Molecular pathogenesis of human hepatocellular carcinoma View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2002-08

AUTHORS

Snorri S. Thorgeirsson, Joe W. Grisham

ABSTRACT

Hepatocarcinogenesis is a slow process during which genomic changes progressively alter the hepatocellular phenotype to produce cellular intermediates that evolve into hepatocellular carcinoma. During the long preneoplastic stage, in which the liver is often the site of chronic hepatitis, cirrhosis, or both, hepatocyte cycling is accelerated by upregulation of mitogenic pathways, in part through epigenetic mechanisms. This leads to the production of monoclonal populations of aberrant and dysplastic hepatocytes that have telomere erosion and telomerase re-expression, sometimes microsatellite instability, and occasionally structural aberrations in genes and chromosomes. Development of dysplastic hepatocytes in foci and nodules and emergence of hepatocellular carcinoma are associated with the accumulation of irreversible structural alterations in genes and chromosomes, but the genomic basis of the malignant phenotype is heterogeneous. The malignant hepatocyte phenotype may be produced by the disruption of a number of genes that function in different regulatory pathways, producing several molecular variants of hepatocellular carcinoma. New strategies should enable these variants to be characterized. More... »

PAGES

339-346

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/ng0802-339

    DOI

    http://dx.doi.org/10.1038/ng0802-339

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1017140614

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/12149612


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