1. ¹Department of Pathology, Pochon CHA University, Sungnam, South Korea
2. ²Department of Pathology, Ulsan University, Seoul, South Korea
3. ³Department of Pathology, Korea University, Seoul, South Korea
4. ⁴Department of Pathology, Soonchunhyang University, Seoul, South Korea
5. ⁵Department of Pathology, Hanyang University, Seoul, South Korea
6. ⁶Department of Pathology, Seoul University, Seoul, South Korea
7. ⁷Department of Pathology, Chungnam University, Daejon, South Korea
8. ⁸Department of Pathology, Catholic University, Seoul, South Korea
9. ⁹Department of Pathology, Ewha University, Seoul, South Korea
10. ¹⁰Department of Pathology, Sungkyunkwan University, Seoul, South Korea
11. ¹¹Department of Pathology, Inje University, Busan, South Korea
12. ¹²Department of Pathology, Gachon University, Inchon, South Korea
13. ¹³Department of Pathology, Inha University, Inchon, South Korea

Correspondence: Dr GH Ahn, MD, Department of Pathology, Samsung Medical Center, Sungkyunkwan University College of Medicine, 50, Ilwon-Dong, Kangnam-Gu, Seoul 143-230, South Korea. E-mail: gahn@smc.samsung.co.kr

Received 26 July 2004; Revised 9 September 2004; Accepted 9 September 2004; Published online 22 October 2004.

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.