作者: Maria Raidl , Christine Pirker , Rolf Schulte-Hermann , Michaela Aubele , Daniela Kandioler-Eckersberger
DOI: 10.1016/J.JHEP.2003.12.020
关键词: DNA 、 Hepatocellular carcinoma 、 HCCS 、 Chromosome 、 Pathology 、 Hepatocellular adenoma 、 Focal nodular hyperplasia 、 Biology 、 Lung 、 Nodule (medicine)
摘要: Abstract Background/Aims In human hepatocarcinogenesis the tumor precursor lesions and sequence of genetic aberrations are not known. We therefore compared alterations different types benign liver to those hepatocellular carcinoma. Methods By comparative genomic hybridisation (CGH) 40 cases, including cirrhotic (CL), focal nodular hyperplasia (FNHs), adenoma (HCAs), dysplastic nodules (DNs), primary carcinoma (HCCs), metastases lung were studied. Results FNHs HCAs exhibited few chromosomal abnormalities. Frequency pattern in DNs highly resembled HCCs: gains DNA clustered chromosome arms 1p/q, 7q, 15q, 16p, 17q, 20q losses often found at 3p, 4q, 9p, 11q. Aberrations on 1p, 6q, 8p/q, 13q occurred almost exclusively HCCs; gain 8q encompassed amplification c-myc, as verified by fluorescence situ hybridisation. Conclusions The HCCs more than HCAs, suggesting that may be actual precursors. Furthermore, 11q, 17q appear early events being crucial for hepatocarcinogenesis.