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Human papillomavirus in head and neck squamous cell carcinoma.

机译：人乳头瘤病毒在头颈部鳞状细胞癌中。

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The discovery of human papillomavirus (HPV) as a necessary cause of cervical cancer in the 1980's was a great stride in the field of tumor viruses. HPV is now known to cause almost 100% of cervical cancers and during the last two decades, has also been implicated in 20-25% of head and neck squamous cell carcinomas (HNSCC). Unlike cervical cancer, where viral presence is the prominent risk factor, the role of HPV in oral cancers appears to be more complex, as oral cancers have been associated predominantly with alcohol and tobacco exposure. Also unknown is whether HPV is associated with changes in genomic instability in HNSCC. We examined the association of HPV16 DNA and risk for HNSCC in a case only study and that between HPV serology and risk for HNSCC in a case-control study, examining the association between HPV and alcohol and tobacco consumption, patient demographics, and clinical correlates such as tumor location and patient survival. In a case only analysis of HNSCC, we also studied the relationship between viral presence and LINE-1 hypomethylation, a measure of genomic instability in the tumor. We assessed HPV16 DNA status by PCR-amplification of a region of the L1 gene of HPV16. Serology to the L1 protein of HPV6, 11, 16 and 18 was determined by the competitive luminex immunoassay. LINE-1 hypomethylation was measured by PCR amplification of the LINE-1 promoter region, followed by restriction digests. We found that HPV16 DNA was prevalent in 25% of HNSCC cases and was associated with lighter drinking behavior. Antibodies to HPV6 and HPV 16 were associated with increased risk for HNSCC. Among cases, both HPV16 DNA and serology to L1 were associated with an increasing number of oral sex partners, better patient survival, and oropharyngeal location. Hypomethylation of LINE-1 was not associated with HPV status but was associated with smoking and drinking behaviors, gene specific promoter hypermethylation and p53 status. We have shown evidence supporting the idea that HPV6 and HPV16 are important risk factors for HNSCC and that changes in genomic instability may account for distinct clinical and molecular characteristics of HNSCC tumors.
机译：人类乳头瘤病毒（HPV）作为宫颈癌的必要病因的发现在1980年代是肿瘤病毒领域的一大进步。现在已知HPV会导致近100％的宫颈癌，并且在过去的二十年中，HPV也与20-25％的头颈部鳞状细胞癌（HNSCC）有关。与宫颈癌不同，宫颈癌中病毒的存在是最主要的危险因素，HPV在口腔癌中的作用似乎更为复杂，因为口腔癌主要与酒精和烟草接触有关。 HPV是否与HNSCC中基因组不稳定性的变化有关还不清楚。我们仅在个案研究中检查了HPV16 DNA与HNSCC风险之间的关联，在个案对照研究中检查了HPV血清学与HNSCC风险之间的关联，研究了HPV与烟酒和烟草消费，患者人口统计学以及临床相关性之间的关联。取决于肿瘤的位置和患者的生存率。在仅对HNSCC进行分析的情况下，我们还研究了病毒存在与LINE-1低甲基化之间的关系，LINE-1低甲基化是衡量肿瘤中基因组不稳定性的一种方法。我们通过PCR扩增HPV16的L1基因区域来评估HPV16的DNA状态。通过竞争性luminex免疫测定来确定HPV6、11、16和18的L1蛋白的血清学。通过对LINE-1启动子区域进行PCR扩增，然后进行限制性酶切，测量LINE-1的低甲基化程度。我们发现HPV16 DNA在25％的HNSCC病例中普遍存在，并且与较轻的饮酒行为有关。 HPV6和HPV 16抗体与HNSCC风险增加相关。在这些病例中，HPV16 DNA和L1血清学都与越来越多的口交伴侣，更好的患者生存率和口咽位置有关。 LINE-1的低甲基化与HPV状态无关，但与吸烟和饮酒行为，基因特异性启动子高甲基化和p53状态有关。我们已经显示出证据支持以下观点：HPV6和HPV16是HNSCC的重要危险因素，而基因组不稳定性的变化可能解释了HNSCC肿瘤的独特临床和分子特征。

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