title: [Quantitative detection of HER-2 oncogene amplification in primary hepatocellular carcinoma using dual FISH technique and its clinical significance].
abstract: To investigate the frequency of HER-2 oncogene amplification in primary hepatocellular carcinoma (HCCs) and its relationships with clinicopathological parameters and prognosis, 42 surgical samples from patients with primary HCCs were detected for their HER-2 oncogene amplification by dual FISH technique, and then the correlations between HER-2 amplification and clinicopathological characteristics and prognosis were analyzed statistically. HER-2 oncogene amplification was detected in 9 of 42 (21.4%) primary HCCs, including 4 (9.5%) cases with high copy (HC) and 5 (11.9%) ones with low copy (LC). HER-2 amplification was associated significantly with postoperative survival time of HCC patients examined (P = 0.046) and the presence of HER-2 gene amplification showed a trend toward a correlation with tumor size (P = 0.085), but wasn't relative to sex, age, AFP level, HBV infection, postoperative relapse and clinical staging of HCC patients tested (P > 0.05). On the other hand, gain of the HER-2 oncogene copy was examined in 31 of 42(73.8%) primary HCCs, consisting of 9 (21.4%) cases with HER-2 amplification and 22(52.4%) ones with aneusomy 17/polysomy 17. There weren't significant relationships between gain of HER-2 oncogene copy and, HCC patient's sex, tumor size, clinical staging, postoperative relapse and survival time (P > 0.05), but gain of HER-2 oncogene copy correlated significantly to patients' age, AFP level and HBV infection (P < 0.05). The study indicated that there were a lower frequency of HER-2 oncogene amplification and a higher frequency of aneusomy 17/polysomy 17 in primary HCCs and that HER-2 oncogene amplification activation might be involved in the development and progression of a subset of HCCs, and seemed to be a valuably independent prognosis factor predicting postoperative poorer survival for patients with HCC.
authors.affiliation: Department of Etiology, Cancer Institute, Sun Yat-sen University of Medical Sciences, Guangzhou 510060, China.
authors.forename: B J
authors.initials: BJ
authors.lastname: Huang
authors.forename: T J
authors.initials: TJ
authors.lastname: Huang
authors.forename: Q W
authors.initials: QW
authors.lastname: Liang
authors.forename: C W
authors.initials: CW
authors.lastname: Huang
authors.forename: Y
authors.initials: Y
authors.lastname: Fang
mesh_terms: D000328:Adult; D000368:Aged; D006528:Carcinoma, Hepatocellular / Q000235:genetics*; D005260:Female; D005784:Gene Amplification; D018734:Genes, erbB-2; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D008113:Liver Neoplasms / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D011379:Prognosis