Abstract
A major advance in analysing the mechanisms of chemical carcinogenesis has been the development of cell culture systems in which normal rodent cells can be transformed as a result of in vitro exposure to specific chemicals or radiation1–6. An unexpected finding in these systems is that the frequency of transformation is often much greater than that of induction of drug-resistant mutants3,6–10. In addition, studies using the technique of cell spreading have suggested that the latent period between exposure of cell cultures to carcinogens and the emergence of cells having the heritable ability to form transformed foci is also much greater than that for the induction of drug-resistant mutants8,11,12. In most of the above transformation studies, the cells were exposed to carcinogens at low cell densities and, therefore, mutation-like events that might be induced with a low frequency could have been missed. Thus, we have now analysed the kinetics of cell transformation of C3H 10T1/2 cells when exposed to the potent ultimate carcinogen (±)7β,8α-dihydroxy-9α,10α-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene (BPDE) in conditions of high cell density. We report here that in these conditions acquisition of the ability to form transformed foci and acquisition of ouabain resistance occur with similar kinetics and within 2 days of carcinogen exposure.
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References
Berwald, Y. & Sachs, L. J. natn. Cancer Inst. 35, 641–661 (1965).
Chen, T. T. & Heidelberger, C. Int. J. Cancer 4, 166–178 (1969).
Heidelberger, C. et al. Mutat. Res. (in the press).
DiPaolo, J. A., Donovan, P. J. & Nelson, R. L. Nature new Biol. 230, 240–242 (1971).
DiPaolo, J. A., Takano, K. & Popescu, N. C. Cancer Res. 32, 2686–2695 (1972).
Barrett, J. C. & Elmore, E. in Mutagenesis and Carcinogenesis (eds Andrews, L. S., Lorentzen, R. J. & Flamm, W. G.) (Springer, Berlin, in the press).
Parodi, S. & Brambilla, G. Mutat. Res. 47, 53–74 (1977).
Kennedy, A. R. et al. Proc. natn. Acad. Sci. U.S.A. 77, 7262–7266 (1980).
Fernandez, A., Mondal, S. & Heidelberger, C. Proc. natn. Acad. Sci. U.S.A. 77, 7272–7276 (1980).
Weinstein, I. B. J. supramolec. Struct. 17, 99–120 (1981).
Haber, D. A. et al. Cancer Res. 37, 1644–1648 (1977).
Peterson, A. R. et al. Cancer Res. 41, 3095–3099 (1981).
Landolph, J. R. & Heidelberger, C. Proc. natn. Acad. Sci. U.S.A. 76, 930–934 (1979).
Chan, G. & Little, J. B. Proc. natn. Acad. Sci. U.S.A. 75, 3363–3366 (1978).
Rezinikoff, C. A., Brankow, D. W. & Heidelberger, C. Cancer Res. 33, 3231–3238 (1973).
Kirschmeier, P. et al. Proc. natn. Acad. Sci. U.S.A. 79, 273–277 (1982).
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Backer, J., Boerzig, M. & Weinstein, I. When do carcinogen-treated 10T1/2 cells acquire the commitment to form transformed foci?. Nature 299, 458–460 (1982). https://doi.org/10.1038/299458a0
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DOI: https://doi.org/10.1038/299458a0
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