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Journal of Clinical Microbiology, May 2006, p. 1755-1762, Vol. 44, No. 5
0095-1137/06/$08.00+0     doi:10.1128/JCM.44.5.1755-1762.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Human Papillomavirus Type 16 Integration in Cervical Carcinoma In Situ and in Invasive Cervical Cancer

Hugo Arias-Pulido,1 Cheri L. Peyton,1,{dagger} Nancy E. Joste,2 Hernan Vargas,3,4,{ddagger} and Cosette M. Wheeler1*

Departments of Molecular Genetics and Microbiology,1 Department of Pathology, University of New Mexico, Health Sciences Center, School of Medicine, Albuquerque, New Mexico,2 Grupo Farmacogenética del Cáncer, Dep. Farmacia, Universidad Nacional de Colombia, Bogotá, Colombia,3 Grupo de Biología Molecular Tumoral, Instituto Nacional de Cancerología, Bogotá, Colombia4

Received 24 October 2006/ Returned for modification 5 January 2006/ Accepted 20 February 2006

Integration of human papillomavirus type 16 (HPV-16) into the host DNA has been proposed as a potential marker of cervical neoplastic progression. In this study, a quantitative real-time PCR (qRT-PCR) was used to examine the physical status of HPV-16 in 126 cervical carcinoma in situ and 92 invasive cervical cancers. Based on criteria applied to results from this qRT-PCR assay, HPV-16 was characterized in carcinoma in situ cases as episomal (61.9%), mixed (i.e., episomal and integrated; 29.4%), and integrated (8.7%) forms. In invasive cervical cancer samples, HPV-16 was similarly characterized as episomal (39.1%), mixed (45.7%), and integrated (15.2%) forms. The difference in the frequency of integrated or episomal status estimated for carcinoma in situ and invasive cervical cancer cases was statistically significant (P = 0.003). Extensive mapping analysis of HPV-16 E1 and E2 genes in 37 selected tumors demonstrated deletions in both E1 and E2 genes with the maximum number of losses (78.4%) observed within the HPV-16 E2 hinge region. Specifically, deletions within the E2 hinge region were detected most often between nucleotides (nt) 3243 and 3539. The capacity to detect low-frequency HPV-16 integration events was highly limited due to the common presence and abundance of HPV episomal forms. HPV-16 E2 expressed from intact episomes may act in trans to regulate integrated genome expression of E6 and E7.

* Corresponding author. Mailing address: Department of Molecular Genetics and Microbiology, School of Medicine, Health Sciences Center, University of New Mexico, Albuquerque, NM 87111. Phone: (505) 272-5785. Fax: (505) 277-0265. E-mail: cwheeler{at}salud.unm.edu.

{dagger} Present address: Department of Zoology, Oregon State University, Corvallis, Oreg.

{ddagger} Present address: Grupo Farmacogenética del Cáncer, Dep. Farmacia, Universidad Nacional de Colombia, Bogotá, Colombia.

Journal of Clinical Microbiology, May 2006, p. 1755-1762, Vol. 44, No. 5
0095-1137/06/$08.00+0     doi:10.1128/JCM.44.5.1755-1762.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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