Rapid Communication
Copyright ©2008 The WJG Press and Baishideng. All rights reserved.
World J Gastroenterol. Jun 14, 2008; 14(22): 3526-3533
Published online Jun 14, 2008. doi: 10.3748/wjg.14.3526
Fragile histidine triad gene alterations are not essential for hepatocellular carcinoma development in South Korea
Chang Woo Nam, Jung Woo Shin, Neung Hwa Park
Chang Woo Nam, Department of Surgery, University of Ulsan College of Medicine, Biomedical Research Center, Ulsan University Hospital, Ulsan 682-714, South Korea
Jung Woo Shin, Neung Hwa Park, Internal Medicine, University of Ulsan College of Medicine, Biomedical Research Center, Ulsan University Hospital, Ulsan 682-714, South Korea
Author contributions: Park NH and Nam CW designed the research; Nam CW and Park NH performed the research; Shin JW and Park NH analyzed the data; and Nam CW and Park NH wrote the paper.
Correspondence to: Dr. Neung Hwa Park, Department of Internal Medicine, Ulsan University Hospital, 290-3 Jeonha-dong, Dong-gu, Ulsan 682-714, South Korea. nhpark@uuh.ulsan.kr
Telephone: +82-52-2508845
Fax: +82-52-2518235
Received: February 9, 2008
Revised: May 6, 2008
Accepted: May 13, 2008
Published online: June 14, 2008
Abstract

AIM: To establish the role of FHIT in the pathogenesis hepatocellular carcinoma (HCC).

METHODS: We examined genomic alterations, as well as, mRNA and protein expression patterns from the FHIT gene, in 48 surgically resected hepatocellular carcinoma (HCC) tissues. Additionally, p53 mutations were analyzed.

RESULTS: Aberrant FHIT transcripts were detected in 11 of 48 surrounding non-tumor liver tissues and 27 of 48 HCC samples (22.9% vs 56.3%, P = 0.002). No point mutations were identified within the open reading frame region of FHIT. Loss of heterozygosity (LOH) of the FHIT locus was detected in 4 of 42 informative cases for D3S1300, and 3 of 29 informative cases for D3S1313. Reduced expression of FHIT protein (Fhit) was observed in 8 (16.7%) of 48 HCC samples, with complete loss of Fhit in only 1 case. There were no associations with abnormal transcripts, LOH, and Fhit expression. p53 mutations were identified in 9 of the 48 HCC cases. However, none of the cases displayed a G to T transversion at p53 codon 249.

CONCLUSION: Aberrant FHIT transcripts were more common in HCC tissues as compared to non-cancerous liver tissues. However, Fhit expression was lost or reduced in a minor fraction of HCC tissues, while it was strongly expressed in non-cancerous liver tissues. Therefore, our study suggests that FHIT plays a role in relatively few HCC cases in South Korea.

Keywords: Fragile histidine triad; Aberrant transcripts; Microsatellite instability; Protein expression; Hepatocellular carcinoma