI
mutations necessary to turn an otherwise healthy cell into a cancerous cell. More than three-
Iourths oI all cancers in North America are diagnosed in people over age 55.
Statistics show that men are more likely to develop cancer than women. In the United States,
nearly halI oI all men will develop cancer at some point in their liIetimes, whereas slightly more
than one-third oI women will. Cancer statistics Ior Canada are similar. Stomach cancer is nearly
twice as common in men as in women, as are certain types oI kidney cancer. However, the
reasons Ior the discrepancy between the sexes are unknown.
Some cancers are more prevalent in particular races than others. In the United States, Ior
example, bladder cancer is twice as common in white people as in black people. White women
are slightly more likely to develop breast cancer than are black women, but black women are
more likely to die oI the disease. Asian, Hispanic, and Native American women have the lowest
breast cancer risk. On the whole, AIrican Americans, especially men, are more likely to develop
cancerand more likely to die Irom itthan members oI any other group in the United States.
Reasons Ior the discrepancies between races are still not entirely clear, but many epidemiologists
trace them to diIIerences in diet and exercise, unequal access to medical care, and exposure to


Epithelial Cells

Epithelial Cells
Epithelial tissue Iorms a protective layer oI cells that covers organ surIaces and lines body
cavities. Shown here is a layer oI simple squamous (scaly) epithelium under magniIication.
Cancers that arise in epithelial tissues, called carcinomas, account Ior approximately 90
percent oI all human cancers.
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More than 100 types oI cancer develop in the various organs in the body. Cancers are described
according to where in the body the cancer originated, what type oI tissue it originated in, and
what type oI cell it started in. For example, breast cancer describes any cancer that originated in
the breast. II the cancer spreads to a new organ, such as the lungs, the tumor is called metastatic
breast cancer, not lung cancer.

Connective Cell Tissues

Connective Cell Tissues
Connective tissues include bone, cartilage, Iat, ligaments, and tendons. These tissues
support and connect parts oI the body. The structure varies depending on the purpose oI the
tissue. The diagonal red band in this image shows elastin Iiber, which allows connective
tissue to spring back into shape Iollowing deIormation. Cancers called sarcomas orginate
in connective tissues. Rare, sarcomas constitute only about 2 percent oI all human cancers.
Sarcomas are elusive in their early stages. They may arise deep within connective tissues,
making them more likely to spread to distant parts oI the body beIore they are detected.
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Each organ in the body is composed oI diIIerent types oI tissue, and most cancers arise in one oI
three main typesepithelial, connective, or blood-Iorming tissue. Carcinomas are cancers that
occur in epithelial tissuesthe skin and inner membrane surIaces oI the body, such as those oI
the lungs, stomach, intestines, and blood vessels. Carcinomas account Ior approximately 90
percent oI human cancers. Sarcomas originate in connective tissuessuch as muscle, bone,
cartilage, and Iatthat support and connect other parts oI the body. Much rarer than carcinomas,
sarcomas account Ior less than 2 percent oI all cancers. Leukemias develop in blood cells, and
lymphomas originate in the lymphatic system. Combined, these cancers oI the blood-Iorming
tissues account Ior about 8 percent oI all human cancers.
Cancers are Iurther identiIied according to the type oI cell aIIected. For example, squamous cells
are Ilat, scalelike cells Iound in epithelial tissue. Cancers that originate in these cells are called
squamous cell carcinomas. Adenomatous cells are glandular or ductal cells, and carcinomas that
originate in these cells are called adenocarcinomas. Sarcomas that develop in Iat cells are called
liposarcomas, and those that develop in bone cells are called osteosarcomas.
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