Human papillomavirus 16/18 expression of endocervical glandular lesions: relationship with p53 and MIB-1 Expressions.
The pathogenesis of endocervical glandular lesions are not clearly understood. The aims of this study are to evaluate the etiologic role of human papillomavirus (HPV) 16/18 and the relationship of HPV 16/18, p53 and MIB-1 expressions in endocervical glandular dysplasia (EGD), adenocarcinoma in situ (AIS) and adenocarcinoma. The materials included 14 endocervical adenocarcinoma and 5 AIS and 18 high grade EGD and 39 low grade EGD. Immunohistochemistry for p53 and MIB-1, and in situ PCR for HPV 16/18 were done. HPV 16/18 positivity was 84.2%, 16.7% and 17.9% in malignant glandular lesion (adenocarcinoma and AIS), high grade EGD and low grade EGD, respectively. P53 protein expression rates of malignant glandular lesions, high grade EGD and low grade EGD were 31.6%, 11.1%, and 0%, respectively. High MIB-1 labelling index was found in 73.7% of malignant glandular lesions, but in only 5.7% and 3.6% of high and low grade EGD, respectively. There were statistically significant differences in HPV 16/18, p53 and MIB-1 expressions between malignant endocervical glandular lesions and EGD, but no significant difference in p53 and MIB-1 expressions in relation to HPV 16/18 expression. In malignant endocervical glandular lesions, HPV 16/18 infection may be a major causative factor, but not be related to p53 and MIB-1 expressions.
Yoon
H K
HK
Department of Anatomic Pathology, Pusan Paik Hospital, Pusan, Korea. pathyoon@ijnc.inje.ac.kr
Kim
Y J
YJ
Kang
M S
MS
D000230:Adenocarcinoma / Q000473:pathology / Q000503:physiopathology / Q000821:virology*; D034961:Antigens, Nuclear; D002294:Carcinoma, Squamous Cell / Q000473:pathology / Q000503:physiopathology / Q000821:virology; D005260:Female; D006801:Humans; D019394:Ki-67 Antigen; D009687:Nuclear Proteins / Q000032:analysis / Q000235:genetics*; D009856:Oncogene Proteins, Viral / Q000235:genetics; D027383:Papillomaviridae; D030361:Papillomavirus Infections / Q000473:pathology* / Q000503:physiopathology; D016159:Tumor Suppressor Protein p53 / Q000032:analysis / Q000235:genetics*; D014412:Tumor Virus Infections / Q000473:pathology* / Q000503:physiopathology; D002583:Uterine Cervical Neoplasms / Q000473:pathology / Q000503:physiopathology / Q000821:virology*
D034961:Antigens, Nuclear; D019394:Ki-67 Antigen; D009687:Nuclear Proteins; D009856:Oncogene Proteins, Viral; D016159:Tumor Suppressor Protein p53