DOI:10.1007/s00423-011-0812-9 - Corpus ID: 8069716
Promoter methylation status of hMLH1, hMSH2, and MGMT genes in colorectal cancer associated with adenoma–carcinoma sequence
@article{Lee2008PromoterMS,
title={Promoter methylation status of hMLH1, hMSH2, and MGMT genes in colorectal cancer associated with adenoma–carcinoma sequence},
author={Kyung‐Hwa Lee and Ji-Shin Lee and Jong Hee Nam and Chan Choi and Min‐Cheol Lee and Chang‐soo Park and Sang Woo Juhng and Jae-Hyuk Lee},
journal={Langenbeck's Archives of Surgery},
year={2008},
volume={396},
pages={1017-1026},
url={https://api.semanticscholar.org/CorpusID:8069716}
}- Kyung‐Hwa Lee, Ji-Shin Lee, Jae-Hyuk Lee
- Published in Langenbeck's archives of… 1 May 2008
- Biology, Medicine
- Langenbeck's Archives of Surgery
Data suggest that CpG island methylation in hMSH2 and MGMT, but not hMLH1, is closely related to carcinogenesis in colorectal carcinomas presenting with a conventional adenoma–carcinoma sequence, and may have clinical significance in the evaluation of colon cancer patients and in tumor-specific management of the disease.
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39 Citations
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The findings suggest that DNA methylation is a useful marker for tumor progression monitoring and that promoter methylation in certain genes is associated with more advanced tumor stage, poor differentiation, and metastasis.
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A meta-analysis of 45 articles identified a significant association between hMLH1 hypermethylation and colorectal cancer risk using the fixed-effects model and random effects model pooled.
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The methylation levels of MGMT and MLH1 were moderately and weakly correlated between the patient-matched leukocytes and the normal colorectal tissue, respectively.
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Early epigenetic methylation of WIF1 gene is one of the mechanisms for ACF development in human colon, although a statistically significant difference was observed only for the WIF1 gene.
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The hypothesis that MGMT expression may be an OS biomarker as useful as tumor stage or differentiation grade and that CD133 expression may be a predictive biomarker of DFS is supported.
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This study suggests that aberrant DNA methylation and epigenetic inactivation of hMSH2 play an important role in the development of ALL through altering cell growth and survival.
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