Objectives: In the past several years, much evidence has accumulated that strongly implicates human papillomavirus (HPV) as an etiological agent of cervical cancer. However, the natural history of HPV infection is not yet completely understood, and at present there is no good marker to predict progression to invasive cancer in individual patients with dysplasia.
Methods: Tissue specimens from 45 patients with cervical dysplasia were classified as showing progression to carcinoma (progression group; 26 women), spontaneous regression (regression group; 16 women), and persistence (persistence group; 3 women). The presence of HPV 16, 18, 33, and 52 DNA was examined in 90 formalin-fixed, paraffin-embedded surgical and biopsy specimens of dysplasia using the PCR method, and the relationship between the presence of HPV and cervical carcinogenesis was analyzed. The mean follow-up period was 25.8 months in the progressed group and 34.0 months in both the persistent and regressed groups. The mean ages were 46.4 in the progressed group and 46.8 in the persistent and regressed groups.
Results: HPV 16, 18, 33, and 52 DNA were detected in 19 of the 26 patients (73.1%) in the progressed group. All patients with HPV 16, 18, or 52 DNA showed progression to carcinoma. The HPV 33 DNA was detected in 5 of the 16 patients (31.3%) in the regressed group and in 2 of the 3 patients (66.7%) in the persistent group, while HPV 16, 18, and 52 DNA were not detected in the 19 patients that comprised the regressed and persistent groups.
Conclusion: This retrospective study suggests that cervical dysplasia in patients with high-risk types of HPV possessed the potential to progress to carcinoma in situ and eventually to invasive carcinoma as well.