During the last years new perspectives have arisen in the field of cancer therapy, when it has been generally accepted that the mechanisms which regulate cell death play an equally important role in tumorgenesis as the mechanisms which regulate cell proliferation. Apoptosis constitutes an intrinsic program of cell suicide which is necessary for the depletion of undesired cells and for the maintenance of tissue homeostasis. Its regulation is extremely complex process and a large number of genes contribute to this process. These genes are divided to the ones that induce apoptosis (p53, c-myc, E2F, Fas, Bax, Bad, Bak, Bcl-x_s) and to those that suppress apoptosis (Bcl-2, Bcl-X_L, Bcl-w, MCL-1, A-I, crmA, p35). Apoptosis exists in most malignant tumors and a high apoptotic rate has been found in rapidly proliferating tumors. The variable types of cancer therapy (chemotherapy, radiation therapy, hormonotherapy) have the capability, under certain circumstances, to induce apoptosis. The understanding of the biochemistry and genetics of apoptosis creates new possibilities of therapeutic intervention which aim, on the one hand, in the increase of automatic cell death of tumor cells and on the other hand in the diminution of the resistance of the tumor cells to the different types of therapy. These aims will be obtained if the expression of the genes that induce apoptosis increases with the use of drugs that will cause overexpression of the wild type of p53 or will mimick its effect or will act as antibodies Fas which trigger apoptosis. The discovery of drugs that will suppress the expression of bcl-2 aims to the same effect. In the same way the diminution of the expression of mutant genes, such as the mutant type of p53 or the Bcr-Abl chimerical gene of chronic myeloid leukemia, will have the same results. Future searches in the field of apoptosis will help significantly in cancer therapy.

Key words: Apoptosis, cancer, chemotherapy.

Full text in Greek