PMID: 8975319Sep 1, 1996Paper

Antioncogene p53 and apoptosis response: new hypotheses on the molecular bases of tumor resistance to radiotherapy

La Radiologia medica
R Corvò

Abstract

Recent experimental data indicate that in normal or neoplastic cells, DNA damage induced by ionizing radiation may work as a signal to trigger apoptosis, a characteristic suicide program inherent to multicellular organisms. The morphological signatures of apoptosis are cell shrinkage, nuclear condensation and genomic fragmentation down to the size of individual nucleosome units (apoptotic bodies). A number of genes have been identified as involved regulators of apoptosis. The tumor suppressor gene p53 has emerged as a main modulator and inducer of apoptosis. Cells containing wild-type p53 function undergo G1 arrest following DNA damage by ionizing radiations. DNA repair processes are, then, activated before the damaged genome can be replicated, with resultant genetic instability. If DNA repair fails, the wild p53 gene may trigger apoptosis and the cell with persisting DNA damage, dies. Cells with loss of functional p53 gene by either gene mutation or deletion appear unable to undergo radiation-induced apoptosis. This evidence may underlie the increased likelihood for p53 deficient cells to develop oncogenetic processes after irradiation exposure. According to p53-triggering apoptosis patterns, cancer cells with a normal p53 gen...Continue Reading

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