Brief Article
Copyright ©2010 Baishideng. All rights reserved
World J Gastroenterol. Aug 14, 2010; 16(30): 3847-3852
Published online Aug 14, 2010. doi: 10.3748/wjg.v16.i30.3847
Germline mutation analysis of hPMS2 gene in Chinese families with hereditary nonpolyposis colorectal cancer
Xia Sheng, Heng-Hua Zhou, Xiao-Yan Zhou, Xiang Du, Tai-Ming Zhang, San-Jun Cai, Wei-Qi Sheng, Da-Ren Shi
Xia Sheng, Xiao-Yan Zhou, Xiang Du, Tai-Ming Zhang, Wei-Qi Sheng, Da-Ren Shi, Department of Pathology, Shanghai Cancer Center, Fudan University, Shanghai 200032, China; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China
Heng-Hua Zhou, Department of Pathology, Shanghai Ninth People’s Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China
San-Jun Cai, Department of Abdominal Surgery, Cancer Center, Fudan University, Shanghai 200032, China
Author contributions: Sheng X and Zhou HH contributed equally to this work, participated in the treatment of patients, analyzed the data, performed the research and wrote the manuscript; Zhou XY, Du X, Sheng WQ and Shi DR participated in the treatment of patients, collected the data and designed the research; Cai SJ participated in the treatment of patients, collected the data; Zhang TM contributed to the new reagents/analytic tools.
Supported by The Initiation Fund for Prominent Young Researchers of Shanghai Medical College, Fudan University
Correspondence to: Wei-Qi Sheng, MD, PhD, Associate Professor, Department of Pathology, Shanghai Cancer Center, Fudan University, 270 Dong An Road, Shanghai 200032, China. shengweiqi2006@yahoo.com.cn
Telephone: +86-21-64175590 Fax: +86-21-64046008
Received: March 25, 2010
Revised: May 21, 2010
Accepted: May 28, 2010
Published online: August 14, 2010
Abstract

AIM: To study the germline mutation of hPMS2 gene in 26 unrelated Chinese hereditary nonpolyposis colorectal cancer (HNPCC) probands and to fulfill the screening strategy for HNPCC in Chinese.

METHODS: Genomic DNA was extracted from the peripheral blood. To avoid the interference of pseudogene in detection of the remaining 11 exons (exon 1-5, 9, 11-15), long-range polymerase chain reaction (PCR) was conducted to amplify the complete coding region of hPMS2 gene firstly. Then 1/8 of the PCR products were used as template to amplify the individual exon respectively and DNA sequencing was done. Direct DNA sequencing of the conventional PCR products of exon 6, 7, 8 and 10 of hPMS2 gene was performed. The same analysis was made in 130 healthy persons without family histories of HNPCC to further investigate the pathological effects of the detected missense mutation.

RESULTS: One HNPCC proband fulfilled Bethesda guidelines and was found to carry the germline mutation of hPMS2 gene, which has not been reported in Chinese HNPCC families. It was a missense mutation at c.1532C>T of exon 11. It was detected in three controls as well with an occurrence rate of 2.3% (3/130). Since it could not be found in the PMS2-single nucleotide polymorphism (SNP) database, this missense mutation is a new SNP unreported up to date. Meanwhile, 260 reported SNPs of hPMS2 gene were detected in the 26 HNPCC probands. The 2nd and 5th exons were probably the hot SNP regions of hPMS2 gene in Chinese HNPCC families involving 53.1% of all reported SNP.

CONCLUSION: The germline mutation of hPMS2 gene may be rare in Chinese HNPCC families. The 2nd and 5th exons are hot SNP regions of hPMS2 gene.

Keywords: Hereditary nonpolyposis colorectal cancer; hPMS2; Missense mutation; Single nucleotide polymorphism; Colorectal cancer