2011
DOI: 10.1309/lm532dspduxirjvn
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Association of TNF-α Gene Promoter Polymorphisms With Susceptibility of Cervical Cancer in Southwest China

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Cited by 11 publications
(8 citation statements)
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“…In our meta-analysis, a significant association was found between the TNF-α 308G/A polymorphism and urogenital cancer risk, indicating that the -308A allele might be a genetic risk factor for susceptibility to urogenital cancer. In the subgroup analysis of cancer type, our study suggested that the TNF-α 308G/A polymorphism led to an increased incidence of cervical cancer risk in the allele contrast model (OR = 1.28, 95%CI = 1.08-1.52, P = 0.004), the heterozygote model (OR = 1.27, 95%CI = 1.02-1.60, P = 0.034), and the dominant model (OR = 1.29, 95%CI = 1.06-1.58, P = 0.013), which was consistent with several of the studies we included (Duarte et al, 2005;Kohaar et al, 2007;Singh, 2009;Zuo et al, 2011;Badano et al, 2012;Sousa et al, 2014), but not with some of the other studies (Jang et al, 2001;Calhoun et al, 2002;Gostout et al, 2003;Deshpande et al, 2005;Ivansson, 2010;Wang et al, 2011;Barbisan et al, 2012;Wang et al, 2012). Furthermore, previous meta-analyses have produced the same conclusion.…”
Section: Discussionsupporting
confidence: 86%
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“…In our meta-analysis, a significant association was found between the TNF-α 308G/A polymorphism and urogenital cancer risk, indicating that the -308A allele might be a genetic risk factor for susceptibility to urogenital cancer. In the subgroup analysis of cancer type, our study suggested that the TNF-α 308G/A polymorphism led to an increased incidence of cervical cancer risk in the allele contrast model (OR = 1.28, 95%CI = 1.08-1.52, P = 0.004), the heterozygote model (OR = 1.27, 95%CI = 1.02-1.60, P = 0.034), and the dominant model (OR = 1.29, 95%CI = 1.06-1.58, P = 0.013), which was consistent with several of the studies we included (Duarte et al, 2005;Kohaar et al, 2007;Singh, 2009;Zuo et al, 2011;Badano et al, 2012;Sousa et al, 2014), but not with some of the other studies (Jang et al, 2001;Calhoun et al, 2002;Gostout et al, 2003;Deshpande et al, 2005;Ivansson, 2010;Wang et al, 2011;Barbisan et al, 2012;Wang et al, 2012). Furthermore, previous meta-analyses have produced the same conclusion.…”
Section: Discussionsupporting
confidence: 86%
“…The TNF-α 308G/A polymorphism is a G/A polymorphism at nucleotide (nt) -308, and is associated with the development of several urogenital cancers, including prostate cancer (Zabaleta et al, 2008;Moore et al, 2009;Jones et al, 2013), cervical cancer (Singh, 2009;Zuo et al, 2011), bladder cancer (Jeong et al, 2004;Kim et al, 2005;Leibovici et al, 2005), and renal cell carcinoma (Jang et al, 2001). For example, Jeong et al (2004) studied 113 patients with bladder cancer and 109 healthy subjects and found that the genotype of the 308 nucleotide in the TNF-α promoter had a statistically significant effect on TNF-α production and was related to the bladder tumor grade.…”
Section: Discussionmentioning
confidence: 99%
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“…They are mainly secreted by activated macrophages and are able to promote the host's defense mechanism by activating inflammatory processes (8). Although a moderate TNF level is necessary to maintain cell protected and prevent certain diseases through regulation of the immune response, excessive TNF secretion due to pathological conditions is associated with autoimmune diseases, infectious diseases and malignant tumors (9). In cervical cancer, TNF promotes cell cycle progression by increasing cyclin-dependent kinase activity and HPV16 E6/E7 RNA expression in HPV-immortalized keratinocytes (9, 10).…”
Section: Introductionmentioning
confidence: 99%
“…Although a moderate TNF level is necessary to maintain cell protected and prevent certain diseases through regulation of the immune response, excessive TNF secretion due to pathological conditions is associated with autoimmune diseases, infectious diseases and malignant tumors (9). In cervical cancer, TNF promotes cell cycle progression by increasing cyclin-dependent kinase activity and HPV16 E6/E7 RNA expression in HPV-immortalized keratinocytes (9, 10). It also enhances the transcription and stability of epidermal growth factor receptor (EGFR), resulting in cell proliferation and tumorigenesis (9, 11).…”
Section: Introductionmentioning
confidence: 99%