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American Journal of Pathology, Vol 134, 1183-1188, Copyright © 1989 by American Society for Investigative Pathology
REGULAR ARTICLES |
CP Crum, M Symbula and BE Ward
Department of Pathology, University of Virginia Medical Center, Charlottesville 22908.
The extent to which human papillomavirus (HPV) type 16 is transcribed and the nature of the transcripts produced in genital precancers has not been clearly defined. The authors analyzed 28 cases of cervical (CIN) or vulvar (VIN) intraepithelial neoplasia by RNA-RNA in situ hybridization, using probes generated from HPV 16 open reading frames (ORFs) either upstream (E6-E7) or downstream (E2-E5-L2) to the E1 ORF, where HPV 16 genomic integration most commonly occurs. Hybridization signals corresponding to one or both probes were detected in a high proportion of cells throughout the lesional epithelium of low- and high- grade CIN, including basal layers. In serial sections analyzed with the two probes, hybridization signals were obtained from both, and in similar proportion, irrespective of CIN grade. The distribution and character of hybridization signals suggests that the morphologic progression of precancers is not associated with either cessation of HPV 16 early transcription or a change in the general character of the transcripts produced.
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