Cytogenetic alterations in liver cell tumors as detected by comparative genomic hybridization.

Hepatocellular carcinoma (HCC) is one of the most frequent neoplasia worldwide. Environmental risk factors as hepatitis B virus (HBV) and hepatitis C virus (HCV) play a critical role in liver carcinogenesis. Liver carcinogenesis is probably a multistep process involving several genes, but morphological and molecular features of premalignant and malignant hepatic lesions are yet far from being fully elucidated. This study summarizes chromosomal imbalances of a wide variety of precancerous and cancerous lesions of the liver as detected by Comparative Genomic Hybridization (CGH). Preneoplastic nodules, classified as macroregenerative nodules (MRN), low-grade dysplastic nodules (LG-DN) and high-grade dysplastic nodules (HG-DN), showed only few aberrations (mean 1.1/case), without any significant pattern. This finding is comparable to what happens in non-neoplastic tissue. On the contrary, in three of six HG-DN we found deletions of 8p and gains of 1q. LG-DN and MRN never showed these chromosomal imbalances. Furthermore some chromosomal changes appeared to be quite characteristic for some of the investigated tumor entities: HCC. 8p- might be relatively specific for HCC (44% with 8p) since it was hardly found in fibrolamellar carcinoma (FLC) or hepatoblastoma (HB). The same applies for 17q+ which was much more frequent in HCC (41%) than in FLC (0 of 5) or HB (9%). FLC. There were 4 alterations that were more frequent in FLC than in other tumor types. These changes included 4q+, 9p-, 16p- and Xq-. HB. Alterations that were typical for hepatoblastoma included Xp+ and Xq+, which were found both in the mesenchymal and in the epithelial parts of HBs. Other frequent changes in these tumor types included 1p-, 9p- and 2q+.