JCP

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS REGISTER
[Advanced]

Published Online First: 12 December 2007. doi:10.1136/jcp.2007.052027
Journal of Clinical Pathology 2008;61:627-631
Copyright © 2008 by the BMJ Publishing Group Ltd & Association of Clinical Pathologists.

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
jcp.2007.052027v1
61/5/627    most recent
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this link to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Add article to my folders
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Huang, L-W
Right arrow Articles by Lee, B-H
PubMed
Right arrow PubMed Citation
Right arrow Articles by Huang, L-W
Right arrow Articles by Lee, B-H
Right arrowPubmed/NCBI databases
Medline Plus Health Information
*Cervical Cancer

ORIGINAL ARTICLES

Integration of human papillomavirus type-16 and type-18 is a very early event in cervical carcinogenesis

L-W Huang1,2,3, S-L Chao4, B-H Lee5

1 Department of Obstetrics and Gynecology, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan
2 School of Medicine, Fu Jen Catholic University, Hsinchuang, Taipei Hsien, Taiwan
3 School of Medicine, Taipei Medical University, Taipei, Taiwan
4 Department of Chinese Medicine, Renai Branch, Taipei City Hospital, Taipei, Taiwan
5 King Car Food Industrial Co., Ltd, Yuan Shan Research Institute, Ilan, Taiwan

Correspondence to:
Lee-Wen Huang, MD, Department of Obstetrics and Gynecology, Shin Kong Wu Ho-Su Memorial Hospital, 95 Wen Chang Road, Shih-Lin District, Taipei 111, Taiwan; m002057{at}ms.skh.org.tw

Aim: Human papillomavirus (HPV) integration is a critical event in cervical carcinogenesis. The aim of this study was to explore the physical status of HPV-16 and HPV-18 during the progression of cervical precancerous lesions.

Methods: A series of 101 HPV-16 or HPV-18 positive cervical neoplasms (32 cervical intraepithelial neoplasia (CIN) cases and 69 cervical carcinoma (CC) cases) were evaluated. The physical status of both types of HPV was assessed from paraffin-embedded formaldehyde-fixed surgical specimens by real-time PCR.

Results: For HPV-16, integrated DNA was observed in 5 (83.3%) of 6 CIN I cases, 10 (90.9%) of 11 CIN II/III cases, 29 (82.9%) of 35 FIGO (International Federation of Gynecology and Obstetrics) stage I CC cases and 16 (94.1%) of 17 FIGO stages II~IV CC cases. For HPV-18, integrated DNA was observed in 3 (50%) of 6 CIN I cases, 5 (55.6%) of 9 CIN II/III cases, 9 (64.3%) of 14 FIGO stage I CC cases, and 1 (33.3%) of 3 FIGO stages II~IV CC cases. The mixed form of HPV DNA was the most prevalent physical state in HPV-16. There was no significant difference between the physical state of HPV-16 and HPV-18 DNA with regard to the various grades of cervical lesions.

Conclusions: These data imply that integration of HPV-16 and HPV-18 DNA into the host genome occurs in the very early stage of cervical neoplastic progression. These early events may play an initiating role in the malignant transformation of HPV-16- and HPV-18-related low-grade lesions into high-grade dysplasia and invasive carcinoma.








HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS REGISTER
Journal of Clinical Pathology Molecular Pathology
Terms and conditions relating to subscriptions purchased online  ¦  Website terms and conditions  ¦  Privacy policy
Copyright © 2008 by the BMJ Publishing Group Ltd & Association of Clinical Pathologists.