| |
Although
not often inherited, cancer is undoubtedly a disease of the genetic
material of somatic cells, resulting in ncontrolled or unregulated
cell division. Many of the agents that cause cancer (e.g., carsonagens,
X rays) also cause mutations or chromosome abnormalities. There
is no doubt that understanding the role of DNA is central to understanding
the causes of cancer, and, without this, prevention and treatment
cannot be optimal. Biological approaches provided by recombinant
DNA technology have illuminated some of the basic pathways leading
to the malignant process at the molecular level. Researchers have
found that certain genes normally present in our cells-the so-called
proto-oncogenes, which are highly conserved in the evolution of
vertebrates-are altered in a variety of ways in cancer cells so
that their expression is changed and the regulation of cell division
is disturbed.
No more than
a weak hereditary influence has been noted in the occurrence of
most common adult malignancies, with up to 90 percent of all cancer
being related to environmental factors (carcinogens); e.g., about
30 percent of cancer deaths are attributable to cigarette smoking.
However, about 5 percent of cancers have a pronounced genetic
causal component. Many individuals with this latter type are members
of families with a single-gene disease that carries a marked predisposition
toward developing cancer. One group of such diseases, inherited
in a recessive fashion, are the chromosome instability syndromes
in which there is an increased tendency toward chromosomal breakage
and rearrangement, often with defects in DNA repair mechanisms.
One example is congenital
aplastic (Fanconi's) anemia. Individuals with immunological
deficiency diseases, a group of single-gene disorders that produce
defects in the immune response, also often develop malignancies.
Persons with chromosomal abnormalities, most commonly those with
Down
syndrome, have an increased risk of developing leukemia,
a malignancy of the white blood cells.
Rick
Weiss
|
|