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Genomic instability (GI) is a hallmark of tumorigenic progression and is observed as delayed genetic damage in the progeny of irradiated and unirradiated bystander cells. The expression of GI can be influenced by genotype, cell type and radiation quality. While several studies have demonstrated the induction of GI by high and low-linear energy transfer (LET) radiation, our work on human and mouse primary cell systems has shown LET-dependent differences in the induction and expression of GI. These differences might be attributed to differences in radiation track structure, dose rate, contribution of bystander cells and radiation dose. This paper reviews the role of radiation quality in the induction of GI and describe the possible mechanisms underlining the observed differences between radiation types on its induction. The experimental results presented suggest that dose might be the most significant factor in determining induction of GI after low-LET radiation.

Original publication

DOI

10.1093/rpd/ncl445

Type

Journal article

Journal

Radiat Prot Dosimetry

Publication Date

2006

Volume

122

Pages

221 - 227

Keywords

Bystander Effect, DNA Damage, Dose-Response Relationship, Radiation, Genome, Genomic Instability, Linear Energy Transfer, Models, Genetic, Radiation Dosage, Radiation, Ionizing