Abstract
Background Defects in mismatch repair (MMR) have been extensively documented as the underlying cause of several cancers, most notably colon cancer. Recently, MMR has been proposed to play a role in the transition to hormone independence in prostate cancer. It is proposed that MMR mediates the cytotoxic effects of DNA damaging agents by exerting a futile repair pathway which leads to double strand breaks (DSBs). Previous reports indicate that the sensitivity of cells defective in homologous recombination (HR) to the DNA alkylation is reduced by defects in MMR genes. The involvement of MMR in the pathogenesis of prostate cancer has only recently been investigated. Genetic differences in MMR genes between ethnic populations may account for different outcomes after therapy. These genetic backgrounds should be investigated further.
Highlights
Defects in mismatch repair (MMR) have been extensively documented as the underlying cause of several cancers, most notably colon cancer
Previous reports indicate that the sensitivity of cells defective in homologous recombination (HR) to the DNA alkylation is reduced by defects in MMR genes
We have assessed the contribution of different MMR genes to the processing of alkylation damage in vivo
Summary
Defects in mismatch repair (MMR) have been extensively documented as the underlying cause of several cancers, most notably colon cancer. Differential contribution of mismatch repair genes in the processing of DNA damage Hernan Flores-Rozas From The Science of Global Prostate Cancer Disparities in Black Men Jacksonville, FL, USA. Background Defects in mismatch repair (MMR) have been extensively documented as the underlying cause of several cancers, most notably colon cancer.
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