Basic Research
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Dec 15, 2004; 10(24): 3597-3601
Published online Dec 15, 2004. doi: 10.3748/wjg.v10.i24.3597
Genetic alterations and reduced expression of tumor suppressor p33ING1b in human exocrine pancreatic carcinoma
Guan-Zhen Yu, Ming-Hua Zhu, Zhi Zhu, Can-Rong Ni, Jian-Ming Zheng, Fang-Mei Li
Guan-Zhen Yu, Ming-Hua Zhu, Zhi Zhu, Can-Rong Ni, Jian-Ming Zheng, Fang-Mei Li, Department of Pathology, Changhai Hospital, Second Military Medical University, Shanghai 200433, China
Author contributions: All authors contributed equally to the work.
Supported by the “258” Project Foundation of Changhai Hospital, Shanghai, China
Correspondence to: Ming-Hua Zhu, Department of Pathology, Changhai Hospital, Second Military Medical University, Shanghai 200433, China. mhzhu2000@hotmail.com
Telephone: +86-21-25074604 Fax: +86-21-25074604
Received: January 16, 2004
Revised: February 17, 2004
Accepted: February 24, 2004
Published online: December 15, 2004
Abstract

AIM: To detect the expression of p33ING1b protein and the change of p33ING1b gene in pancreatic carcinoma and to evaluate the significance of p33ING1b in pancreatic cell carcinogenesis.

METHODS: Pathological specimens from pancreatic carcinoma and matched non-tumor pancreatic tissues were examined for p33ING1b expression and mutation by immunohistochemistry, polymerase chain reaction single-strand conformation polymorphisms (PCR-SSCP) and loss of heterozygosity (LOH).

RESULTS: The rate of p33ING1b protein expression was 85% (34/40). A single germline missense mutation was detected in 1 of 40 tumors located at codon 215: TGC-TCC (Cys-Ser). Fourteen (60.9%) of 23 tumor samples showed LOH in all of the informative markers tested, but no mutation was detected in these tumors and only two of the informative tumors lacked expressions of p33ING1b protein.

CONCLUSION: Mutation and loss of expression are not the main reasons for the disfunction of p33ING1b in pancreatic carcinoma, an abnormality at the level of chromosome and/or transcription may inhibit their normal functions, potentially contributing to pancreatic cell carcinogenesis.

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