Pintos Javier, Black Martin J, Sadeghi Nader, Ghadirian Parviz, Zeitouni Anthony G, Viscidi Raphael P, Herrero Rolando, Coutlée François, Franco Eduardo L
Division of Cancer Epidemiology, McGill University, Montreal, Canada.
Oral Oncol. 2008 Mar;44(3):242-50. doi: 10.1016/j.oraloncology.2007.02.005. Epub 2007 Apr 27.
The objective of the present study was to examine the association between human papillomavirus (HPV) infection and risk of developing oral cancer. The investigation followed a hospital-based case-control design. Cases consisted of newly diagnosed patients with squamous cell carcinoma of the oral cavity and oropharynx. Controls were frequency matched to cases on gender, age, and hospital. Subjects were interviewed to elicit information on putative risk factors. Oral exfoliated cells were tested for detection of HPV DNA by the PGMY09/11 polymerase chain reaction protocol. Serum antibodies against HPV 16, 18, and 31 viral capsids were detected using an immunoassay technique. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CI) of oral cancer according to HPV exposure variables. HPV DNA was detected in 19% of cases (14 out of 72), and 5% of controls (six out of 129). Among tonsil-related cancers (palatine tonsil and base of tongue) viral DNA was detected in 43% of cases (nine out of 21). The OR for tonsil-related cancers for high-risk HPV types was 19.32 (95%CI: 2.3-159.5), after adjustment for socio-demographic characteristics, tobacco, and alcohol consumption. The equivalent OR for HPV 16 seropositivity was 31.51 (95%CI: 4.5-219.7). The ORs of non-tonsillar oral cancers for high risk HPV DNA in oral cells and for seropositivity were 2.14 (95%CI: 0.4-13.0) and 3.16 (95%CI: 0.8-13.0), respectively. These results provide evidence supporting a strong causal association between HPV infection and tonsil-related cancers. The evidence for an etiologic link is less clear for non-tonsillar oral cancers.
本研究的目的是检验人乳头瘤病毒（HPV）感染与患口腔癌风险之间的关联。该调查采用基于医院的病例对照设计。病例包括新诊断的口腔和口咽鳞状细胞癌患者。对照在性别、年龄和医院方面与病例进行频数匹配。对受试者进行访谈以获取有关假定风险因素的信息。采用PGMY09/11聚合酶链反应方案检测口腔脱落细胞中的HPV DNA。使用免疫测定技术检测针对HPV 16、18和31病毒衣壳的血清抗体。根据HPV暴露变量，采用逻辑回归估计口腔癌的比值比（OR）和95%置信区间（CI）。19%的病例（72例中的14例）检测到HPV DNA，5%的对照（129例中的6例）检测到HPV DNA。在与扁桃体相关的癌症（腭扁桃体和舌根）中，43%的病例（21例中的9例）检测到病毒DNA。在调整了社会人口统计学特征、烟草和酒精消费因素后，高危HPV类型导致扁桃体相关癌症的OR为19.32（95%CI：2.3 - 159.5）。HPV 16血清阳性的等效OR为31.51（95%CI：4.5 - 219.7）。口腔细胞中高危HPV DNA导致非扁桃体口腔癌的OR为2.14（95%CI：0.4 - 13.0），血清阳性导致非扁桃体口腔癌的OR为3.16（95%CI：0.8 - 13.0）。这些结果提供了证据，支持HPV感染与扁桃体相关癌症之间存在强烈的因果关联。对于非扁桃体口腔癌，病因学联系的证据不太明确。
