肝细胞癌和胆管癌干细胞起源的证据。

Sell S, Dunsford H A

University of Texas Health Science Center, Department of Pathology and Laboratory Medicine, Houston 77225.

Am J Pathol. 1989 Jun;134(6):1347-63.

A review of the morphologic, autoradiographic, and phenotypic analysis of the cellular changes seen during induction of cancer of the liver in rats by chemical carcinogens is used to develop an alternative to the established hypothesis that chemically induced hepatocellular carcinoma arises from premalignant nodules. The authors propose that hepatocellular and ductular carcinomas arise from a pluripotent liver stem cell and that enzyme-altered foci and nodular changes are adaptive non-oncogenic responses to the toxic effects of carcinogens. It is further postulated that persistent nodules may provide an environment that nurtures development of neoplastic cells other than the altered hepatocytes that originally form the nodule. It is possible, however, that there may be more than one cellular lineage to hepatocellular cancer and that persistent nodules contain these different lineages.

通过化学致癌物诱导大鼠肝癌过程中细胞变化的形态学、放射自显影和表型分析综述，旨在为已确立的化学诱导肝细胞癌起源于癌前结节的假说提供一种替代观点。作者提出，肝细胞癌和胆管癌起源于多能肝干细胞，酶改变灶和结节性变化是对致癌物毒性作用的适应性非致癌反应。进一步推测，持续性结节可能提供一种环境，促进除最初形成结节的改变肝细胞之外的肿瘤细胞的发育。然而，肝细胞癌可能存在不止一种细胞谱系，持续性结节可能包含这些不同的谱系。