A total of 311 smears from the lower genital tract were examined by the filter in situ hybridization method to identify human papillomavirus (HPV) DNA. Of these 311 smears, 229 came from clinically and cytologically negative patients and served as a control group. In this group HPV-DNA was detected in 5 cases (2.2%). Of 82 cytologically positive cases (25 confirmed by histology) 56 (68%) contained HPV-DNA. A high prevalence of HPV 6/11 and absence of HPV 16/18 was found in cases with cytological signs of permissive HPV infection. In mild and moderate dysplasia all viruses occurred at almost the same frequency. In severe dysplasia/carcinoma in situ HPV 16/18 was found 5 times more frequently than HPV 6/11. HPV 16/18 was identified in all 4 invasive cancer cases. Cervical irrigation of colposcopically suspect areas was performed in 15 cytologically and HPV-DNA positive cases using the hydrodynamic filtration method. In 12 cases only the cells obtained from the colposcopically positive areas contained HPV-DNA. The sensitivity and reproducibility of the filter in situ hybridization was shown by: comparing the results obtained by HPV-DNA hybridization using Southern blot analysis of tumor biopsies; analysing the correlation of cytologic diagnosis and presence of HPV-DNA in follow-up examinations, and diagnosing presence or absence of HPV-DNA in parallel filters from the same patients.

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Perinatal morbidity and mortality are increased in both overt and gestational diabetes. Since retardation of placental development has been documented in overt diabetes, we, thus, examined morphometrically the terminal villi of 26 patients with gestational diabetes in order to determine if there is an immaturity of placental development. Investigation of villous surface, degree of vascularization, and development of epithelial plates yielded values lying somewhere between those of non-diabetic patients and those of patients with overt diabetes. Only the surface areas of the vessels were reduced to levels lower than in overt diabetes. Our findings appear to explain the occasional development of acute placental insufficiency.

Comparative cytogenetic and histologic studies on 18 mesothelial ovarian tumors revealed a normal chromosome complement in benign lesions, and the well-known cytogenetic pattern in cystadenocarcinomas. But all borderline tumors of the series evidenced an abnormal stem line and a more or less marked tendency to polyploidization. Serous papillary cystadenomas of this group showed in five out of six cases a stem line with the karyotype 47,XX+C10 (identified by Q-banding), present in both sides of bilateral lesions. It is evidenced that malignant change on the chromosomal level precedes histologically detectable features of malignancy. Histologic equivalents appeared, when the abnormal cell line was established. The initiation of malignant transformation therefore may be signalized by karyotype abnormalities before structural changes can be detected in the corresponding histologic specimens. The results discussed include the concepts of multicentric origin and clonal evolution of malignancy.

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