Abstract
Rats fed a choline-devoid diet as the sole treatment develop hepatocellular carcinomas, the pathogenesis of which appears to reside exclusively in effects of the diet on the liver. Among the latter, most prominent is the induction of repeating cycles of liver cell injury, death, and regeneration. Two other models have been described recently in the literature, in which development of hepatic neoplastic lesions occurs after protracted periods of liver cell injury, death, and regeneration, without exposure of the animals to chemical carcinogens. The possibility is considered that an abnormal increase in cell turnover may result in all of the genomic alterations that are required for initiation, promotion, and neoplastic transformation of liver cells in these models of hepatocarcinogenesis. The possible involvement, in the same models, of endogenously initiated liver cells also is discussed briefly.
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Research supported by National Cancer Institute grant CA 23449 and American Cancer Society grant BC 471 to B.L., and National Cancer Institute grant CA 43909 to J.L.
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Lombardi, B., Chandar, N. & Locker, J. Nutritional model of hepatocarcinogenesis. Digest Dis Sci 36, 979–984 (1991). https://doi.org/10.1007/BF01297151
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DOI: https://doi.org/10.1007/BF01297151