机构地区:[1]Department of Surgery, University of Ulsan College of Medicine, Biomedical Research Center, Ulsan University Hospital, Ulsan 682-714, South Korea [2]Internal Medicine, University of Ulsan College of Medicine, Biomedical Research Center, Ulsan University Hospital, Ulsan 682-714, South Korea
出 处:《World Journal of Gastroenterology》2008年第22期3526-3533,共8页世界胃肠病学杂志(英文版)
基 金:The Korea Research Foundation Grant funded by the Korean Government (MOEHRD, Basic Research Promotion Fund), KRF-2007-412-J00303;Ulsan University Hospital Biomedical Research Center Promotion Fund (UUH-2007-05)
摘 要: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.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.
关 键 词:Fragile histidine triad Aberrant transcripts Microsatellite instability Protein expression Hepatocellular carcinoma
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