Adventures in hepatocarcinogenesis.
Neoplasia is a heritably altered, relatively autonomous growth of tissue. Hepatocarcinogenesis, the pathogenesis of neoplasia in liver, as modeled in the rat exhibits three distinct, quantifiable stages: initiation, promotion, and progression. Simple mutations and/or epigenetic alterations may result in the irreversible stage of initiation. The stage of promotion results from selective enhancement of cell replication and selective inhibition of cellular apoptosis of initiated cells dependent on the genetic and/or epigenetic alterations of the latter. The irreversible stage of progression results from initial karyotypic alterations that evolve into greater degrees of genomic instability. The initial genomic alteration in the transition from promotion to progression may involve primarily epigenetic mechanisms driven by epigenetic and genetic alterations fixed during the stage of promotion.
Pitot
Henry C
HC
McArdle Laboratory for Cancer Research, Department of Oncology and Pathology, University of Wisconsin-Madison, Madison, Wisconsin 53706, USA. pitot@oncology.wisc.edu
D000818:Animals; D002273:Carcinogens; D019175:DNA Methylation; D018450:Disease Progression; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007621:Karyotyping; D008113:Liver Neoplasms / Q000209:etiology / Q000473:pathology*; D008114:Liver Neoplasms, Experimental / Q000209:etiology / Q000473:pathology*; D009385:Neoplastic Processes; D011230:Precancerous Conditions
D002273:Carcinogens