[Growth induction with short-term exposure to carcinogens]

The mechanisms responsible for the phenotypic tumor expression in initially carcinogen-altered cells are largely unknown. Because of functional similarities between restorative and tumorous growing tissues it seems possible that cell multiplication during carcinogenesis similar mechanisms may be involved like those in regenerative cell division. Among other factors, growth stimulators play an important role in regulation of regenerative cell growth due to tissue loss. For example, after partial hepatectomy various proliferation stimulating activities emerge in the blood serum. Their action is not restricted to liver cells, but it is also effective in some extrahepatic tissues including the adrenal cortex. Strikingly, also single oral doses of chemical carcinogens (independent of their organotropism) or chemical promoters cause a mitotic response in the outer region of the zona fasciculata 36 and 48 h after administration. In analogy to liver regeneration, we suppose the mitogenic adrenocortical action of these chemical compounds to be mediated also by endogenous growth factors. It is well known that in advanced stages of chemical carcinogenesis tumors can develop without further carcinogen treatment. From this point of view the question arises whether the so-called promoting action of chemical carcinogens is represented by endogenous growth stimulators.