Abstract
Cancer is essentially a genetic disease at the cellular level. It is caused by abnormalities in the genetic mechanisms which control cellular growth and proliferation. Most gene alterations associated with cancer are acquired through exposure to environmental carcinogens such as certain chemicals, radiation, infectious organisms, or factors in the diet. Only a small minority are inherited in the germline. Almost all cancers in humans have both sporadic and genetic counterparts. Genetic alterations may indirectly increase the risk of mutations occurring in growth related genes by affecting the metabolism of an environmental carcinogen or DNA repair mechanisms. Genetic predisposition to cancer may also result from inherited mutations in genes that are directly concerned with normal growth and differentiation. Included in this category are oncogenes, which, when activated, promote abnormal growth and proliferation, and tumour suppressor genes, which usually have a role in cellular differentiation and repression of proliferation but which may be lost, damaged, or switched off through mutations. Both tumour suppressor genes and DNA repair defects have been shown to account for inherited predisposition to cancer.