Ernster Joel A, Sciotto Cosimo G, O'Brien Maureen M, Finch Jack L, Robinson Linda J, Willson Thomas, Mathews Michael
Department of Otolaryngology-Head and Neck Surgery, University of Colorado Health Sciences Center, Denver, CO 80909, USA.
Laryngoscope. 2007 Dec;117(12):2115-28. doi: 10.1097/MLG.0b013e31813e5fbb.
OBJECTIVES/HYPOTHESIS: To document the increasing incidence of oropharyngeal (OP) cancer and to provide evidence that this increase is caused by oncogenic human papilloma virus (HPV).
Epidemiologic review and retrospective case series analysis.
We collected data from Colorado and the United States comparing the average annual age-adjusted incidence rates of OP and non-OP head and neck cancer between the periods 1980 to 1990 and 1991 to 2001. We obtained data on 72 patients with OP cancer from a single county in Colorado, from 1980 through 2004. HPV status was determined by DNA-polymerase chain reaction. We assessed disease-specific survival.
The average annual age-adjusted incidence of OP cancer in males in Colorado increased from 2.54 per 100,000 to 3.47 (P < .05) or 36.6%, whereas the U.S. rate increased from 4.34 to 4.81 (P < .05) or 10.8%. The rates in females and the rates of non-OP head and neck cancer decreased. Of the 72 cases, 50 (69%) were positive for HPV subtype 16. The ratio of HPV-positive to HPV-negative cases prior to 1995 was 0.72 (8:11) but was 3.81 (42:11) afterward. Survival was positively affected by HPV status (hazard ratio of 0.15, confidence intervals 0.07-0.36, P < .001). Disease-specific survival was 83% in the HPV-positive patients and 15% in the HPV-negative group.
OP cancer incidence is increasing in Colorado males and to a lesser extent in U.S. males. The HPV-positive OP cancer cases were more frequent in the later years of the study. Disease-specific survival was much better in the HPV-positive patients, confirming that HPV testing defines a unique subset of patients. These findings suggest that HPV oncogenesis accounts for the increase in average annual age-adjusted incidence of OP cancer.
目的/假设：记录口咽癌（OP）发病率的上升情况，并提供证据证明这种上升是由致癌性人乳头瘤病毒（HPV）引起的。
流行病学综述和回顾性病例系列分析。
我们收集了科罗拉多州和美国的数据，比较了1980年至1990年以及1991年至2001年期间口咽癌和非口咽头颈癌的年龄调整后年均发病率。我们获取了1980年至2004年期间科罗拉多州一个县72例口咽癌患者的数据。通过DNA聚合酶链反应确定HPV状态。我们评估了疾病特异性生存率。
科罗拉多州男性口咽癌的年龄调整后年均发病率从每10万人2.54例增至3.47例（P <.05），即增长了36.6%，而美国的发病率从4.34例增至4.81例（P <.05），即增长了10.8%。女性发病率以及非口咽头颈癌的发病率下降。在这72例病例中，50例（69%）HPV 16型呈阳性。1995年之前HPV阳性与阴性病例的比例为0.72（8:11），但之后为3.81（42:11）。生存率受HPV状态的正向影响（风险比为0.15，置信区间为0.07 - 0.36，P <.001）。HPV阳性患者的疾病特异性生存率为83%，HPV阴性组为15%。
科罗拉多州男性口咽癌发病率在上升，美国男性上升幅度较小。在研究后期，HPV阳性的口咽癌病例更为常见。HPV阳性患者的疾病特异性生存率要好得多，证实HPV检测确定了一个独特的患者亚组。这些发现表明，HPV致癌作用导致了口咽癌年龄调整后年均发病率的上升。
