Seglen P, Saeter G, Schwarze P
Int J Oncol. 1994 Oct;5(4):805-10. doi: 10.3892/ijo.5.4.805.
Treatment of rats with the carcinogen 2-acetylaminofluorene (2-AAF) during liver regeneration (Solt-Farber protocol) induced a selective outgrowth of diploid, gamma-glutamyltranspeptidase (GGT)-positive hepatocytes (3-4 times increase) as well as of nonparenchymal (oval) liver cells. After cessation of treatment the oval cells rapidly disappeared, while the population of diploid, GGT-positive hepatocytes declined more slowly over the subsequent ten weeks. In animals pretreated with the initiating carcinogen diethylnitrosamine (DEN) a large fraction of the diploid, GGT-positive hepatocytes persisted. The results differ from those obtained with our standard, sequential treatment protocol (2-AAF given after completed regeneration), where there is no hyperproliferation of oval cells and where GGT-positive hepatocytes are found only in DEN-pretreated animals (Saeter et al, Carcinogenesis 9: 581-587, 1988). Different experimental models of liver carcinogenesis may thus present different patterns of liver cell proliferation, which should be taken into account when general hypotheses on the cellular origin of liver cancer are proposed.
在肝脏再生过程中（索尔-法伯方案）用致癌物2-乙酰氨基芴（2-AAF）处理大鼠，会诱导二倍体、γ-谷氨酰转肽酶（GGT）阳性肝细胞选择性增殖（增加3至4倍）以及非实质（卵圆）肝细胞增殖。停止处理后，卵圆细胞迅速消失，而二倍体、GGT阳性肝细胞群体在随后十周内下降得较为缓慢。在用起始致癌物二乙基亚硝胺（DEN）预处理的动物中，大部分二倍体、GGT阳性肝细胞持续存在。这些结果与我们的标准序贯处理方案（再生完成后给予2-AAF）所得到的结果不同，在标准方案中没有卵圆细胞的过度增殖，并且仅在DEN预处理的动物中发现GGT阳性肝细胞（塞特等人，《癌变》9: 581 - 587，1988年）。因此，不同的肝癌发生实验模型可能呈现不同的肝细胞增殖模式，在提出关于肝癌细胞起源的一般假说时应予以考虑。
