PMID- 15633221 OWN - NLM STAT- MEDLINE DCOM- 20050222 LR - 20190430 IS - 1007-9327 (Print) IS - 2219-2840 (Electronic) IS - 1007-9327 (Linking) VI - 11 IP - 2 DP - 2005 Jan 14 TI - Expression of fragile histidine triad in primary hepatocellular carcinoma and its relation with cell proliferation and apoptosis. PG - 228-31 AB - AIM: To evaluate the expression of fragile histidine triad (FHIT) gene protein, product of a candidate tumor suppressor, and to investigate the relationship between FHIT, cell apoptosis and proliferation, and pathological features of primary hepatocellular carcinoma (HCC). METHODS: Forty-seven HCC and ten normal liver specimens were collected during surgical operation between 2001 and 2003. FHIT and proliferating cell nuclear antigen (PCNA) expression were detected by immunohistochemistry, and apoptotic level was evaluated by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay on the tissue sections. RESULTS: All normal liver tissues showed a strong expression of FHIT, whereas 28 of 47 (59.6%) carcinomas showed a significant loss or absence of FHIT expression (P = 0.001). The proportion of reduced FHIT expression in those carcinomas at stages III-IV (70.6%) and in those with extrahepatic metastasis (86.7%) showed an increasing trend compared with those at stages I-II (30.8%, P = 0.013) and those without metastasis (46.9%, P = 0.010) respectively. Apoptotic incidence in advanced TNM stage carcinoma and those with positive FHIT expression was higher than that in early stage carcinoma (P = 0.030) and in those with negative FHIT expression (P = 0.044) respectively. The proliferating potential of hepatocellular carcinoma was associated with FHIT expression (P = 0.016) and the aggressive feature (P = 0.019). Kaplan-Meier analysis demonstrated that the survival time of these 47 patients correlated with TNM stage, FHIT expression and metastasis. CONCLUSION: There is marked loss or absence of FHIT expression, as well as abnormal apoptosis-proliferation balance in HCC. FHIT may play an important role in carcinogenesis and development of HCC. FAU - Nan, Ke-Jun AU - Nan KJ AD - Department of Oncology, First Hospital of Xi'an Jiaotong University, Xi'an 710061, Shaanxi Province, China. FAU - Ruan, Zhi-Ping AU - Ruan ZP FAU - Jing, Zhao AU - Jing Z FAU - Qin, Hai-Xia AU - Qin HX FAU - Wang, Hong-Yan AU - Wang HY FAU - Guo, Hui AU - Guo H FAU - Xu, Rui AU - Xu R LA - eng PT - Journal Article PL - United States TA - World J Gastroenterol JT - World journal of gastroenterology JID - 100883448 RN - 0 (Neoplasm Proteins) RN - 0 (fragile histidine triad protein) RN - 4QD397987E (Histidine) RN - EC 3.6.- (Acid Anhydride Hydrolases) SB - IM MH - Acid Anhydride Hydrolases/*genetics MH - Adult MH - Apoptosis/*genetics MH - Carcinoma, Hepatocellular/*genetics/*pathology MH - Cell Division/*genetics MH - Female MH - *Genes, Tumor Suppressor MH - Histidine/*genetics MH - Humans MH - Liver/physiology MH - Liver Neoplasms/*genetics/*pathology MH - Male MH - Middle Aged MH - Neoplasm Metastasis MH - Neoplasm Proteins/*genetics MH - Neoplasm Staging MH - Reference Values PMC - PMC4205407 EDAT- 2005/01/06 09:00 MHDA- 2005/02/23 09:00 PMCR- 2005/01/14 CRDT- 2005/01/06 09:00 PHST- 2005/01/06 09:00 [pubmed] PHST- 2005/02/23 09:00 [medline] PHST- 2005/01/06 09:00 [entrez] PHST- 2005/01/14 00:00 [pmc-release] AID - 10.3748/wjg.v11.i2.228 [doi] PST - ppublish SO - World J Gastroenterol. 2005 Jan 14;11(2):228-31. doi: 10.3748/wjg.v11.i2.228.