Allelic losses and DNA methylation at DNA mismatch repair loci in sporadic colorectal cancer | Zendy

Nadia Benachenhou | Zendy

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Allelic losses and DNA methylation at DNA mismatch repair loci in sporadic colorectal cancer

Author(s) -

Nadia Benachenhou

Publication year - 1998

Publication title -

carcinogenesis

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.688

H-Index - 204

eISSN - 1460-2180

pISSN - 0143-3334

DOI - 10.1093/carcin/19.11.1925

Subject(s) - dna mismatch repair , biology , locus (genetics) , microsatellite , dna methylation , carcinogenesis , colorectal cancer , allele , genetics , microsatellite instability , methylation , dna repair , cancer research , dna , microbiology and biotechnology , cancer , gene , gene expression

Normal and tumor DNA samples of 35 patients with sporadic colorectal carcinoma were analyzed for microsatellite alterations at 12 markers linked to mismatch repair loci: hMLH1, hMSH2, hMSH3, hMSH6, hPMS1 and hPMS2. Remarkably, no correlation was observed between the replication error phenotype (RER+) and allelic losses at these loci. Hemizygous deletions, seen in 6/35 (17%) informative cases at hMLH1, 4/27 (15%) at hMSH2/hMSH6 and 6/34 (18%) at hMSH3, were rarely found in RER+ tumors. Since mismatch repair protein components act in molecular complexes of defined stoichiometry we propose that hemizygous deletion of the corresponding loci may be involved in colorectal tumorigenesis through defects in cellular functions other than replication error correction. The analysis of the methylation status of the promoter region of hMLH1 revealed that methylation might be an important mechanism of this locus inactivation in RER+ sporadic colorectal cancer.

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