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Cancer Epidemiology Biomarkers & Prevention Vol. 14, 2550-2556, November 2005
© 2005 American Association for Cancer Research

Anal Human Papillomavirus Infection in Women and Its Relationship with Cervical Infection

Brenda Y. Hernandez1, Katharine McDuffie1, Xuemei Zhu1, Lynne R. Wilkens1, Jeffrey Killeen6, Bruce Kessel7, Mark T. Wakabayashi5, Cathy C. Bertram7, David Easa2, Lily Ning3, Jamie Boyd4, Christian Sunoo8, Lori Kamemoto5 and Marc T. Goodman1

1 Cancer Research Center of Hawaii, 2 Clinical Research Center, 3 University Health Services, 4 Leeward Community College, and 5 John A. Burns Medical School, University of Hawaii; 6 Kapiolani Medical Center for Women and Children; 7 Queen's Medical Center; and 8 Kaiser Hawaii Permanente Medical Systems, Honolulu, Hawaii

Requests for reprints: Brenda Y. Hernandez, Cancer Research Center of Hawaii, University of Hawaii, 1236 Lauhala Street, Honolulu, HI 96813. Phone: 808-586-2992; Fax: 808-586-2982. E-mail: brenda{at}crch.hawaii.edu

Human papillomavirus (HPV), the primary cause of cervical cancer, is also associated with the development of anal cancer. Relatively little is known about the epidemiology of anal HPV infection among healthy females and its relationship to cervical infection. We sought to characterize anal HPV infection in a cohort of adult women in Hawaii. Overall, 27% (372 of 1,378) of women were positive for anal HPV DNA at baseline compared with 29% (692 of 2,372) with cervical HPV DNA. Among women with paired anal and cervical samples, anal infection without accompanying cervical infection was observed in 14% (190 of 1,363). Concurrent anal and cervical HPV infections were observed in 13% (178 of 1,363) of women. Women with cervical HPV infection had >3-fold increased risk of concurrent anal infection. Concurrent anal and cervical HPV infection was most prevalent among the youngest women and steadily decreased through age 50 years. By contrast, the prevalence of anal infection alone remained relatively steady in all age groups. Compared with cervical infections, the overall distribution of HPV genotypes in the anus was more heterogeneous and included a greater proportion of nononcogenic types. A high degree of genotype-specific concordance was observed among concurrent anal and cervical infections, indicating a common source of infection. Nevertheless, the association of anal intercourse with anal HPV infection was limited to those women without accompanying cervical infection. The relationship of anal to cervical infection as described in this study has implications for the development of anal malignancies in women.




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
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Molecular Cancer Research Cancer Prevention Research
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Annual Meeting Education Book Meeting Abstracts Online
Copyright © 2005 by the American Association for Cancer Research.