Background: High-risk human papillomavirus (hrHPV) type E6 and E7 oncoproteins contribute to oncogenesis in multiple ways by modulating the activities of host components in cell-cycle regulation including the expressi...Background: High-risk human papillomavirus (hrHPV) type E6 and E7 oncoproteins contribute to oncogenesis in multiple ways by modulating the activities of host components in cell-cycle regulation including the expression of p16 protein (p16) and human telomerase reverse transcriptase (hTERT). The expression of p16 and hTERT protein in Bowenoid papulosis (BP) has not been studied. Methods: Biopsy samples of BP from 26 patients were subjected to in situ hybridization for various HPV strains and immunohistochemical staining for p16 and hTERT. Results: Among the 26 biopsy specimens, in situ hybridization using DNA probes for HPV 16/18 revealed positivity in 18 specimens (69.2%), one of which also showed positivity with the probes for HPV 6/11. HPV 31/33/35 was found in three specimens (11.5%). Two specimens (7.7%) were positive for unclassified HPV. Twenty-one BP specimens that were infected with hrHPV were positive for p16 and/or hTERT. Moderate or strong and diffuse immunostaining was observed for p16 in 15 hrHPV-infected specimens and for hTERT in 16 hrHPVinfected specimens. The expression of p16 or hTERT was each significantly associated with the presence of hrHPV. Conclusions: hrHPVs were involved in inducing p16 and hTERT overexpression in BP. Moreover, our results suggested that immunohistochemical p16 and hTERT expression might be a useful marker of hrHPV infection in BP.展开更多
文摘Background: High-risk human papillomavirus (hrHPV) type E6 and E7 oncoproteins contribute to oncogenesis in multiple ways by modulating the activities of host components in cell-cycle regulation including the expression of p16 protein (p16) and human telomerase reverse transcriptase (hTERT). The expression of p16 and hTERT protein in Bowenoid papulosis (BP) has not been studied. Methods: Biopsy samples of BP from 26 patients were subjected to in situ hybridization for various HPV strains and immunohistochemical staining for p16 and hTERT. Results: Among the 26 biopsy specimens, in situ hybridization using DNA probes for HPV 16/18 revealed positivity in 18 specimens (69.2%), one of which also showed positivity with the probes for HPV 6/11. HPV 31/33/35 was found in three specimens (11.5%). Two specimens (7.7%) were positive for unclassified HPV. Twenty-one BP specimens that were infected with hrHPV were positive for p16 and/or hTERT. Moderate or strong and diffuse immunostaining was observed for p16 in 15 hrHPV-infected specimens and for hTERT in 16 hrHPVinfected specimens. The expression of p16 or hTERT was each significantly associated with the presence of hrHPV. Conclusions: hrHPVs were involved in inducing p16 and hTERT overexpression in BP. Moreover, our results suggested that immunohistochemical p16 and hTERT expression might be a useful marker of hrHPV infection in BP.
