EXPRESSION PATTERNS OF CYCLIN-D1 AND CYCLIN-E IN CONDYLOMA ACUMINATUMIN COMPARISON WITH PSORIATIC PROLIFERATIVE LESIONS

Citation
Jl. Mate et al., EXPRESSION PATTERNS OF CYCLIN-D1 AND CYCLIN-E IN CONDYLOMA ACUMINATUMIN COMPARISON WITH PSORIATIC PROLIFERATIVE LESIONS, Journal of pathology, 184(1), 1998, pp. 83-88
Citations number
19
Categorie Soggetti
Pathology
Journal title
ISSN journal
00223417
Volume
184
Issue
1
Year of publication
1998
Pages
83 - 88
Database
ISI
SICI code
0022-3417(1998)184:1<83:EPOCAC>2.0.ZU;2-H
Abstract
Human papillomavirus (HPV) is able to subvert the host cell replicatio n machinery so as to foster viral reproduction. Specifically, HPV infe ction is known to induce expression of proliferation antigens such as Ki67 and proliferative cell nuclear antigen (PCNA) in differentiated k eratinocytes which have ceased to replicate. In order to determine whe ther cyclin D1 or cyclin E deregulation is also a feature of HPV infec tion, an immunohistochemical investigation of cyclin D1, cyclin E, Ki6 7, and PCNA expression has been carried out in 38 cases of HPV 6/11-re lated condyloma acuminatum (CA). Results were compared with those obta ined from 15 psoriatic proliferative lesions. Whereas 35 (92.1 per cen t) CA samples exhibited positive nuclear immunostaining for cyclin E, no cyclin D1 immunoreaction was detected in any of the CA samples stud ied. AU psoriatic lesions showed immunostaining for both cyclins. All CA cases revealed a positive immunoreaction for Ki67 and 33 for PCNA, both in the parabasal and in the differentiated upper epithelial layer s. Parabasal keratinocytes of psoriatic lesions were always positive f or both Ki67 and PCNA. These results indicate that in the onslaught of HPV 6/11 upon the keratinocyte replication machinery, cyclin E, PCNA, and Ki67 are amongst the targeted cell cycle modulators, whereas cycl in D1 is spared the main effects of virus-cell interplay. In contrast, both cyclins seem to be induced in psoriasis, a non-viral proliferati ve skin condition. (C) 1998 John Wiley & Sons, Ltd.