© 2003 by Oxford University Press
© 2003 Oxford University Press
ARTICLE |
Human Papillomavirus and Oral Cancer: The International Agency for Research on Cancer Multicenter Study
For the IARC Multicenter Oral Cancer Study Group
Affiliations of authors: International Agency for Research on Cancer, Lyon, France (RH, NM, SF); Proyecto Epidemiológico Guanacaste, Costa Rican Foundation for Health Sciences, San José, Costa Rica (RH); Institut Català d’Oncologia, Barcelona, Spain (XC, FXB); Deutsches Krebsforschungszentrum, Heidelberg, Germany (MP, UR); Cancer Center and Institute of Oncology, Warsaw, Poland (JL); Queen’s University Belfast, Northern Ireland, United Kingdom (FK); Regional Cancer Center, Trivandrum, India (PB); Cancer Institute, Women India Association, Chennai, India (TR); Kidwai Memorial Institute of Oncology, Bangalore, India (HS); Sydney Head and Neck Cancer Institute, Royal Prince Alfred Hospital and University of Sydney, Sydney, Australia (BR); McGill University, Montreal, Canada (JP); Instituto Nacional de Oncologia y Radiobiologia, Havana, Cuba (LF); Toombak and Smoking Research Center, Khartoum, Sudan (AI); Escuela Andaluza de Salud Publica, Granada, Spain (MJS); Facultad de Medicina, Seville, Spain (AN); Centro di Riferimento Oncologico di Aviano, Aviano, Italy (RT); Istituto di Ricerche Farmacologiche "Mario Negri," Milan, Italy (AT); Vrije Universiteit Medical Center, Amsterdam, The Netherlands (PJFS, CJLMM); Stanley Division of Developmental Neurovirology, Department of Pediatrics, The Johns Hopkins University School of Medicine, Baltimore, MD (RV).
Correspondence to: Rolando Herrero, MD, PhD, Proyecto Epidemiológico Guanacaste, P.O. Box 125-6151, San José, Costa Rica (e-mail: rherrero{at}amnet.co.cr)
Background: Human papillomavirus (HPV), the causal agent of cervical cancer, appears to be involved in the etiology of cancer of the oral cavity and oropharynx. To investigate these associations, we conducted a multicenter case-control study of cancer of the oral cavity and oropharynx in nine countries. Methods: We recruited 1670 case patients (1415 with cancer of the oral cavity and 255 with cancer of the oropharynx) and 1732 control subjects and obtained an interview, oral exfoliated cells, and blood from all participants and fresh biopsy specimens from case patients. HPV DNA was detected by polymerase chain reaction (PCR). Antibodies against HPV16 L1, E6, and E7 proteins in plasma were detected with enzyme-linked immunosorbent assays. Multivariable models were used for case-control and case-case comparisons. Results: HPV DNA was detected in biopsy specimens of 3.9% (95% confidence interval [CI] = 2.5% to 5.3%) of 766 cancers of the oral cavity with valid PCR results and 18.3% (95% CI = 12.0% to 24.7%) of 142 cancers of the oropharynx (oropharynx and tonsil combined) with valid PCR results. HPV DNA in cancer biopsy specimens was detected less frequently among tobacco smokers and paan chewers and more frequently among subjects who reported more than one sexual partner or who practiced oral sex. HPV16 DNA was found in 94.7% of HPV DNA-positive case patients. HPV DNA in exfoliated cells was not associated with cancer risk or with HPV DNA detection in biopsy specimens. Antibodies against HPV16 L1 were associated with risk for cancers of the oral cavity (odds ratio [OR] = 1.5, 95% CI = 1.1 to 2.1) and the oropharynx (OR = 3.5, 95% CI = 2.1 to 5.9). Antibodies against HPV16 E6 or E7 were also associated with risk for cancers of the oral cavity (OR = 2.9, 95% CI = 1.7 to 4.8) and the oropharynx (OR = 9.2, 95% CI = 4.8 to 17.7). Conclusions: HPV appears to play an etiologic role in many cancers of the oropharynx and possibly a small subgroup of cancers of the oral cavity. The most common HPV type in genital cancers (HPV16) was also the most common in these tumors. The mechanism of transmission of HPV to the oral cavity warrants further investigation.
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