PMID- 12760798 OWN - NLM STAT- MEDLINE DCOM- 20041012 LR - 20160818 IS - 0529-5807 (Print) IS - 0529-5807 (Linking) VI - 32 IP - 1 DP - 2003 Feb TI - [Loss of p53 gene and amplification of HER-2 oncogene in primary hepatocellular carcinoma and their clinical significance]. PG - 20-4 AB - OBJECTIVE: To investigate the deletion of p53 gene and amplification of HER-2 oncogene at chromosome 17 in primary hepatocellular carcinoma (HCC) and the clinical significance. METHODS: Interphase dual fluorescence in situ hybridization (FISH) was applied to detect the ratio of the number of p53 gene copy or HER-2 oncogene copy to that of chromosome 17 copy, to determine the p53 gene deletion and HER-2 oncogene amplification in nuclei prepared from 42 surgical specimens of HCC. Statistical analysis for their clinical significance was performed. RESULTS: Loss of p53 gene and amplification of HER-2 oncogene were detected in 27 (64.3%) and 9 (21.4%) of the 42 HCC respectively including 4 cases with low and 5 with high copy amplification. Six (14.3%) of 42 HCC showed simultaneously p53 gene deletion and HER-2 oncogene amplification. 61.9% (26/42) of HCC were polysomy 17, which correlated positively with p53 gene deletion (chi(2) = 12.286, P < 0.001). No close correlation between p53 gene loss and HER-2 oncogene amplification was found (chi(2) = 0.00, P = 1.00). Loss of p53 gene was related to the serum alpha-fetoprotein (AFP) level and the tumor size (P < 0.05). The postoperative 2-year survival rate (18.5%) of HCC patients with p53 gene deletion was significantly lower than postoperative 2-year survival rate (60.0%) of those without p53 gene loss (chi(2) = 7.467, P = 0.006). Meanwhile, HER-2 oncogene amplification showed a tendency of correlation with the tumor size (chi(2) = 2.973, P = 0.085), and the postoperative 2-year survival rate (0/9) of HCC patients with HER-2 oncogene amplification was significantly lower than those (42.4%) without HER-2 oncogene amplification (chi(2) = 3.977, P = 0.046). CONCLUSION: There were a high frequency of p53 gene deletion and a low frequency of HER-2 oncogene amplification in primary HCC, which might be involved in initiation and development of a subset of primary HCC. FAU - Huang, Bi-jun AU - Huang BJ AD - Department of Etiology, Cancer Institute, Cancer Center, Sun Yat-sen University, Guangzhou 510060, China. FAU - Zhu, Zhen-yu AU - Zhu ZY FAU - Liang, Qi-wan AU - Liang QW FAU - Fang, Yan AU - Fang Y LA - chi PT - English Abstract PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - China TA - Zhonghua Bing Li Xue Za Zhi JT - Zhonghua bing li xue za zhi = Chinese journal of pathology JID - 0005331 RN - 0 (alpha-Fetoproteins) SB - IM MH - Adult MH - Carcinoma, Hepatocellular/*genetics/pathology MH - *Chromosomes, Human, Pair 17 MH - Female MH - Gene Amplification MH - Gene Deletion MH - *Genes, erbB-2 MH - *Genes, p53 MH - Humans MH - In Situ Hybridization, Fluorescence MH - Liver Neoplasms/*genetics/pathology MH - Male MH - Middle Aged MH - Polyploidy MH - Survival Rate MH - alpha-Fetoproteins/metabolism EDAT- 2003/05/23 05:00 MHDA- 2004/10/13 09:00 CRDT- 2003/05/23 05:00 PHST- 2003/05/23 05:00 [pubmed] PHST- 2004/10/13 09:00 [medline] PHST- 2003/05/23 05:00 [entrez] PST - ppublish SO - Zhonghua Bing Li Xue Za Zhi. 2003 Feb;32(1):20-4.