D'Souza Gypsyamber, Kreimer Aimee R, Viscidi Raphael, Pawlita Michael, Fakhry Carole, Koch Wayne M, Westra William H, Gillison Maura L
Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, USA.
N Engl J Med. 2007 May 10;356(19):1944-56. doi: 10.1056/NEJMoa065497.
Substantial molecular evidence suggests a role for human papillomavirus (HPV) in the pathogenesis of oropharyngeal squamous-cell carcinoma, but epidemiologic data have been inconsistent.
We performed a hospital-based, case-control study of 100 patients with newly diagnosed oropharyngeal cancer and 200 control patients without cancer to evaluate associations between HPV infection and oropharyngeal cancer. Multivariate logistic-regression models were used for case-control comparisons.
A high lifetime number of vaginal-sex partners (26 or more) was associated with oropharyngeal cancer (odds ratio, 3.1; 95% confidence interval [CI], 1.5 to 6.5), as was a high lifetime number of oral-sex partners (6 or more) (odds ratio, 3.4; 95% CI, 1.3 to 8.8). The degree of association increased with the number of vaginal-sex and oral-sex partners (P values for trend, 0.002 and 0.009, respectively). Oropharyngeal cancer was significantly associated with oral HPV type 16 (HPV-16) infection (odds ratio, 14.6; 95% CI, 6.3 to 36.6), oral infection with any of 37 types of HPV (odds ratio, 12.3; 95% CI, 5.4 to 26.4), and seropositivity for the HPV-16 L1 capsid protein (odds ratio, 32.2; 95% CI, 14.6 to 71.3). HPV-16 DNA was detected in 72% (95% CI, 62 to 81) of 100 paraffin-embedded tumor specimens, and 64% of patients with cancer were seropositive for the HPV-16 oncoprotein E6, E7, or both. HPV-16 L1 seropositivity was highly associated with oropharyngeal cancer among subjects with a history of heavy tobacco and alcohol use (odds ratio, 19.4; 95% CI, 3.3 to 113.9) and among those without such a history (odds ratio, 33.6; 95% CI, 13.3 to 84.8). The association was similarly increased among subjects with oral HPV-16 infection, regardless of their tobacco and alcohol use. By contrast, tobacco and alcohol use increased the association with oropharyngeal cancer primarily among subjects without exposure to HPV-16.
Oral HPV infection is strongly associated with oropharyngeal cancer among subjects with or without the established risk factors of tobacco and alcohol use.
大量分子证据表明人乳头瘤病毒（HPV）在口咽鳞状细胞癌的发病机制中起作用，但流行病学数据并不一致。
我们进行了一项基于医院的病例对照研究，纳入100例新诊断的口咽癌患者和200例无癌症的对照患者，以评估HPV感染与口咽癌之间的关联。采用多因素逻辑回归模型进行病例对照比较。
一生中有大量阴道性伴侣（26个或更多）与口咽癌相关（比值比，3.1；95%置信区间[CI]，1.5至6.5），一生中有大量口交性伴侣（6个或更多）也与之相关（比值比，3.4；95%CI，1.3至8.8）。关联程度随阴道性伴侣和口交性伴侣数量的增加而增加（趋势P值分别为0.002和0.009）。口咽癌与口腔HPV16型（HPV-16）感染显著相关（比值比，14.6；95%CI，6.3至36.6），与37种HPV中的任何一种口腔感染相关（比值比，12.3；95%CI，5.4至26.4），以及与HPV-16 L1衣壳蛋白血清阳性相关（比值比，32.2；95%CI，14.6至71.3）。在100例石蜡包埋的肿瘤标本中，72%（95%CI，6到81）检测到HPV-16 DNA，64%的癌症患者HPV-16癌蛋白E6、E7或两者血清呈阳性。在有大量吸烟和饮酒史的受试者中（比值比，19.4；95%CI，3.3至113.9）以及无此类病史的受试者中（比值比，33.6；95%CI，13.3至84.8），HPV-16 L1血清阳性与口咽癌高度相关。无论吸烟和饮酒情况如何，在口腔HPV-16感染的受试者中，这种关联同样增加。相比之下，吸烟和饮酒主要在未接触HPV-16的受试者中增加与口咽癌的关联。
无论有无吸烟和饮酒等既定危险因素，口腔HPV感染与口咽癌均密切相关。
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