Methylation tolerance due to an O6-methylguanine DNA methyltransferase (MGMT) field defect in the colonic mucosa: an initiating step in the development of mismatch repair-deficient colorectal cancers

@article{Svrcek2010MethylationTD,
  title={Methylation tolerance due to an O6-methylguanine DNA methyltransferase (MGMT) field defect in the colonic mucosa: an initiating step in the development of mismatch repair-deficient colorectal cancers},
  author={M. Svrcek and O. Buhard and C. Colas and F. Coulet and S. Dumont and Illiasse Massaoudi and A. Lamri and R. Hamelin and J. Cosnes and Carla Oliveira and R. Seruca and M. Gaub and M. Legrain and A. Collura and O. Lascols and E. Tiret and J. Fl{\'e}jou and A. Duval},
  journal={Gut},
  year={2010},
  volume={59},
  pages={1516 - 1526}
}
Background and aims O6-Methylguanine-DNA methyltransferase (MGMT) removes methyl adducts from O6-guanine. Known as methylation tolerance, selection for mismatch repair (MMR)-deficient cells that are unable to initiate lethal processing of O6-methylguanine-induced mismatches in DNA is observed in vitro as a consequence of MGMT deficiency. It was therefore hypothesised that an MGMT field defect may constitute a preneoplastic event for the development of MMR-deficient tumours displaying… Expand
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  • P. Minoo
  • Biology, Medicine
  • Front. Oncol.
  • 2013
TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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The accumulation of DNA demethylation in Sat α in normal gastric tissues with Helicobacter pylori infection renders susceptibility to gastric cancer in some individuals.
TLDR
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Expression and promoter methylation status of hMLH1, MGMT, APC, and CDH1 genes in patients with colon adenocarcinoma
TLDR
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TLDR
The data suggest that epigenetic silencing of MGMT by promoter hypermethylation may lead to a particular genetic change in human cancer, specifically G to A transitions in the K-ras oncogene. Expand
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TLDR
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TLDR
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TLDR
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