Although numerous allelic chromosome losses have been reported in hepatocellular carcinomas (HCC), ations of a limited number of specific genes, the sochromosome analysis by cytogenetic methods has rarely called oncogenes and tumor suppressor genes. 1,2 Some been performed in these tumors, unlike in other solid of these alterations have been shown to be related to malignant tumors. The purpose of the current study was chromosomal changes because specific chromosomal to analyze primary liver tumors by conventional cytogeabnormalities have been demonstrated by cytogenetic netic methods and by a new molecular cytogenetic techstudies of cancer cells. 3 For instance, more than 100 nique, called fluorescent in situ hybridization (FISH), a recurrent chromosomal translocations have been detechnique that has been recently proposed to count the scribed in approximately 14,000 cases of different manumber of chromosome copies in interphase nuclei with lignant neoplasms. 4 The cytogenetic study of chromochromosome centromeric probes. Primary cultures of somal changes and the possible consequences on tumoral cells were prepared to obtain metaphases. Specellular function are therefore important for a more cific chromosomes probes 7, 17, and 20 were used to percomplete understanding of carcinogenesis.
form in situ hybridization on isolated intact tumoral cells. Seven cases of primary liver tumors (six cases of Hepatocellular carcinoma (HCC) is one of the most HCC and one case of benign focal hepatic nodular hypercommon cancers worldwide. Epidemiological studies plasia) were investigated. A few metaphases were obhave shown frequent associations between HCC and tained in five of the seven tumors, and in most cases chronic hepatitis B or C virus infections, alcohol abuse, numerical abnormalities were difficult to interpret. In or hemochromatosis. [5][6][7] The oncogenic effects of these contrast with in situ hybridization, all cases of HCC factors remain unclear despite numerous hypotheses showed losses and/or gains of chromosomes. Loss of one and extensive investigations. 6,8,9 Although numerous to three chromosomes occurred in five tumors. A gain chromosome allelic losses have been reported in of two chromosomes was observed in two of these five HCC, 10,11 specific regions have not been determined. tumors. In only one case, a gain of only three chromo-Moreover, very few primary HCCs have been studied somes occurred. In addition, a loss of chromosome 17 by conventional cytogenetic techniques, 12-14 and, as far was recorded for the benign tumor. These results demas we know, none have been studied by molecular cytoonstrate that FISH with specific probes can provide ingenetic techniques. formation on chromosome number in the tumoral cells of primary liver tumors even in the absence of analyz-A major advance in cytogenetics was the introduction able metaphases. This technique opens new possibilities of fluorescent in situ hybridization (FISH) with cloned for the investigation of chromosome abnormalities in DNA probes that can recognize chromosome-specific HCC. (HEPATOLOGY 1996;23:429-435.)
repeat sequences, such as a-satellite centromeric DNAs. An important advantage of this method is that the chromosome copy number can be determined in the interphase nuclei of solid tumors. This study analyzed Abbreviations: HCC, hepatocellular carcinoma; FISH, fluorescent in situ six cases of primary HCC and one case of focal hepatic hybridization; SSC, sodium saline citrate.