ABSTRACT
Multistage carcinogenesis in mouse skin can be considered to comprise initiation, promotion, and conversion events, and the relative ineffectiveness of Tetradecanoylphorbolacetate (TPA) in the conversion of papillomas to carcinomas is probably the result of its inactivity as a mutagen. This chapter discusses "TPAology" with only limited reference to the equally potent but structurally unrelated tumor promoter’s teleocidin B and dihydroteleocidin B. However, two-stage carcinogenesis has been demonstrated in systems other than mouse skin and has been shown to involve promoting agents other than the phorbol esters. The application of the initiation-promotion model to carcinogenesis should relate the biochemical effects of initiators and promoters to a biological end point. The role of inflammation and cellular proliferation in both carcinogenesis and tumor promotion has been studied extensively. Cytogenetic events have always been considered important in an overall view of carcinogenesis and would seem to have relevance to the later stages, i.e., promotion.
