Activation of endogenous type‐C viral p30 antigen in chemically‐induced rat hepatocellular carcinomas

Abstract

Chemically induced rat hepatocellular carcinomas were prospectively examined for expression of the major group-specific antigen (p 30) of genetically transmitted rat type-C viruses. Ten primary tumors induced following oral administration of the carcinogen N-2-acetylaminofluorine did not express elevated levels of viral antigen as compared to antigen levels detected in normal liver tissue. By contrast, rapidly growing transplantable hepatocellular carcinomas (THCs) derived from primary tumor expressed increased quantities of viral antigen. The expression of antigen was marginally elevated after only one transplanation, increased to maximal levels after several transplant generations and, once achieved, was stably maintained throughout subsequent transplants. Studies with additional previously established THCs showed that poorly differentiated, rapidly proliferating tumors tended to express elevated levels of viral antigen, while more differentiated, slowly growing tumors did not. The results show that the expression of endogenous type-C viral 30 antigen is a stable phenotypic property of many rat THC lines.