The poor prognosis of hepatocellular carcinoma (HCC) has been associated with recurrence and metastasis. Recently, we established a pair of HCC cell lines from a primary (H2-P) and its matched metastatic (H2-M) HCC tumors. A high density of cDNA microarray with 9184 human cDNA was used to identify the differentially expressed genes between H2-P and H2-M. Comparing with H2-P, eight upregulated and six downregulated genes were detected in H2-M. One interesting finding is the overexpression of Vimentin (VIM), a well-defined intermediate filament, which has been linked to a more aggressive status in various tumors. The correlation of overexpression of VIM and HCC metastasis was studied by immunohistochemistry using a tissue microarray with 200 primary HCCs and 60 pairs of primary and matched metastatic HCC samples. Tissue microarray demonstrated that the overexpression of VIM was significantly associated with HCC metastasis (Po0.01). This finding strongly suggests that the overexpression of VIM may play an important role in the metastasis of HCC.

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

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