Earlier research indicates that within the human population there are consi
derable differences in the response to the carcinogenic activity of environ
mental carcinogens. Genetic polymorphism associated with several variants o
f the gene products participating in the biotransformation of various xenob
iotics (including carcinogens) found in human populations constitutes a maj
or cause of those differences. Enzymes coded by different variants of the s
ame gene can differ in their catalytic activities. Up to the present time,
most information on the effect of genetic polymorphism on the individual's
ability to activate or deactivate environmental carcinogenic xenobiotics, a
nd the associated risk of cancer, has been collected from studies of cytoch
romes P-450 belonging to gene families CYP1, CYP2 and CYP3, and of glutathi
one S-transferases and N-acetyltransferases. As carcinogen metabolism compr
ises a chain of chemical reactions involving numerous enzymes and enzyme-co
ding genes, research performed hitherto is able to offer only a very limite
d explanation of the associations between genetic polymorphism and the indi
vidual's susceptibility to cancer.