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© 1985 Oxford University Press

research-article

Integration of a mutant c-Ha-ras oncogene into C3H/10T1/2 cells and its relationship to tumorigenic transformation

T. Herbert Manoharan, Jeffrey A. Burgess, Dominic Ho 1, Christine L. Newell and William E. Fahl 2

Northwestern University Cancer Center 8315 Olson Pavilion, 303 East Chicago Avenue, Chicago, IL 60611, USA

2To whom reprint requests should be sent

C3H/10T1/2-CL8 mouse cells were shown to take up and express a plasmid-cloned drug resistance gene (Ecogpt) after DNA transfection at a frequency (2–6 x 10–4) which is acceptable for routine recovery of gene-transformed populations. Transfection of 10T1/2 cells with a mutant c-Ha-ras oncogene (pEJ6.6 plasmid) results in neoplastically transformed 10T1/2 cell populations as judged by colony morphology and tumorigenic growth in nude mice. The levels of mutant c-Ha-ras gene integration and expression in the tumorigenic cell populations and 10T1/2 cell controls were determined, and the highest level of mutant ras transcript was seen in the most tumorigenic cell population. A preliminary comparison of 10T1/2 and NIH/3T3 cells showed similar frequencies for pEJ6.6-induced transformed foci and a similar lack of sensitivity to the transforming effects of a cloned B-lym oncogene. The results identify a genetic event, which has previously been shown to be carcinogen-inducible, that is permissive for neoplastic transformation of the widely used carcinogen-transformable 10T1/2 mouse cell line.


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