Gingerich Morgan A, Smith Joshua D, Michmerhuizen Nicole L, Ludwig Megan, Devenport Samantha, Matovina Chloe, Brenner Chad, Chinn Steven B
Program in Cellular and Molecular Biology, University of Michigan Medical School, Ann Arbor, Michigan.
Department of Otolaryngology - Head and Neck Surgery, University of Michigan Medical School, Ann Arbor, Michigan.
Head Neck. 2018 May;40(5):943-954. doi: 10.1002/hed.25057. Epub 2018 Feb 10.
The past 2 decades have seen an increased incidence of head and neck squamous cell carcinoma (HNSCC) in a nontraditional, low-risk patient population (ie, ≤45 years of age, no substance use history), owing to a combination of human papillomavirus (HPV) infection and individual genetic variation.
Articles positing genetic variants as contributing factors in HNSCC incidence in low-risk, nontraditional patients were identified using a PubMed search, reviewed in detail, and concisely summarized herein.
Recent data suggest that common polymorphisms in DNA repair enzymes, cell-cycle control proteins, apoptotic pathway members, and Fanconi anemia-associated genes likely modulate susceptibility to HNSCC development in low-risk, nontraditional patients.
At present, there is a lack of robust, comprehensive data on genetic drivers of oncogenesis in low-risk patients and a clear need for further research on genetic alterations underlying the rising incidence of HNSCC in low-risk, nontraditional patients.
在过去20年中，由于人乳头瘤病毒（HPV）感染和个体基因变异共同作用，在非传统的低风险患者群体（即年龄≤45岁、无物质使用史）中，头颈部鳞状细胞癌（HNSCC）的发病率有所上升。
通过PubMed检索，找出将基因变异作为低风险、非传统患者发生HNSCC的影响因素的文章，并进行详细审阅，在此进行简要总结。
近期数据表明，DNA修复酶、细胞周期调控蛋白、凋亡途径成员以及范可尼贫血相关基因中的常见多态性可能会调节低风险、非传统患者发生HNSCC的易感性。
目前，缺乏关于低风险患者肿瘤发生的基因驱动因素的有力、全面的数据，并且显然需要进一步研究低风险、非传统患者中HNSCC发病率上升背后的基因改变。
