Prognostic significance of c‐myc and AIB1 amplification in hepatocellular carcinoma

Abstract

BACKGROUNDAmplifications of 1q21, c‐myc at 8q24.1, and AIB1 at 20q12 are genetic alterations that are detected frequently in hepatocellular carcinoma (HCC). The authors evaluated the association of these amplifications with the prognosis of patients with HCC.METHODSIn the current study, amplification of 1q21, c‐myc, and AIB1 was analyzed in 560 specimens from 400 patients with HCC and 20 patients with benign liver lesions using fluorescence in situ hybridization with high‐throughput tissue microarray. Differences of amplification patterns were compared between small and large HCC, single nodular and multiple nodular HCC, primary and metastatic HCC, and primary and recurrent HCC.RESULTSSignificant differences between single nodular and multiple nodular HCC were detected in c‐myc amplification (12% vs. 38%; P < 0.01) and AIB1 amplification (16% vs. 30%; P < 0.05). More frequent c‐myc amplification was detected in metastatic HCC (45%) compared with primary HCC (29%) and in recurrent HCC (60%) compared with primary HCC (38%). Similarly, more frequent AIB1 amplification was observed in metastatic HCC (41%) compared with primary HCC (23%) and in recurrent HCC (60%) compared with primary HCC (29%). However, no significant differences in 1q21 amplification were observed.CONCLUSIONSThe current results strongly suggest that amplifications of the c‐myc and AIB1 oncogenes are late genetic alterations in the progression of HCC and are correlated with a poor prognosis. Cancer 2002;95:2346–52. © 2002 American Cancer Society.DOI 10.1002/cncr.10963

Ulcerative Colitis and Colorectal Cancer: Aneuploidy and Implications for Improved Screening

“…Thus, it is reasonable to suggest that the genomic instability reflected by aneuploidy has to be followed by multiple cellular alterations in order to reach malignant properties. One of the decisive steps in this transformational process is the ability of genomically altered cells to proliferate, which is compulsory for clonal expansion (Wang et al 2002). In the present study, six out of eight UCC specimens exhibited an increased cyclin A expression pattern.…”

Genomic instability and oncogene amplifications in colorectal adenomas predict recurrence and synchronous carcinoma

“…26 It has also been described to be amplified in endometrial, stomach, prostate, pancreatic, and hepatocellular carcinomas. [27][28][29] NCOA3 is as transcription coactivator involved in cell proliferation, migration, differentiation, and growth. 30 Henke et al 31 could show that NCOA3 amplification seems to be an early event during pancreatic cancer development.…”

Analysis of DNA copy number aberrations in hepatitis C virus-associated hepatocellular carcinomas by conventional CGH and array CGH

“…Amplification of MYC has been observed frequently in large HCC nodules, suggesting that it is a late genetic alteration in the progression of HCC. 24 The PTK2 gene has also been identified as a target for the amplification event at 8q23-24, and elevated expression of PTK2 is associated with a large tumor size in HCC. 25 Our data revealed that four genes were correlated with poor differentiation of HCV-HCC.…”