Gamma-radiation sensitivity and polymorphisms in RAD51L1 modulate glioma risk.

ABSTRACT:

Background

DNA strand breaks pose the greatest threat to genomic stability. Genetically determined mutagen sensitivity predisposes individuals to a variety of cancers, including glioma. However, polymorphisms in DNA strand break repair genes that may determine mutagen sensitivity are not well studied in cancer risk, especially in gliomas.

Methods

We correlated genotype data for tag single-nucleotide polymorphisms (tSNPs) of DNA strand break repair genes with a gamma-radiation-induced mutagen sensitivity phenotype [expressed as mean breaks per cell (B/C)] in samples from 426 glioma patients. We also conducted analysis to assess joint and haplotype effects of single-nucleotide polymorphisms (SNPs) on mutagen sensitivity. We further validate our results in an independent extern

SUBMITTER: Liu Y 

PROVIDER: S-EPMC2981459 | biostudies-literature | 2010 Oct

REPOSITORIES: biostudies-literature