Anil K. Chaturvedi, Eric A. Engels, Ruth M. Pfeiffer, Nicolas Wentzensen, William F. Anderson, and Philip S. Rosenberg, National Cancer Institute; Sean Altekruse, Surveillance, Epidemiology, and End Results Program, National Cancer Institute, Rockville, MD; Brenda Y. Hernandez and Marc T. Goodman, Cancer Research Center of Hawaii, Honolulu, HI; Weihong Xiao, Esther Kim, Bo Jiang, and Maura L. Gillison, The Ohio State University, Columbus, OH; Maria Sibug-Saber, Wendy Cozen, and Lihua Liu, University of Southern California at Los Angeles, Los Angeles; Richard C. Jordan, University of California and Radiation Therapy Oncology Group Biospecimen Resource, San Francisco, CA; and Charles F. Lynch, University of Iowa, Iowa City, IA.
J Clin Oncol. 2023 Jun 10;41(17):3081-3088. doi: 10.1200/JCO.22.02625.
Recent increases in incidence and survival of oropharyngeal cancers in the United States have been attributed to human papillomavirus (HPV) infection, but empirical evidence is lacking.
HPV status was determined for all 271 oropharyngeal cancers (1984-2004) collected by the three population-based cancer registries in the Surveillance, Epidemiology, and End Results (SEER) Residual Tissue Repositories Program by using polymerase chain reaction and genotyping (Inno-LiPA), HPV16 viral load, and HPV16 mRNA expression. Trends in HPV prevalence across four calendar periods were estimated by using logistic regression. Observed HPV prevalence was reweighted to all oropharyngeal cancers within the cancer registries to account for nonrandom selection and to calculate incidence trends. Survival of HPV-positive and HPV-negative patients was compared by using Kaplan-Meier and multivariable Cox regression analyses.
HPV prevalence in oropharyngeal cancers significantly increased over calendar time regardless of HPV detection assay ( trend < .05). For example, HPV prevalence by Inno-LiPA increased from 16.3% during 1984 to 1989 to 71.7% during 2000 to 2004. Median survival was significantly longer for HPV-positive than for HPV-negative patients (131 20 months; log-rank < .001; adjusted hazard ratio, 0.31; 95% CI, 0.21 to 0.46). Survival significantly increased across calendar periods for HPV-positive ( = .003) but not for HPV-negative patients ( = .18). Population-level incidence of HPV-positive oropharyngeal cancers increased by 225% (95% CI, 208% to 242%) from 1988 to 2004 (from 0.8 per 100,000 to 2.6 per 100,000), and incidence for HPV-negative cancers declined by 50% (95% CI, 47% to 53%; from 2.0 per 100,000 to 1.0 per 100,000). If recent incidence trends continue, the annual number of HPV-positive oropharyngeal cancers is expected to surpass the annual number of cervical cancers by the year 2020.
Increases in the population-level incidence and survival of oropharyngeal cancers in the United States since 1984 are caused by HPV infection.
美国口咽癌的发病率和存活率的最近增长归因于人类乳头瘤病毒（HPV）感染，但缺乏经验证据。
通过聚合酶链反应和基因分型（Inno-LiPA）、HPV16 病毒载量和 HPV16 mRNA 表达，使用来自监测、流行病学和最终结果（SEER）残余组织储存库计划的三个基于人群的癌症登记处收集的所有 271 例口咽癌（1984-2004 年）确定 HPV 状态。使用逻辑回归估计四个日历期间 HPV 流行率的趋势。通过重新加权癌症登记处中所有口咽癌的观察 HPV 流行率，以考虑非随机选择并计算发病率趋势。使用 Kaplan-Meier 和多变量 Cox 回归分析比较 HPV 阳性和 HPV 阴性患者的生存情况。
无论 HPV 检测方法如何（趋势<.05），口咽癌中的 HPV 流行率都随着时间的推移而显著增加。例如，通过 Inno-LiPA 检测的 HPV 流行率从 1984 年至 1989 年的 16.3%增加到 2000 年至 2004 年的 71.7%。HPV 阳性患者的中位生存期明显长于 HPV 阴性患者（131 20 个月；对数秩<.001；调整后的危险比，0.31；95%CI，0.21 至 0.46）。HPV 阳性患者的生存时间随着时间的推移显著增加（=0.003），而 HPV 阴性患者则没有（=0.18）。HPV 阳性口咽癌的人群发病率从 1988 年到 2004 年增加了 225%（95%CI，208%至 242%）（从每 100,000 人 0.8 例增加到每 100,000 人 2.6 例），而 HPV 阴性癌症的发病率下降了 50%（95%CI，47%至 53%；从每 100,000 人 2.0 例降至每 100,000 人 1.0 例）。如果最近的发病率趋势持续下去，到 2020 年，HPV 阳性口咽癌的年发病数预计将超过宫颈癌的年发病数。
自 1984 年以来，美国口咽癌的人群发病率和存活率的增加是由 HPV 感染引起的。
