摘要

The infectivity of human papillomavirus (HPV) is closely linked to the characteristics of the epithelial lesions that they induce in the uterine cervix. Recent epidemiological studies have shown that not all HPV-infected patients necessarily develop carcinoma. It is therefore of importance to determine the molecular mechanism of tumorigenesis following HPV infection. In our previous study of amplification in the oncogenes c-myc and N-myc, amplification was observed in the c-myc but not in the N-myc gene. In the present study, we attempted to determine whether amplification occurs in other major oncogenes other than c-myc and N-myc, including c-erbB-2, N-ras and H-ras, using a quantitative dot-blot hybridization imaging plate method. Frequencies of gene amplification were 28.1% in c-myc, 25.0% in H-ras and 7.1% in c-erbB-2. No amplification of the N-myc or N-ras gene was observed. We also developed a simple and rapid method for detection of point mutations at codon 12 of the K-ras gene based on the PCR-RFLP technique and using a mismatched primer. Two cases of point mutation at codon 12 of the K-ras gene were observed in a total of 32 cervical cancer patients tested. These findings suggest that chromosomal alterations are critical steps in the progression to cervical carcinoma during the tumorigenetic process following HPV infection.

  • 出版日期1993-12