The C3H/10T1/2 cell system has been widely used as a quantitative assay for neoplastic transformation. Following exposure to chemical or physical carcinogens, there is a dose-dependent induction of neoplastic transformation in a small percentage of surviving cells. The ability of carcinogen-initiated cells to undergo transformation is highly dependent upon the effects of cell population density and is also inhibited by cancer chemo-preventive retinoids. It is proposed that these observations are functionally related. Inhibition of transformation by retinoids correlates strongly with their ability to up-regulate intercellular gap junctional communication in normal and carcinogen-initiated cells while inhibition due to density effects correlates with the proximity of initiated cells to normal cells. It is hypothesized that junctional communication allows the transfer of signal molecules which suppress neoplastic transformation.

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