Chen X, Gao L, Sturgis E M, Liang Z, Zhu Y, Xia X, Zhu X, Chen X, Li G, Gao Z
Department of Otolaryngology-Head and Neck Surgery, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.
Department of Head and Neck Surgery, The University of Texas MD Anderson Cancer Center, Houston, USA.
Ann Oncol. 2017 May 1;28(5):1105-1110. doi: 10.1093/annonc/mdx027.
Molecular evidence suggests that human papillomavirus (HPV) has a role in the etiology of oropharyngeal squamous cell carcinoma. However, the role of HPV in laryngeal squamous cell carcinoma (LSCC) is unclear.
We conducted a case-control study using tumor tissue specimens from 300 LSCC patients and vocal cord polyp specimens from 300 cancer-free controls. HPV genotype, HPV16 viral load and viral integration status, and p16 expression were determined.
The prevalence of HPV (all types) was higher in cases than controls [21 (7.0%) versus 10 (3.3%), adjusted odds ratio (aOR) 2.37, 95% CI 1.08-5.21]. The prevalence of HPV16 was higher in cases than controls [20 (6.7%) versus 8 (2.7%), aOR 2.84, 95% CI 1.21-6.68]. The risk of LSCC associated with HPV16 DNA positivity was even higher in patients aged 55 years or younger (aOR 3.52, 95% CI 1.07-11.54), males (aOR 4.74, 95% CI 1.33-16.90), never-smokers (aOR 5.57, 95% CI 1.41-22.10), and never-drinkers (aOR 3.72, 95% CI 1.09-12.72). HPV DNA was partly or fully integrated in all 20 HPV16-positive cases but was episomal in all 8 HPV16-positive controls; however, the HPV16-positive cases and controls had similar viral loads (P = 0.28). P16 immunostaining was positive in 31 of the 300 cases (10.3%) and negative in all 300 controls.
These results suggest that prior infection with HPV16 may play a role in the etiology of some LSCC. This larger case-control study will offer for the first time the possibility to address in depth the understanding of a tissue-specific role of HPV in laryngeal carcinogenesis. Further studies with larger samples are needed to confirm these findings.
分子证据表明，人乳头瘤病毒（HPV）在口咽鳞状细胞癌的病因学中起作用。然而，HPV在喉鳞状细胞癌（LSCC）中的作用尚不清楚。
我们进行了一项病例对照研究，使用了300例LSCC患者的肿瘤组织标本和300例无癌对照的声带息肉标本。测定了HPV基因型、HPV16病毒载量和病毒整合状态以及p16表达。
病例组中HPV（所有类型）的患病率高于对照组[21例（7.0%）对10例（3.3%），校正优势比（aOR）2.37，95%可信区间1.08 - 5.21]。病例组中HPV16的患病率高于对照组[20例（6.7%）对8例（2.7%），aOR 2.84，95%可信区间1.21 - 6.68]。在55岁及以下的患者（aOR 3.52，95%可信区间1.07 - 11.54）、男性（aOR 4.74，95%可信区间1.33 - 16.90）、从不吸烟者（aOR 5.57，95%可信区间1.41 - 22.10）和从不饮酒者（aOR 3.72，95%可信区间1.09 - 12.72）中，与HPV16 DNA阳性相关的LSCC风险甚至更高。在所有20例HPV16阳性病例中，HPV DNA部分或完全整合，但在所有8例HPV16阳性对照中为游离型；然而，HPV16阳性病例和对照的病毒载量相似（P = 0.28）。300例病例中有31例（10.3%）p16免疫染色呈阳性，所有300例对照均为阴性。
这些结果表明，既往HPV16感染可能在某些LSCC的病因学中起作用。这项更大规模的病例对照研究将首次为深入了解HPV在喉癌发生中的组织特异性作用提供可能。需要进一步进行更大样本量的研究来证实这些发现。
