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World J Gastroenterol. Dec 14, 2007; 13(46): 6254-6258
Published online Dec 14, 2007. doi: 10.3748/wjg.v13.i46.6254
Two novel germline mutations of MLH1 and investigation of their pathobiology in hereditary non-polyposis colorectal cancer families in China
Chao-Fu Wang, Xiao-Yan Zhou, Tai-Ming Zhang, Ye Xu, San-Jun Cai, Da-Ren Shi
Chao-Fu Wang, Xiao-Yan Zhou, Tai-Ming Zhang, Da-Ren Shi, Department of Pathology, Cancer Hospital of Fudan University, Shanghai 200032; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China
Ye Xu, San-Jun Cai, Department of Abdominal Surgery, Cancer Hospital of Fudan University, Shanghai 200032, China
Author contributions: All authors contributed equally to the work.
Supported by the Key Project of Shanghai Medical Subjects, No.05 III 004 and Shanghai Pujiang Program, No. 06PJ14019
Correspondence to: Dr. Xiao-Yan Zhou, Laboratory of Molecular Pathology, Cancer Hospital of Fudan University, 270 Dongan Road, Shanghai 200032, China. xyzhou100@yahoo.com
Telephone: +86-21-64175590-3646
Received: May 16, 2007
Revised: August 20, 2007
Accepted: October 15, 2007
Published online: December 14, 2007
Abstract

AIM: To detect germline mutations of MLH1, and investigate microsatellite instability and expression of MLH1 in tumor tissues of hereditary non-polyposis colorectal cancer (HNPCC) with two novel germline mutations, and further investigate the pathobiology of the two novel mutations of MLH1.

METHODS: RNA was extracted from the peripheral blood of 12 patients from 12 different families that fulfilled the Amsterdam II Criteria for HNPCC. Germline mutations of MLH1 were determined by RT-PCR, followed by cDNA sequencing analysis. PCR-GeneScan analysis was used to investigate microsatellite instability with a panel of five microsatellite markers (BAT26, BAT25, D5S346, D2S123 and mfd15), along with immunohistochemical staining to detect the expression of MLH1 protein in two patients' tumor tissues with novel mutations.

RESULTS: Three germline mutations were found in four patients, one of the mutations has previously been reported, but the other two, CGC→TGC at codon 217 of exon 8 and CCG→CTG at codon 581 of exon 16, have not been reported. The two patients' tumor tissues with novel mutations had high-frequency microsatellite instability that showed more than two unstable loci, and both tumors lost their MLH1 protein expression.

CONCLUSION: The two novel germline mutations of MLH1 in HNPCC families i.e. CGC→TGC at codon 217 of exon 8 and CCG→CTG at codon 581 of exon 16, are very likely to have pathological significance.

Keywords: Colorectal cancer; Hereditary non-polyposis colorectal cancer; MLH1 gene; Germline mutation; Microsatellite instability; Gene sequencing