Case–Control Study of Human Papillomavirus and Oropharyngeal Cancer
Gypsyamber D'Souza, Ph.D., Aimee R. Kreimer, Ph.D., Raphael Viscidi, M.D., Michael Pawlita, M.D., Carole Fakhry, M.D., M.P.H., Wayne M. Koch, M.D., William H. Westra, M.D., and Maura L. Gillison, M.D., Ph.D.
TRANSLATED TITLE: Fall–Kontroll-Studie zum humanen Papillomvirus und Oropharynxkarzinom
Hintergrund Es wurde der hinreichende molekulare Nachweis erbracht,dass das humane Papillomvirus (HPV) in der Pathogenese einesPlattenepithelkarzinoms des Oropharynx eine Rolle spielt, jedochsind die epidemiologischen Daten nicht schlüssig.
Methoden Wir führten eine krankenhausbasierte Fall–Kontroll-Studiean 100 Patienten mit frisch diagnostiziertem Oropharynxkarzinomund 200 Kontrollpersonen ohne Karzinom durch, um Zusammenhängezwischen einer HPV-Infektion und dem Auftreten eines Oropharynxkarzinomszu definieren. Multivariate logistische Regressionsmodelle wurdenfür die Erstellung von Fall–Kontroll-Vergleichenverwendet.
Ergebnisse Eine hohe Zahl an Vaginalsex-Partnern währenddes Lebens (26 oder mehr) war mit einem Oropharynxkarzinom (OddsRatio 3,1; 95%-Konfidenzintervall [KI] 1,5 bis 6,5) ebenso assoziiertwie eine hohe Zahl an Oralsex-Partnern während des Lebens(6 oder mehr) (Odds Ratio 3,4; 95%-KI 1,3 bis 8,8). Der Gradder Assoziation stieg mit der Anzahl an Vaginalsex- und Oralsex-Partnern(p-Werte für den Trend 0,002 bzw. 0,009). Ein Oropharynxkarzinomwar signifikant mit einer oralen Infektion mit dem HPV-Typ 16(HPV-16) (Odds Ratio 14,6; 95%-KI 6,3 bis 36,6), einer oralenInfektion mit einem sonstigen von 37 HPV-Typen (Odds Ratio 12,3;95%-KI 5,4 bis 26,4) und der Seropositivität für dasHPV-16 L1 Capsidprotein (Odds Ratio 32,2; 95%-KI 14,6 bis 71,3)assoziiert. HPV-16-DNS wurde in 72% (95%-KI 62 bis 81) von 100in Paraffin-eingebetteten Tumorproben nachgewiesen, und 64%der Tumorpatienten waren für das HPV-16 Onkoprotein E6bzw. E7 oder beide seropositiv. HPV-16 L1-Seropositivitätwar für Patienten mit starkem Tabak- und Alkoholkonsumin der Anamnese hochgradig mit einem Oropharynxkarzinom (OddsRatio 19,4; 95%-KI 3,3 bis 113,9) assoziiert, jedoch auch fürPatienten ohne diese Anamnese (Odds Ratio 33,6; 95%-KI 13,3bis 84,8). Die Assoziation war in vergleichbarer Weise fürPatienten mit oraler HPV-16-Infektion erhöht, unabhängigvon deren Tabak- und Alkoholkonsum. Dagegen steigerten Tabak-und Alkoholkonsum das Risiko für ein Oropharynxkarzinominsbesondere bei Patienten ohne HPV-16-Exposition.
Schlussfolgerungen Eine orale HPV-Infektion ist hochgradig mitdem Auftreten eines Oropharynxkarzinoms bei Patienten mit oderohne die bekannten Risikofaktoren von Tabak- oder Alkoholkonsumassoziiert.
Source Information
From the Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health (G.D.); the Departments of Pediatrics (R.V.), Otolaryngology–Head and Neck Surgery (C.F., W.M.K.), and Pathology (W.H.W.), Johns Hopkins Hospital; and the Division of Viral Oncology, Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University (M.L.G.) — all in Baltimore; the Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (A.R.K.); and the Infection and Cancer Control Program, German Cancer Research Center, Heidelberg, Germany (M.P.).
Address reprint requests to Dr. Gillison at Johns Hopkins University, Cancer Research Bldg. I, Rm. 3M 54A, 1650 Orleans St., Baltimore, MD 21231, or to gillima{at}jhmi.edu.
Human Papillomavirus and Oropharyngeal Cancer
Ukpo O. C., Moore E. J., Smith D. I., Williams H., Higgins C. D., Crawford D. H., Braakhuis B. J., Snijders P. J., Leemans C. R., Gillison M. L.
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N Engl J Med 2007;
357:1156-1158, Sep 13, 2007.
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