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Combined p53-related genetic variants together with HPV infection increase oral cancer risk

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机构: [1]Department of Head and Neck Surgery, The University of Texas M. D. Anderson Cancer Center, Houston, TX [2]Department of Medical Imaging, Jinling Hospital, Medical School of Nanjing University, Nanjing, China [3]Department of Epidemiology, The University of Texas M. D. Anderson Cancer Center, Houston, TX [4]Department of Otolaryngology Head and Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing, China [5]Department of Tumor Biological Treatment, The Third Affiliated Hospital, Soochow University, Changzhou, Jiangsu, China
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关键词: p53 p73 MDM2 MDM4 HPV infection oral cancer

摘要:
To explore the role of polymorphisms of p53-related genes in etiology of oral cancer, we investigated joint effects of seven putatively functional polymorphisms of p53 (codon 72 Arg/Pro), p73 (4/14 GC/AT), murine double minute 2 gene (MDM2; A2164G and T2580G) and MDM4 (rs11801299 G > A, rs10900598 G > T and rs1380576 C > G) on risk of human papillomavirus (HPV)16-associated oral cancer in a casecontrol study with 325 cases and 335 cancer-free controls. We found that HPV16 seropositivity alone was associated with an increased risk of oral cancer [adjusted odds ratio (OR), 3.1; 95% confidence interval (CI), 2.14.6]. After combining genotypes of seven polymorphisms and using the low-risk group (03 combined risk genotypes) and HPV16 seronegativity as the reference group, the medium-risk (4 combined risk genotypes) and high-risk groups (57 combined risk genotypes) and HPV16 seronegativity were associated with only an OR of 1.6 (95% CI, 1.12.5) and 1.2 (95% CI, 0.71.9) for oral cancer risk, respectively, whereas the low-risk, medium-risk and high-risk groups and HPV16 seropositivity were significantly associated with a higher OR of 2.1 (95% CI, 1.23.6), 4.0 (95% CI, 1.89.1) and 19.1 (95% CI, 5.764.2), respectively. Notably, such effect modification by these combined risk genotypes was particularly pronounced in young subjects (aged < 50 years), never smokers and patients with oropharyngeal cancer. Taken together, these findings suggest that the combined risk genotypes of p53-related genes may modify risk of HPV16-associated oral cancer, especially in young patients, never-smokers and patients with oropharyngeal cancer. Larger studies are needed to validate our findings.

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出版当年[2011]版:
大类 | 2 区 医学
小类 | 2 区 肿瘤学
最新[2023]版:
大类 | 2 区 医学
小类 | 2 区 肿瘤学
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出版当年[2010]版:
Q1 ONCOLOGY
最新[2023]版:
Q1 ONCOLOGY

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第一作者机构: [1]Department of Head and Neck Surgery, The University of Texas M. D. Anderson Cancer Center, Houston, TX [2]Department of Medical Imaging, Jinling Hospital, Medical School of Nanjing University, Nanjing, China
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通讯机构: [1]Department of Head and Neck Surgery, The University of Texas M. D. Anderson Cancer Center, Houston, TX [3]Department of Epidemiology, The University of Texas M. D. Anderson Cancer Center, Houston, TX [*1]Univ Texas MD Anderson Canc Ctr, Dept Head & Neck Surg, Unit 1445, 1515 Holcombe Blvd, Houston, TX 77030 USA
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