AMERICAN ASSOCIATION FOR CANCER RESEARCH 19
Five to 10 percent of all new U. S. cancer cases are linked to inherited genetic mutations ( 22).
Some mutations are acquired during cell multiplication,
and the number of times a cell multiplies
increases the chance it will acquire a mutation.
Some mutations are acquired as a result of exposure
to factors that damage genetic material, such as toxins
in tobacco smoke and ultraviolet (UV) light from the sun.
Simplified estimates of the relative contribution of each of the various sources of mutations to developing particular types
of cancer are illustrated based on a recent study ( 23). This understanding can influence approaches for prevention and
early detection of these and other types of cancer. Because cancer is caused by the accumulation of mutations over time,
the older a person gets, the more likely he or she is to have a cell that has acquired a combination of genetic mutations
causing it to become cancerous.
WHY DID I GET THIS CANCER?
Cancer initiation and progression are predominantly caused by the accumulation of changes, or mutations,
in the genetic material of a cell over time. Some genetic mutations are inherited from your parents and are
present in each cell of the body from birth but most genetic mutations are acquired during your lifetime.
These factors come together to determine the chance that an individual cell has of acquiring mutations
over time. This, in turn, helps determine the overall risk that a person will develop a particular type of cancer.
Acquired genetic mutations
related to exposure to the
toxins in cigarette smoke are
the primary, but not the only,
contributors to the risk of developing
lung cancer. Eliminating tobacco use and
exposure to smoke can prevent cancer
(see Eliminate Tobacco Use, p. 24).
Polyposis–dependent Colorectal Cancer
For individuals who inherit a
mutation in the adenomatous
polyposis coli (APC) gene,
the inherited genetic
mutation is the primary,
but not the only, contributor
to their risk of developing
colorectal cancer. Such individuals, however, can
alter their personal prevention plans to proactively
survey for the earliest signs of disease and
intervene as appropriate
(see Finding Cancer, p. 38).
Basal Cell Carcinoma
Basal cells in the outermost layer
of the skin are constantly
multiplying to replace skin
damaged by normal wear
and tear. Thus, the number of
cell multiplications is the
primary contributor to the risk of
developing basal cell carcinoma. However,
it is not the only contributor. Exposure to UV
radiation from the sun or tanning beds can also
cause basal cells to acquire genetic mutations,
and a person can reduce his or her risk for
this cancer by adopting sun-safe
habits and avoiding UV tanning
devices (see Protect Skin
From UV Exposure, p. 32).
Hepatitis C Virus–dependent
Chronic infection with hepatitis C virus (HCV) increases
a person’s risk for liver cancer because it causes damage
to the liver, which triggers a tissue-repair process that
involves extensive multiplication of cells in the liver.
Thus, chronic HCV infection is the primary, but not the
only, contributor to the risk of developing liver cancer in
infected individuals. HCV infection is treatable and preventable
(see Prevent Infection With Cancer-causing Pathogens, p. 33). Adapted from ( 24)