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Radiation-induced genomic instability and its implications for radiation carcinogenesis

Abstract

Radiation-induced genomic instability is characterized by an increased rate of genetic alterations including cytogenetic rearrangements, mutations, gene amplifications, transformation and cell death in the progeny of irradiated cells multiple generations after the initial insult. Chromosomal rearrangements are the best-characterized end point of radiation-induced genomic instability, and many of the rearrangements described are similar to those found in human cancers. Chromosome breakage syndromes are defined by chromosome instability, and individuals with these diseases are cancer prone. Consequently, chromosomal instability as a phenotype may underlie some fraction of those changes leading to cancer. Here we attempt to relate current knowledge regarding radiation-induced chromosome instability with the emerging molecular information on the chromosome breakage syndromes. The goal is to understand how genetic and epigenetic factors might influence the onset of chromosome instability and the role of chromosomal instability in carcinogenesis.

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Acknowledgements

This work was supported by the Biological and Environmental Research Program (BER), US Department of Energy, Grant No. DE-FG02-01ER63230 and National Institute of Health Awards CA73924 and CA 83872.

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Correspondence to Lei Huang.

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Huang, L., Snyder, A. & Morgan, W. Radiation-induced genomic instability and its implications for radiation carcinogenesis. Oncogene 22, 5848–5854 (2003). https://doi.org/10.1038/sj.onc.1206697

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