ArticleVirchows Archiv : an international journal of pathology2003
The promoter methylation status of the DNA repair gene O6-methylguanine-DNA methyltransferase in ulcerative colitis.
Article in Virchows Archiv : an international journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 28 citations in OpenAlex.
- MGMT-Methylation in Non-Neoplastic Diseases of the Central Nervous System.International journal of molecular sciences · 2021Article
- Whole-Exome Sequencing Analyses of Inflammatory Bowel Disease-Associated Colorectal Cancers.Gastroenterology · 2016Article
- Unique patterns of CpG island methylation in inflammatory bowel disease-associated colorectal cancers.Inflammatory bowel diseases · 2012Article
- Silencing of MGMT expression by promoter hypermethylation in the metaplasia-dysplasia-carcinoma sequence of Barrett's esophagus.Cancer letters · 2009Article
- Contributions of integrin-linked kinase to breast cancer metastasis and tumourigenesis.Journal of cellular and molecular medicineReview
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8 authors at 2 institutions in 1 country.
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Abstract
Patients with long-standing and extensive ulcerative colitis (UC) have an increased incidence of colorectal cancer (CRC). It has been reported that a DNA repair gene, O6-methylguanine-DNA methyltransferase (MGMT) is inactivated by promoter hypermethylation in sporadic CRCs. Hence, we investigated the promoter methylation status of MGMT by methylation specific polymerase chain reaction (PCR) in a total of 67 tissue samples (61 non-cancerous tissues and 6 cancer tissues) from 24 patients with UC. Promoter hypermethylation of MGMT was detected in one well-differentiated adenocarcinoma (16.7%) of 6 cancer samples and not detected in any of adenomas and dysplasias. In non-dysplastic tissues, promoter hypermethylation of MGMT was detected in 2 (3.7%, mucosa with mild inflammation) of 54 samples. The frequency of MGMT promoter hypermethylation in UC-associated CRCs found in this study (16.7%) is obviously lower than previously reported in sporadic CRCs (39.0-42.0%). We also confirmed that 42.9% (6/14) of sporadic CRCs showed the promoter methylation. These findings indicated that promoter hypermethylation of the MGMT gene is infrequent in patients with UC, and may not closely contribute to UC-associated colorectal tumorigenesis. A different genetic pathway for tumor progression may exist between sporadic CRC and UC-associated CRC.
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