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2. Most cells divide at some time during their life cycle, and some divide dozens of times before
they die. Organisms rely on cell division for reproduction, growth, and repair and replacement of
damaged or worn out cells. Organisms could not grow or function properly if the genetic
information encoded in DNA was not passed from cell to cell. Within all organisms, cells divide
to produce new cells, each of which requires the genetic information found in DNA. Yet simply
splitting the DNA of a dividing cell between two new cells would lead to disaster—the two new
cells would have different instructions and each subsequent generation of cells would have less
and less genetic information to work with.
3. Organisms use two types of cell division to ensure that DNA is passed down from cell to cell
during reproduction. Simple one-celled organisms and other organisms that reproduce asexually
—that is, without the joining of cells from two different organisms—reproduce by a process
called mitosis. During mitosis a cell doubles its DNA before dividing into two cells and
distributing the DNA evenly to each resulting cell. Organisms that reproduce sexually use a
different type of cell division. These organisms produce special cells called gametes, or egg and
sperm. In the cell division known as meiosis, the chromosomes in a gamete cell are reduced by
half. During sexual reproduction, an egg and sperm unite to form a zygote, in which the full
number of chromosomes is restored.
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Another busy area in cell biology concerns programmed cell death, or apoptosis. Millions of


times per second in the human body, cells commit suicide as an essential part of the normal cycle
of cellular replacement. This also seems to be a check against disease: When mutations build up
within a cell, the cell will usually self-destruct. If this fails to occur, the cell may divide and give
rise to mutated daughter cells, which continue to divide and spread, gradually forming a growth
called a tumor. This unregulated growth by rogue cells can be benign, or harmless, or cancerous,
which may threaten healthy tissue. The study of apoptosis is one avenue that scientists explore in
an effort to understand how cells become cancerous.

CARCINOGENS
One of the greatest risk factors for cancer is prolonged or repeated exposure to carcinogens—
chemical, biological, or physical agents that cause the cellular damage that leads to cancer. The
details of how carcinogens causes cancer remain unclear.
- TOBACCO SMOKE
Smoking is associated with cancer in the lungs, esophagus, respiratory tract, bladder,
pancreas, and probably cancers of the stomach, liver, and kidneys. The risk of cancer
increases depending on the number of cigarettes smoked per day, the cigarette’s tar
content, and how many years a person smokes. Starting to smoke while young
significantly increases the risk of developing cancer.
- DIET
Diet can also contribute to cancer. Saturated fats from red meats, such as hamburger or
steak, and high-fat dairy products are linked with several cancers. High salt intake
increases the risk of stomach cancer. Adult obesity increases the risk for cancer of the
uterus in women and also appears to increase the risk for cancers in the breast, colon,
kidney, and gallbladder. Alcohol consumption increases the risk of cancer of the
esophagus and stomach, especially when combined with smoking.
- PATHOGENS
Cancer-causing viruses include the human papillomavirus (HPV), a sexually transmitted
virus responsible for 70 to 80 percent of all cases of cancer of the cervix. Hepatitis B and
C viruses cause almost 80 percent of all liver cancer in the world. Epstein-Barr virus can
also be carcinogenic, causing cancer of the lymphatic system. Human immunodeficiency
virus (HIV) or a type of herpesvirus can lead to rare cancers of the lymphatic and
circulatory systems.
- RADIATION
Exposure to electromagnetic radiation, invisible, high-energy light waves such as sunlight
and X rays, accounts for a small percentage of cancer deaths (see Radiation Effects,
Biological). Most cancer deaths from radiation are from skin cancer, which is triggered
by too much sun exposure. Sunlight that reaches the Earth’s surface contains two kinds of
ultraviolet (UV) radiation. UV-A and UV-B both contribute to sunburn and skin cancer
as well as to conditions such as premature wrinkling of the skin. Depletion of the ozone
layer, which absorbs ultraviolet radiation in the upper atmosphere, will continue to
increase skin damage and skin cancer rates in the future.
- ENVIRONMENTAL AND OCCUPATIONAL CHEMICALS
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 traffic produce air pollution. Some people encounter
carcinogenic chemicals in their working environment.

STEROID HORMONES

Medical research suggests that cancers of the reproductive organs may be affected 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
female sex hormone estrogen seems to increase the risk of breast and uterine cancers

POPULATION DEMOGRAPHICS

Population studies show that a person’s age, race, and gender affect the probability that he or she
will develop cancer. Most cancers occur in adults middle-aged or older. The risk of 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 of
mutations necessary to turn an otherwise healthy cell into a cancerous cell.
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 of developing breast cancer. About 50
to 60 percent of women with inherited BRCA1 or BRCA2 mutations will develop breast cancer
by the age of 70. Inherited mutations in the genes MSH2, MLH1, PMS1, and PMS2, all of which
repair DNA, are especially prevalent in a rare form of hereditary colon cancer.
Scientists suspect that many other hereditary factors contribute to cancer. In addition to inherited
mutations, other genetic variations, particularly those influencing how the body responds to
carcinogens, may create a greater susceptibility to cancer. The identities of the majority of these
genetic variations are not yet known.

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