Mismatch repair system decreases cell survival by stabilizing the tetraploid G1 arrest in response to SN-38.

@article{Bhonde2010MismatchRS,
  title={Mismatch repair system decreases cell survival by stabilizing the tetraploid G1 arrest in response to SN-38.},
  author={Mandar Ramesh Bhonde and M. T. Hanski and Jenny Stehr and Britta Jebautzke and Roser Peir{\'o}-Jord{\'a}n and H. Fechner and Kazunari Kazushige Yokoyama and Weei-Chin Lin and Martin Zeitz and Christoph Hanski},
  journal={International journal of cancer},
  year={2010},
  volume={126 12},
  pages={2813-25}
}
The role of the mismatch repair (MMR) system in correcting base-base mismatches is well established; its involvement in the response to DNA double strand breaks, however, is less clear. We investigated the influence of the essential component of MMR, the hMLH1 protein, on the cellular response to DNA-double strand breaks induced by treatment with SN-38, the active metabolite of topoisomerase I inhibitor irinotecan, in a strictly isogenic cell system (p53(wt), hMLH1(+)/p53(wt), hMLH1(-)). By… CONTINUE READING
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