The past and the future of cancer genetics.

Carcinogenesis represents a multistep process associated with accumulation of somatic mutations in the classes of genes that regulate cell proliferation, apoptosis as well as DNA repair. Oncogenes, positive regulators of cell proliferation are activated during carcinogenesis. On the contrary, tumor suppressor genes, negative regulators of cell proliferation have to be inactivated. Mutations in genes that function in the maintenance of genomic stability are manifested by increase in the mutation rate in cancer cells that drive tumor progression. In general, on the basis of malignant transformation lies the abrogation of the balance between cell proliferation and cell apoptosis. The genetic mechanisms included in the transformation of normally acting genes comprise a wide spectrum of events, such as gene mutation, gene and chromosome rearrangement and gene amplification. Besides the role of somatic gene alteration in the development of sporadic cancer, germline mutations are the basis of a substantial number of inherited cancer syndromes. The future decades will be marked with the expansion of data exploiting cancer genetics, epigenetics and genomics into clinical practice. Consequently, translational cancer research should provide the generating of new targeted therapies, since individual molecular profiling of a patient?s tumor should increase efficacy of conventional anticancer therapies such as chemotherapy and radiotherapy.