Step-wise progression in human skin carcinogenesis in vitro involves mutational inactivation of p53, rasH oncogene activation and additional chromosome loss.

Abstract excerpt

Two mechanisms relevant for skin carcinogenesis in man are mutational inactivation of p53 and oncogenic activation of c-rasH gene. Previously, we transfected c-rasH oncogene into human skin keratinocytes (HaCaT) with u.v.-typic mutations in both p53 alleles, which produced benign and malignant tumorigenic clones, expressing similar amounts of mutant Ras protein. Here we show that neither the ras integration site...

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