Significances of COX-2, p21, Ki-67 expression and HPV infection in nasal inverted papilloma.
- Author:
Xianying MENG
;
Xu WU
;
Yibing YUAN
- Publication Type:Journal Article
- MeSH:
Case-Control Studies;
Cyclin-Dependent Kinase Inhibitor p21;
biosynthesis;
Cyclooxygenase 2;
biosynthesis;
Humans;
Ki-67 Antigen;
biosynthesis;
Nasal Mucosa;
Nasal Polyps;
Nose Neoplasms;
genetics;
virology;
Papilloma, Inverted;
genetics;
virology;
Papillomavirus Infections
- From:
Journal of Clinical Otorhinolaryngology Head and Neck Surgery
2014;28(23):1823-1827
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the significance of expression of COX-2, p21, Ki67 and HPV in nasal inverted papilloma.
METHOD:Detecting COX-2, p21, Ki-67 in 30 cases of nasal inverted papilloma (NIP), 20 cases of nasal polyps (NP) and 10 cases of normal nasal mucosa (NM) by two step immunohistochemical method, and HPV virus by flow-through hybridization method.
RESULT:The positive expression rate of COX-2 and Ki-67 in NIP, NP and NM group was decreased in turn, COX-2 had significant difference in the groups(χ2 = 30.00, P< 0. 05); the positive expression rate of Ki-67 had significant differences between NIP and NM group (χ2 = 8. 533, P<0. 05). The expression of COX-2 in NIP tissues was positively correlate with that of Ki-67 by using Spearman rank correlation analysis (r=0.78, P<0.05). Expression of p21 were not observed in NIP group. The positive rate of HPV was 26. 67% in 30 cases of NIP, all of HPV16 type.
CONCLUSION:COX-2, Ki-67 and HPV infection have certain correlation with the occurrence of NIP. The occurrence of NIP has relationship with inflammatory reaction mediated by COX-2. Ki-67 can well reflect the proliferation activity of tumor cells, and can be used to measure the proliferation rate of nasal inverted papilloma. The COX-2 and Ki-67 have a synergistic role in the pathogenesis of NIP. p21 has no significant relationship with the incidence of NIP. HPV infection is related to the pathogenesis of NIP, but not as a;major factor in the pathogenesis of NIP.
