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JNCI Journal of the National Cancer Institute 2001 93(4):315-318; doi:10.1093/jnci/93.4.315
© 2001 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 93, No. 4, 315-318, February 21, 2001
© 2001 Oxford University Press


BRIEF COMMUNICATION

Human Papillomavirus Type 16 Variants and Risk of Cervical Cancer

Allan Hildesheim, Mark Schiffman, Christina Bromley, Sholom Wacholder, Rolando Herrero, Ana Cecilia Rodriguez, Maria Concepcion Bratti, Mark E. Sherman, Ulysses Scarpidis, Quan-Qiu Lin, Masonoria Terai, Ronald L. Bromley, Kenneth Buetow, Raymond J. Apple, Robert D. Burk

Affiliations of authors: A. Hildesheim, M. Schiffman, C. Bromley, S. Wacholder, K. Buetow, Division of Cancer Epidemiology and Genetics, National Cancer Institute (NCI), Bethesda, MD; R. Herrero, A. C. Rodriguez, M. C. Bratti, Caja Costarricense de Seguro Social, San Jose, Costa Rica; M. E. Sherman, Division of Cancer Epidemiology and Genetics, NCI, and Department of Pathology, The Johns Hopkins University, Baltimore, MD; U. Scarpidis, Q.-Q. Lin, M. Terai, R. D. Burk, Departments of Pediatrics, Microbiology and Immunology and Epidemiology and Social Medicine, Albert Einstein College of Medicine, Bronx, NY; R. L. Bromley, LI-COR Inc., Biotechnology Division, Lincoln, NE; R. J. Apple, Roche Molecular Systems, Alameda, CA.

Correspondence to: Allan Hildesheim, Ph.D., National Institutes of Health, 6120 Executive Blvd., Rm. 7062, Rockville, MD 20852 (e-mail: Hildesha@exchange.nih.gov).

There are substantial data demonstrating that human papillomaviruses (HPVs) are the sexually transmitted etiologic agents of cervical cancer (1). HPV type 16 (HPV16) is the most common HPV type detected in tumors, accounting for 50% of cancers and their precursors, called high-grade squamous intraepithelial lesions (HSILs) (2). Preliminary studies (316) have suggested that variants of HPV16 may show varying degrees of association with cervical neoplasia. This may partially explain why some HPV16 infections progress to HSIL or cancer, while others do not. If causal, these associations may be explained by differences in the transcriptional regulation of the virus by different variants, in the biologic activities of the proteins encoded by HPV16 variants (e.g., enhanced transforming abilities of E6/E7), or in the ability of the host to respond immunologically to specific viral epitopes encoded by variants. This last effect is likely to be . . . [Full Text of this Article]

NOTES

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