TY - JOUR
T1 - Expression patterns of cyclins D1 and E in condyloma acuminatum in comparison with psoriatic proliferative lesions
AU - Mate, José L.
AU - Ariza, Aurelio
AU - Roca, Xavier
AU - López, Dolores
AU - Ferrándiz, Carlos
AU - Pérez-Piteira, Javier
AU - Navas-Palacios, José J.
PY - 1998/1/1
Y1 - 1998/1/1
N2 - Human papillomavirus (HPV) is able to subvert the host cell replication machinery so as to foster viral reproduction. Specifically, HPV infection is known to induce expression of proliferation antigens such as Ki67 and proliferative cell nuclear antigen (PCNA) in differentiated keratinocytes which have ceased to replicate. In order to determine whether cyclin D1 or cyclin E deregulation is also a feature of HPV infection, an immunohistochemical investigation of cyclin D1, cyclin E, Ki67, and PCNA expression has been carried out in 38 cases of HPV 6/11-related condyloma acuminatum (CA). Results were compared with those obtained from 15 psoriatic proliferative lesions. Whereas 35 (92.1 per cent) CA samples exhibited positive nuclear immunostaining for cyclin E, no cyclin D1 immunoreaction was detected in any of the CA samples studied. All 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 layers. Parabasal keratinocytes of psoriatic lesions were always positive for 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 cyclin D1 is spared the main effects of virus-cell interplay. In contrast, both cyclins seem to be induced in psoriasis, a non- viral proliferative skin condition.
AB - Human papillomavirus (HPV) is able to subvert the host cell replication machinery so as to foster viral reproduction. Specifically, HPV infection is known to induce expression of proliferation antigens such as Ki67 and proliferative cell nuclear antigen (PCNA) in differentiated keratinocytes which have ceased to replicate. In order to determine whether cyclin D1 or cyclin E deregulation is also a feature of HPV infection, an immunohistochemical investigation of cyclin D1, cyclin E, Ki67, and PCNA expression has been carried out in 38 cases of HPV 6/11-related condyloma acuminatum (CA). Results were compared with those obtained from 15 psoriatic proliferative lesions. Whereas 35 (92.1 per cent) CA samples exhibited positive nuclear immunostaining for cyclin E, no cyclin D1 immunoreaction was detected in any of the CA samples studied. All 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 layers. Parabasal keratinocytes of psoriatic lesions were always positive for 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 cyclin D1 is spared the main effects of virus-cell interplay. In contrast, both cyclins seem to be induced in psoriasis, a non- viral proliferative skin condition.
KW - Condyloma acuminatum
KW - Cyclin D1
KW - Cyclin E
KW - Human papillomavirus
KW - Ki67
KW - PCNA
KW - Psoriasis
U2 - 10.1002/(SICI)1096-9896(199801)184:1<83::AID-PATH963>3.0.CO;2-B
DO - 10.1002/(SICI)1096-9896(199801)184:1<83::AID-PATH963>3.0.CO;2-B
M3 - Article
VL - 184
SP - 83
EP - 88
JO - Journal of Pathology
JF - Journal of Pathology
SN - 0022-3417
IS - 1
ER -