ABSTRACT
A consensus of experimental and clinical data suggests that carcinogenesis is a multistep process. Several theories of carcinogenesis propose that one necessary step in the development of cancer is the inactivation of cellular anticancer mechanisms. The term anticancer activity includes any process that prevents or reverses the transformed phenotype, including activities previously designated anti-oncogenesis, tumor/cancer suppression, recessive oncogenesis, and other similar terms. Suppression of the transformed phenotype by fusing nontumorigenic cells with tumorigenic cells has been reported by numerous investigators and this topic has been covered extensively in the last few years. A great deal of evidence suggests that the hereditary predisposition to cancer is due to the inactivation, via mutations, and deletions of anticancer mechanisms. This evidence comes from the study of inherited cancers in many species including Drosophila and man. The classical experiments demonstrating the induction of anticancer activity by extracellular factors involve the placement of teratocarcinoma or embryonal carcinoma cells into the blastocyst of mice.
