Department of Environmental Health Sciences, University of Michigan, Ann Arbor, MI, United States; Department of Otolaryngology - Head and Neck Surgery, University of Michigan, Ann Arbor, MI, United States.
Pathology, The University of Michigan Health System, Ann Arbor, MI, United States; Department of Otolaryngology - Head and Neck Surgery, University of Michigan, Ann Arbor, MI, United States.
J Clin Virol. 2020 Nov;132:104637. doi: 10.1016/j.jcv.2020.104637. Epub 2020 Sep 9.
Human papillomavirus (HPV) is etiologically linked to increasing oropharyngeal squamous cell carcinoma (OPSCC) rates in the Western world. However, the role of HPV in Southeast Asia, a high incidence region, hasn't been assessed.
96 formalin-fixed, paraffin-embedded (FFPE) tissue blocks and corresponding patient data were obtained from Srinagarind Hospital, Thailand from 2012-2017. DNA from areas of 70 %+ cellularity were genotyped using polymerase chain reaction (PCR) and stained for p16, a surrogate marker for HPV. Inverse probability weights based on data from the hospital-based cancer registry were used in statistical analyses. Adjusted linear regression was used to assess changes in OPSCC HPV prevalence and conduct projections. Kaplan-Meier and Cox proportional hazard models were used to determine HPV-specific survival differences.
14 patients exhibited monoinfection with HPV16, two with HPV18 and one was HPV16/18 coinfected. PCR results were in agreement with p16 staining. On average, HPV + patients were more likely to have tonsil cancer (p-value:0.002). HPV prevalence increased by 2% annually (pvalue: 0.01), from 16 % in 2012 to 26 % in 2017. At the current rate, OPSCC HPV positivity will exceed 50 % by 2030. HPV positivity was shown to be protective in Kaplan-Meier (log-rank p = 0.02) and sex, age and stage adjusted Cox models (HR:0.34 [95 %CI:0.22, 0.52]).
Given the increased prevalence and similarities in presentation of HPV + OPSCC to those observed in Western countries, the data suggest the adaptation of p16 staining and subsequent restaging of OPSCC tumors as suggested by the American Joint Committee on Cancer in Southeast Asia.
人乳头瘤病毒（HPV）与西方世界口咽鳞状细胞癌（OPSCC）发病率的增加有关。然而，HPV 在东南亚这一高发地区的作用尚未得到评估。
从 2012 年至 2017 年，从泰国诗里叻医院获得了 96 个福尔马林固定、石蜡包埋（FFPE）组织块和相应的患者数据。使用聚合酶链反应（PCR）对具有 70%+细胞密度的区域的 DNA 进行基因分型，并对 p16 进行染色，p16 是 HPV 的替代标志物。基于医院癌症登记处的数据，使用逆概率权重进行统计分析。调整线性回归用于评估 OPSCC HPV 患病率的变化并进行预测。Kaplan-Meier 和 Cox 比例风险模型用于确定 HPV 特异性生存差异。
14 例患者表现为 HPV16 单一感染，2 例患者为 HPV18 感染，1 例患者为 HPV16/18 合并感染。PCR 结果与 p16 染色一致。平均而言，HPV+患者更有可能患有扁桃体癌（p 值：0.002）。HPV 患病率每年增加 2%（p 值：0.01），从 2012 年的 16%增加到 2017 年的 26%。按照目前的速度，到 2030 年 OPSCC HPV 阳性率将超过 50%。Kaplan-Meier（对数秩 p=0.02）和性别、年龄和分期调整的 Cox 模型显示 HPV 阳性具有保护作用（HR：0.34 [95%CI：0.22, 0.52]）。
鉴于 HPV+OPSCC 的患病率增加以及与西方国家观察到的表现相似，数据表明在东南亚地区应采用 p16 染色并根据美国癌症联合委员会的建议对 OPSCC 肿瘤进行重新分期。
