PMID: 8940748Sep 1, 1996Paper

The p53 gene as a modifier of intrinsic radiosensitivity: implications for radiotherapy

Radiotherapy and Oncology : Journal of the European Society for Therapeutic Radiology and Oncology
R G BristowR P Hill

Abstract

Experimental studies have implicated the normal or "wild type' p53 protein (i.e. WTp53) in the cellular response to ionizing radiation and other DNA damaging agents. Whether altered WTp53 protein function can lead to changes in cellular radiosensitivity and/or clinical radiocurability remains an area of ongoing study. In this review, we describe the potential implications of altered WTp53 protein function in normal and tumour cells as it relates to clinical radiotherapy, and describe novel treatment strategies designed to re-institute WTp53 protein function as a means of sensitizing cells to ionizing radiation. A number of experimental and clinical studies are critically reviewed with respect to the role of the p53 protein as a determinant of cellular oncogenesis, genomic stability, apoptosis, DNA repair and radioresponse in normal and transformed mammalian cells. In normal fibroblasts, exposure to ionizing radiation leads to a G1 cell cycle delay (i.e. a "G1 checkpoint') as a result of WTp53 mediated inhibition of G1-cyclin-kinase and retinoblastoma (pRb) protein function. The G1 checkpoint response is absent in tumour cells which express a mutant form of the p53 protein (i.e. MTp53), leading to acquired radioresistance in vit...Continue Reading

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