Modification of sister chromatid exchanges and radiation-induced transformation in mouse C3H/10T1/2 and Syrian hamster embryo cells by the tumor promoter 12-O-tetradecanoylphorbol-13-acetate and two retinoids, the trimethylmethoxy-phenyl analog of N-ethyl retinamide and β-all-trans-retinoic acid, has been studied. 12-O-tetradecanoylphorbol-13-acetate alone enhances, and retinoids alone reduce radiation-induced transformation. When both compounds were present, the retinoids not only reduced the oncogenic effects of radiation but completely eliminated the promoting effects of 12-O-tetrade-canoylphorbol-13-acetate. These results were not paralleled by changes in sister chromatid exchange frequencies, indicating that, while sister chromatid exchanges may be useful as indicators of primary carcinogen mutagens, they may have little utility when secondary agents alter the response of cells to a primary initiator.

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This investigation was supported by Contract DE-AS02-78EV0-4733 from the United States Department of Energy, Grants CA 12536 and CA 23952 to the Radiological Research Laboratory, Department of Radiology; and Grant CA 13696 to the Cancer Center, Institute of Cancer Research, awarded by the National Cancer Institute, Department of Health, Education and Welfare.

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