HUMAN PAPILLOMAVIRUS DETECTION BY POLYMERASE CHAIN-REACTION IN BENIGNAND MALIGNANT PROSTATE TISSUE IS DEPENDENT ON THE PRIMER SET UTILIZED

Citation
Mk. Terris et Dm. Peehl, HUMAN PAPILLOMAVIRUS DETECTION BY POLYMERASE CHAIN-REACTION IN BENIGNAND MALIGNANT PROSTATE TISSUE IS DEPENDENT ON THE PRIMER SET UTILIZED, Urology, 50(1), 1997, pp. 150-156
Citations number
22
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
00904295
Volume
50
Issue
1
Year of publication
1997
Pages
150 - 156
Database
ISI
SICI code
0090-4295(1997)50:1<150:HPDBPC>2.0.ZU;2-H
Abstract
Objectives. Prior investigations evaluating the presence of human papi llomavirus (HPV) in prostatic tissue by polymerase chain reaction (PCR ) technology have yielded detection rates of 0% to 100%. Contamination by viral DNA from prostatic urethral colonization or less than optima l laboratory conditions have been suggested to explain this discrepanc y. In addition, the various investigations have differed in the specif ic oligonucleotide primers utilized for amplification and, therefore, have searched for different segments of the viral genome. The objectiv e of this study is to address these differences. Methods. Forty-one ar chival radical prostatectomy specimens were evaluated, identifying are as of normal and abnormal histology. Meticulous technique was used dur ing tissue acquisition, histologic confirmation, DNA isolation, PCR am plification, polyacrylamide gel electrophoresis, and staining. Primers for a 126- and 99-base pair (bp) fragment of the E6 portion of HPV 16 as well as a consensus primer for the L1 portion of the papillomaviru s genome were utilized. Results. Of the normal prostatic tissues, 13.5 % (5/37) contained the 126-bp E6 viral DNA as did 33.3% (7/ 21) of ben ign prostatic hyperplasia (BPH) samples, 25% (5/20) of dysplasia, 18.2 % (2/1 1) of Gleason grades 1 and 2 adenocarcinoma, 25.9% (7/27) of Gl eason grade 3 adenocarcinoma, and 6.7% (1/15) of Gleason grade 4 adeno carcinoma. Sections from the urethras of the prostatectomy specimens c ontained viral DNA in 31.7% (13/41). Viral detection was variable amon g different specimens in the same patient. With amplification for the 99-bp fragment of HPV 16, 1 of 37 normal (2.7%), 2 of 21 BPH (9.5%), 1 of 20 dysplasia (5.0%), and 2 of 55 cancer (3.8%) specimens revealed HPV DNA. In none of the specimens was DNA amplified using primers for a 450-bp fragment of the L1 portion of HPV. Conclusions. Previously pu blished discrepancies in HPV detection may be solely due to the differ ences in primer sets utilized. (C) 1997, Elsevier Science Inc. All rig hts reserved.