Molecular changes in hepatocellular dysplastic nodules on microdissected liver biopsies

Marco Maggioni, Guido Coggi, Barbara Cassani, Paolo Bianchi, Solange Romagnoli, Alessandra Mandelli, Mauro Borzio, Piergiuseppe Colombo, Massimo Roncalli

Research output: Contribution to journalArticlepeer-review


The genetic profile of dysplastic hepatocellular nodules arising in cirrhosis is poorly understood. We assessed loss of heterozygosity (LOH) and microsatellite instability (MI) in 10 dysplastic nodules (4 low-grade and 6 high-grade) with surrounding cirrhosis and in 10 hepatocellular carcinomas (HCC). Six microsatellite loci were selected and investigated on microdissected needle biopsies. Twenty-four (24.4%) informative loci showed allelic loss, while MI was seen in 3 loci only (3%). The most involved sites were located on chromosomes 4q (54.5%) and 8p (50%). LOH was documented in 16.6%, cirrhotic, 50% low-grade dysplastic nodules (LGDN), 83% high-grade dysplastic nodules (HGDN), and 70% malignant nodules. LOH at multiple loci was increasingly seen from cirrhotic to HGDN, but not from the latter to HCC. The fractional allelic loss (FAL) was significantly increased in dysplastic and neoplastic nodules as compared with cirrhosis (P <.01). The progressive accumulation of genetic changes in cirrhotic, dysplastic, and malignant hepatocellular nodules is in keeping with a multistep process of carcinogenesis; within this spectrum, HGDN can be considered advanced precursors of HCC.

Original languageEnglish
Pages (from-to)942-946
Number of pages5
Issue number5
Publication statusPublished - 2000

ASJC Scopus subject areas

  • Hepatology


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