To discriminate among the chromosomal abnormalities associated with the eti
ology of hepatocellular carcinoma (HCC), we performed a comparative genomic
hybridization (CGH) analysis on 34 HCCs resected on noncirrhotic livers fr
om patients serologically negative for both hepatitis B (HBV) and C (HCV) v
iruses. The results mere compared to those of a previous analysis of 50 HCC
s selected on the basis of their positivity for HBV infection, The majority
of the abnormalities found in the HBV positive cases (losses of chromosome
arms 1p, 8p, 6q, 13q and 14q and gains of 1q, 8q, 6p and 17q) were similar
ly detected in the virus negative specimens. In contrast, a significant dec
rease (40% on average) was observed for losses at 4q, 16q and 17p in non-vi
ral HCC samples, suggesting that these abnormalities are tightly associated
with HBV infection. Thus, in addition to a common pathway towards malignan
cy, a subset of alterations may preferentially contribute to virus-induced
carcinogenesis. In a parallel CGH study of 10 fibrolamellar carcinomas, a r
are subtype of HCC, me found in sis out of the seven informative cases, gai
ns of chromosome arm Iq, This region, which is also preferentially amplifie
d in non fibrolamellar tumors (58%), may contain an essential proto-oncogen
e commonly implicated in liver carcinogenesis.