During the past decade molecular biology and molecular genetics have greatly increased our understanding of the basic mechanisms in cancer development. The essential outcome of these molecular studies is that cancer can be considered as a genetic disease of cells. Both the non-hereditary (sporadic) cancers, as well as the hereditary forms of cancer are caused by genetic accidents that perturb the complex and delicate cellular growth control systems. Thus, at the molecular level, no principal difference exists between hereditary-and non-hereditary forms of cancer and it can be stated that both at the level of the single cell as well at the level of the individual, cancer is a genetic disease. Whereas in hereditary cancer, the risk gene is passed through the germline to the next generation, in. sporadic cancer, a cancer cells passes its abnormal genes to its daughter cells at cell division. It is therefore not surprising that one of the main priorities in cancer research today is the identification of the culprit genes and characterizing the function of their normal products. Genes associated with hereditary cancer syndromes essentially encompass two classes of genes viz. tumor suppressor genes and genes controlling genomic stability (DNA-mismatch repair genes). Although germline mutations in these susceptibility genes are associated with signficantly increased cancer risk, even up to 90%, additional genetic factors and interaction with environmental factors eventually determine if a carrier of a germline mutation will develop cancer. (C) 1997 Elsevier Science Ireland Ltd.