Brief Reports
Copyright ©2005 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Jan 14, 2005; 11(2): 285-288
Published online Jan 14, 2005. doi: 10.3748/wjg.v11.i2.285
Loss of heterozygosity on 10q23.3 and mutation of tumor suppressor gene PTEN in gastric cancer and precancerous lesions
Yi-Ling Li, Zhong Tian, Dong-Ying Wu, Bao-Yu Fu, Yan Xin
Yi-Ling Li, Bao-Yu Fu, Department of Gastroenterology, First Hospital of China Medical University, Shenyang 110001, Liaoning Province, China
Zhong Tian, Department of Surgery, Second Hospital of China Medical University, Shenyang 110003, Liaoning Province, China
Dong-Ying Wu, Yan Xin, The Fourth Laboratory, Cancer Institute, First Hospital of China Medical University, Shenyang 110001, Liaoning Province, China
Author contributions: All authors contributed equally to the work.
Supported by the National Natural Science Foundation of China, No. 30070845
Correspondence to: Professor Yan Xin, The Fourth Laboratory, Cancer Institute, First Hospital of China Medical University, Shenyang 110001, Liaoning Province, China. yxin@mail.cmu.edu.cn
Telephone: +86-24-23256666 Ext. 6351 Fax: +86-24-23253443
Received: April 7, 2004
Revised: April 8, 2004
Accepted: May 24, 2004
Published online: January 14, 2005
Abstract

AIM: To investigate the loss of heterozygosity (LOH) and mutation of tumor suppressor gene PTEN in gastric cancer and precancerous lesions.

METHODS: Thirty cases of normal gastric mucosa, advanced and early stage gastric cancer, intestinal metaplasia, atrophic gastritis, and atypical hyperplasia were analyzed for PTEN LOH and mutations within the entire coding region of PTEN gene by PCR-SSCP denaturing PAGE gel electrophoresis, and PTEN mutation was detected by PCR-SSCP sequencing followed by silver staining.

RESULTS: LOH rate found in respectively atrophic gastritis was 10% (3/30), intestinal metaplasia 10% (3/30), atypical hyperplasia 13.3% (4/30), early stage gastric cancer 20% (6/30), and advanced stage gastric cancer 33.3% (9/30), None of the precancerous lesions and early stage gastric cancer showed PTEN mutations, but 10% (3/30) of the advanced stage gastric cancers, which were all positive for LOH, showed PTEN mutation.

CONCLUSION: LOH of PTEN gene appears in precancerous lesions, and PTEN mutations are restricted to advanced gastric cancer, LOH and mutation of PTEN gene are closely related to the infiltration and metastasis of gastric cancer.

Keywords: Gastric cancer, Precancerous lesions, PTEN gene, Loss of heterozygosity, Mutation