Rapid Communication
Copyright ©2007 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Feb 21, 2007; 13(7): 1090-1097
Published online Feb 21, 2007. doi: 10.3748/wjg.v13.i7.1090
Frequent loss of heterozygosity in two distinct regions, 8p23.1 and 8p22, in hepatocellular carcinoma
Tomoe Lu, Hiroshi Hano, Chenxi Meng, Keisuke Nagatsuma, Satoru Chiba, Masahiro Ikegami
Tomoe Lu, Hiroshi Hano, Chenxi Meng, Keisuke Nagatsuma, Satoru Chiba, Masahiro Ikegami, Department of Pathology, Jikei University School of Medicine, Tokyo, Japan
Author contributions: All authors contributed equally to the work.
Supported by The Jikei University Research Fund
Correspondence to: Tomoe Lu, MD, PhD, Department of Pathology, The Jikei University School of Medicine, 3-25-8 Nishishinbashi, Minato-ku, Tokyo 105-8461, Japan. luwei@jikei.ac.jp
Telephone: +81-3-34331111-231 Fax: +81-3-54720700
Received: November 25, 2006
Revised: December 16, 2006
Accepted: January 18, 2007
Published online: February 21, 2007
Abstract

AIM: To identify the precise location of putative tumor suppressor genes (TSGs) on the short arm of chromosome 8 in patients with hepatocellular carcinoma (HCC).

METHODS: We used 16 microsatellite markers informative in Japanese patients, which were selected from 61 published markers, on 8p, to analyze the frequency of loss of heterozygosity (LOH) in each region in 33 cases (56 lesions) of HCC.

RESULTS: The frequency of LOH at 8p23.2-21 with at least one marker was 63% (20/32) in the informative cases. More specifically, the frequency of LOH at 8p23.2, 8p23.1, 8p22, and 8p21 was 6%, 52%, 47%, and 13% in HCC cases. The LOH was significantly more frequent at 8p23.1 and 8p22 than the average (52% vs 22%, P = 0.0008; and 47% vs 22%, P = 0.004, respectively) or others sites, such as 8p23.2 (52% vs 6%, P = 0.003; 47% vs 22%, P = 0.004) and 8p21 (52% vs 13%, P = 0.001; 47% vs 13%, P = 0.005) in liver cancer on the basis of cases. Notably, LOH frequency was significantly higher at D8S277, D8S503, D8S1130, D8S552, D8S254 and D8S258 than at the other sites. However, no allelic loss was detected at any marker on 8p in the lesions of nontumor liver tissues.

CONCLUSION: Deletion of 8p, especially the loss of 8p23.1-22, is an important event in the initiation or promotion of HCC. Our results should be useful in identifying critical genes that might lie at 8p23.1-22.

Keywords: Loss of heterozygosity, Chromosome, Hepatocarcinogenesis, Hepatocellular carcinoma, 8p