title: Prevalence of human papillomavirus DNA in various histological subtypes of cervical adenocarcinoma: a population-based study.
abstract: The role of human papilloma virus (HPV) infection in the development of cervical carcinoma is well established, however, the prevalence of HPV DNA in cervical adenocarcinoma varies from study to study. It appears to be caused by a number of factors, one of which is that cervical adenocarcinomas comprise a heterogeneous group of multiple subtypes. To clarify the impact of HPV infection on the development of cervical adenocarcinoma with diverse histological subtypes, we performed a population-based study in Korean women from 15 different institutes for the status of HPV infection in adenocarcinoma of uterine cervix. A total of 432 cervical adenocarcinomas from 1997 to 2001 were reviewed and classified according to the modified WHO classification. For 135 cases, HPV typing was performed with HPV DNA chip (82 cases) and PCR HPV typing (53 cases), using formalin-fixed, paraffin-embedded archival tissue. The overall prevalence of HPV infection in cervical adenocarcinoma was 90%. The infection of HPV 16 and/or HPV 18 accounted for 78% of HPV-positive adenocarcinomas. Multiple HPV types were found in 13% of the cases. The HPV DNA was rarely detected in minimal deviation adenocarcinoma. Interestingly, HPV 16 was a predominant type in endometrioid and villoglandular types, whereas HPV 16 and HPV 18 were detected with equal prevalence in other subtypes. In conclusion, HPV infection, mostly HPV 16 and HPV 18, is highly associated with most of the cervical adenocarcinomas, whereas endometrioid and villoglandular type have a different pattern of HPV infection status. Minimal deviation adenocarcinoma does not seem to be related with HPV infection.
authors.affiliation: Department of Pathology, Pochon CHA University, Sungnam, South Korea.
authors.forename: Hee J
authors.initials: HJ
authors.lastname: An
authors.forename: Kyu R
authors.initials: KR
authors.lastname: Kim
authors.forename: In S
authors.initials: IS
authors.lastname: Kim
authors.forename: Dong W
authors.initials: DW
authors.lastname: Kim
authors.forename: Moon H
authors.initials: MH
authors.lastname: Park
authors.forename: In A
authors.initials: IA
authors.lastname: Park
authors.forename: Kwang S
authors.initials: KS
authors.lastname: Suh
authors.forename: Eun J
authors.initials: EJ
authors.lastname: Seo
authors.forename: Sun H
authors.initials: SH
authors.lastname: Sung
authors.forename: Jin H
authors.initials: JH
authors.lastname: Sohn
authors.forename: Hye K
authors.initials: HK
authors.lastname: Yoon
authors.forename: Eun D
authors.initials: ED
authors.lastname: Chang
authors.forename: Hyun I
authors.initials: HI
authors.lastname: Cho
authors.forename: Ji Y
authors.initials: JY
authors.lastname: Han
authors.forename: Sung R
authors.initials: SR
authors.lastname: Hong
authors.forename: Geung H
authors.initials: GH
authors.lastname: Ahn
mesh_terms: D000230:Adenocarcinoma / Q000473:pathology* / Q000821:virology; D000328:Adult; D004279:DNA, Viral / Q000032:analysis / Q000235:genetics*; D005260:Female; D005838:Genotype; D006801:Humans; D007723:Korea / Q000453:epidemiology; D008875:Middle Aged; D009367:Neoplasm Staging; D027383:Papillomaviridae / Q000235:genetics* / Q000254:growth & development; D030361:Papillomavirus Infections / Q000453:epidemiology / Q000473:pathology* / Q000821:virology; D015995:Prevalence; D002583:Uterine Cervical Neoplasms / Q000473:pathology* / Q000821:virology
chemical_list: D004279:DNA, Viral