Wu GJ, Shan XN, Li MF, Shi SL, Zheng QP, Yu L, Zhao SY. Preliminary study on the loss of heterozygosity at 17p13 in gastric and colorectal cancers. World J Gastroenterol 1997; 3(3): 160-162 [PMID: 27239133 DOI: 10.3748/wjg.v3.i3.160]
Corresponding Author of This Article
Dr. Guo-Jun Wu, Institute of Genetics, Fudan University, Shanghai 200433, China
Article-Type of This Article
Original Research
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This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Guo-Jun Wu, Shao-Lin Shi, Qi-Ping Zheng, Long Yu, Shou-Yuan Zhao, Institute of Genetics, Fudan University, Shanghai 200433, China
Xiang-Nian Shan, Ming-Fa Li, Biological Department of Nanjing Railway Medical College, Nanjing 210009, China
Author contributions: All authors contributed equally to the work.
Supported by the National Natural Science Foundation of China (No. 39480018), Natural Science Foundation of Jiangsu Province, No. BK93154315, and Outstanding Youth Teachers Foundation of Jiangsu Province, No. QZ91014.
Correspondence to: Dr. Guo-Jun Wu, Institute of Genetics, Fudan University, Shanghai 200433, China
Telephone: +86-21-65492222-4107
Received: November 2, 1996 Revised: January 25, 1997 Accepted: February 22, 1997 Published online: September 15, 1997
Abstract
AIM: To evaluate the role of p53 in the development and progression of colorectal cancer and gastric carcinoma by analyzing the loss of heterozygosity (LOH) at 17p13.1 and 17p13.3.
METHODS: LOH at the p53 gene locus and 17p13.3 were examined in 22 cases of gastric carcinoma and 14 cases of colorectal cancer by Southern blot analysis.
RESULTS: Of the 22 gastrocarcinoma cases, 12 (54%) were heterozygous and LOH was detected in 6 (50%) of the 12 informative cases. In the 14 colorectal cancer cases, 10 (71%) were heterozygous, and LOH was detected in 6 (60%) of the 10 informative cases.
CONCLUSION: LOH at the p53 gene locus is a frequent event in multiple step carcinogenesis progression. The high frequency of LOH at 17p13.3 suggests that there may be another tumor suppresser gene in that chromosome region.
