Abstract. Compatible with the epidemiology and natural history of cervical cancer and with experimental findings that HPV-immortalized nontumorigenic cells are similar to cervical carcinoma cells, in terms of the quantity and type of viral RNA expressed, it is believed that additional cellular genetic events are necessary for tumorigenic conversion. In the current study we detected codon 12 point mutations of the K-ras oncogene with an incidence of 28.2% in malignant lesions of the cervix, as well as HPV 18 at a higher rate than HPV16 (30.2% vs 27.9%) in genital lesions, by PCR and RFLP analysis. Codon 12 point mutations of K-, H-and Nras were also found in benign lesions of the cervix, in endometrial and in ovarian carcinomas, although at a lower frequency. It is suggested that the mutationally activated ras oncogenes cooperate with HPV in the early stages of carcinogenesis of the human female reproductive tract.