Lombardi B, Chandar N, Locker J
Department of Pathology, School of Medicine, University of Pittsburgh, Pennsylvania 15261.
Dig Dis Sci. 1991 Jul;36(7):979-84. doi: 10.1007/BF01297151.
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.
仅采用缺乏胆碱的饮食喂养的大鼠会患上肝细胞癌，其发病机制似乎完全在于饮食对肝脏的影响。在这些影响中，最突出的是诱导肝细胞损伤、死亡和再生的反复循环。最近文献中还描述了另外两种模型，在这两种模型中，经过长时间的肝细胞损伤、死亡和再生后会发生肝脏肿瘤性病变，而动物并未接触化学致癌物。有人认为，在这些肝癌发生模型中，细胞更新异常增加可能导致肝细胞启动、促进和肿瘤转化所需的所有基因组改变。还简要讨论了在相同模型中内源性启动的肝细胞可能参与其中的情况。
