Behavior of cervical intraepithelial neoplasia (CIN) associated with various human papillomavirus (HPV) types.

201 cervical punch biopsies which showed CIN lesions and were obtained between 1967 to 1977 from Falu Hospital patients, with long-term follow-up data were examined histologically and by DNA typing for human papillomavirus (HPV). We used in situ hybridization for HPV types 6, 11, 16, 18, 31 and 33 and related our findings to the behaviour of the lesion (103 regressed spontaneously and 98 progressed, some of them to invasive cervical carcinoma). There was evidence of HPV infection in 75.6% (152/201) of these lesions on histological examination, and in 53.2% (107/201) on in situ DNA hybridization. Lesions positive for HPV by both methods occurred in the younger age group (Pearson's correlation coefficient, P = 0.008). HPV 16 was found in 51/152 (33.6%) of the HPV lesions, HPV in 12.5%, and HPV 33 in 8.5% HPV 16 was highly significantly (P = 0.0001), and HPV 18 and HPV 33 were significantly (P = 0.008 and P = 0.007, respectively) associated with increasing grades of CIN. Progression to invasive carcinoma was directly (and regression inversely) correlated with the severity of CIN in the first biopsy (P = 0.005). Almost 74% (17/23) of the HPV-CIN III lesions progressed, while only 25% of the HPV-NCIN lesions (6/24) did so. The progression rate was 84.6% for HPV 33 lesions and 52.9% for HPV 16. On the other hand, progression was less common with HPV 6 (25%), and HPV 31 (30.0%). Histological grade and HPV type appear to be of value as prognostic indices.

Epstein-Barr virus (EBV) genomes and c-myc oncogene in oral Burkitt's lymphomas.

In addition to Burkitt's lymphomas, tentative evidence suggests the involvement of Epstein-Barr virus (EBV) in malignant lymphomas of T-cell origin. The c-myc proto-oncogene is strongly associated with the development of lymphoid neoplasias. In the present study, a series of 38 biopsies of oral lymphomas (29 Burkitt's lymphomas, 9 malignant lymphomas of other type) obtained from patients in Tanzania were studied using in situ hybridization (ISH) and polymerase chain reaction (PCR) for detection of EBV DNA and c-myc oncogene. In ISH applied on formalin-fixed, paraffin wax-embedded biopsies, the Bam HI W fragment of EBV DNA was used as the probe. Amplification of c-myc oncogene was studied by PCR with a primer set from Exon II area. As an internal standard beta-globin gene was simultaneously amplified. EBV DNA was disclosed by ISH in five Burkitt's lymphomas only. Using the PCR, 20 of the 29 cases (70%) of Burkitt's lymphomas showed amplification for EBV DNA. Of the other EBV-positive lymphomas, two were of the lymphocytic type (large non-cleaved cell), one histiocytic and one Burkitt's-like lymphoma. All EBV-positive cases found on the agarose gel were positive also with the dot blot, when hybridized with the 32P-labeled EBV Bam HI W-fragment probe. All lymphomas showed similar bands on the gel for c-myc and beta-globin indicating that no amplification of c-myc was present.