This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Burk, R. D. Articles by Hildesheim, A. Search for Related Content PubMed PubMed Citation Articles by Burk, R. D. Articles by Hildesheim, A.

Distribution of Human Papillomavirus Types 16 and 18 Variants in Squamous Cell Carcinomas and Adenocarcinomas of the Cervix

Departments of Pediatrics, Microbiology and Immunology, Epidemiology and Population Health and Obstetrics, Gynecology and Women’s Health, Albert Einstein College of Medicine, Bronx, New York 10461 [R. D. B., M. T., L. F.]; Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland 20852-7234 [P. E. G., L. A. B., A. H.]; Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287 [R. J. K.]; Lombardi Cancer Center, Georgetown University, Washington, DC 20057 [W. A. B.]; Graduate Hospital, Philadelphia, Pennsylvania 19146 [M. D. G.]; Yale University School of Medicine, New Haven, Connecticut 06510 [O. C. H., P. E. S.]; Division of Genetic Oncology, George Washington University, Washington, DC 20037 [L. M.]; and Milton S. Hershey Medical Center, Hershey, Pennsylvania 17033 [R. M.]

The distributions of human papillomavirus (HPV) types detected in cervical adenocarcinomas and squamous cell tumors differ. However, whether the distributions of intratypic HPV variants seen in these two histological forms of cervical disease differ is unknown. Our objective was to compare the distribution of HPV intratypic variants observed in squamous cell carcinomas (SCC) and cervical tumors of glandular origin (e.g., adenocarcinomas; AC) for two HPV types commonly observed in cervical tumors, HPV16 and HPV18. Participants in a multicenter case-control study of AC and SCC conducted in the eastern United States were studied. A total of 85 HPV16 and/or HPV18 positive individuals (31 diagnosed with AC, 43 diagnosed with SCC, and 11 population controls) were included. For HPV16-positive individuals, both the noncoding long control region and the E6 open reading frame were sequenced, and classified into phylogenetic-based lineage groups (European, Asian-American, African1, and African2). For HPV18-positive individuals, the long control region region only was sequenced and classified into known intratypic lineages (European, Asian-Amerindian, and African). The distribution of these different intratypic lineages among AC cases, SCC cases, and population controls was compared using standard methods. Non-European HPV16 and/or HPV18 intratypic variants were observed in 42% of ACs compared with 16% of SCCs and 18% of population controls (P = 0.04). Intratypic variants from the Asian-American lineage of HPV16 accounted for the differences seen between histological groups. The differences observed between AC and SCC cases were strongest for HPV16, and persisted in analysis restricted to Caucasian women, suggesting that the effect cannot be explained by differences in the ethnic make-up of AC versus SCC cases. Cervical AC and SCC differ not only with respect to the distribution of HPV types detected but also with respect to intratypic variants observed. Non-European HPV16 and/or HPV18 variants are commonly seen in AC. A possible hormonal mechanism is suggested to explain the observed findings.

This article has been cited by other articles:

				J. Chen, O. K. Macdonald, and D. K. Gaffney Incidence, Mortality, and Prognostic Factors of Small Cell Carcinoma of the Cervix Obstet. Gynecol., June 1, 2008; 111(6): 1394 - 1402. [Abstract] [Full Text] [PDF]

				K. J. Yu, A. Bashirova, M. M. Madeleine, J. Cheng, L. G. Johnson, S. M. Schwartz, M. Carrington, and A. Hildesheim Evaluation of the Association with Cervical Cancer of Polymorphisms in Syndecan-1, a Heparan Sulfate Proteoglycan Involved with Viral Cell Entry Cancer Epidemiol. Biomarkers Prev., November 1, 2007; 16(11): 2504 - 2508. [Abstract] [Full Text] [PDF]

				L. F. Xi, L. A. Koutsky, A. Hildesheim, D. A. Galloway, C. M. Wheeler, R. L. Winer, J. Ho, and N. B. Kiviat Risk for High-Grade Cervical Intraepithelial Neoplasia Associated with Variants of Human Papillomavirus Types 16 and 18 Cancer Epidemiol. Biomarkers Prev., January 1, 2007; 16(1): 4 - 10. [Abstract] [Full Text] [PDF]

				R. D. Burk and R. DeSalle The tango and tangle of human papillomavirus and the human genome. J Natl Cancer Inst, August 2, 2006; 98(15): 1026 - 1027. [Full Text] [PDF]

				A. Narechania, Z. Chen, R. DeSalle, and R. D. Burk Phylogenetic Incongruence among Oncogenic Genital Alpha Human Papillomaviruses J. Virol., December 15, 2005; 79(24): 15503 - 15510. [Abstract] [Full Text] [PDF]

				S. Bodaghi, L. V. Wood, G. Roby, C. Ryder, S. M. Steinberg, and Z.-M. Zheng Could Human Papillomaviruses Be Spread through Blood? J. Clin. Microbiol., November 1, 2005; 43(11): 5428 - 5434. [Abstract] [Full Text] [PDF]

				N. F. Schlecht, R. D. Burk, J. M. Palefsky, H. Minkoff, X. Xue, L. S. Massad, M. Bacon, A. M. Levine, K. Anastos, S. J. Gange, et al. Variants of human papillomaviruses 16 and 18 and their natural history in human immunodeficiency virus-positive women J. Gen. Virol., October 1, 2005; 86(10): 2709 - 2720. [Abstract] [Full Text] [PDF]

				M Zoodsma, I M Nolte, M Schipper, E Oosterom, G van der Steege, E G E de Vries, G J te Meerman, and A G J van der Zee Analysis of the entire HLA region in susceptibility for cervical cancer: a comprehensive study J. Med. Genet., August 1, 2005; 42(8): e49 - e49. [Abstract] [Full Text] [PDF]

				M. Terai, T. Uyama, T. Sugiki, X.-K. Li, A. Umezawa, and T. Kiyono Immortalization of Human Fetal Cells: The Life Span of Umbilical Cord Blood-derived Cells Can Be Prolonged without Manipulating p16INK4a/RB Braking Pathway Mol. Biol. Cell, March 1, 2005; 16(3): 1491 - 1499. [Abstract] [Full Text] [PDF]