The association between the polymorphisms of TNF-α and non-Hodgkin lymphoma: a meta-analysis

He, Yong; Zhu, Jin; Huang, Shao Yi; Cui, Zhuo; He, Jing; Jia, Wei Hua

doi:10.1007/s13277-014-2569-6

Cited by 14 publications

(9 citation statements)

References 67 publications

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“…Numerous studies have suggested that polymorphisms in genes encoding inflammatory response factors, such as TNF-alpha -308G>A [6], IL6 -174G>C [90], and NFKBIA -826C>T [91] may contribute to cancer susceptibility. Song et al [92] reported that the NFKB1 -94ins/delATTG polymorphism analyzed here (rs28362491) increased the risk of colorectal cancer in a Southern Chinese population; this association was also observed in several publications [71].…”

Section: Discussionmentioning

confidence: 99%

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NFKB1-94insertion/deletion ATTG polymorphism and cancer risk: Evidence from 50 case-control studies

Zhang

Chen

et al. 2016

Oncotarget

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Nuclear factor-kappa B1 (NF-κB1) is a pleiotropic transcription factor and key contributor to tumorigenesis in many types of cancer. Numerous studies have addressed the association of a functional insertion (I)/deletion (D) polymorphism (-94ins/delATTG, rs28362491) in the promoter region of NFKB1 gene with the risk of various types of cancer; however, their conclusions have been inconsistent. We therefore conducted a meta-analysis to reevaluate this association. PubMed, EMBASE, China National Knowledge infrastructure (CNKI), and WANFANG databases were searched through July 2016 to retrieve relevant studies. After careful assessment, 50 case-control studies, comprising 18,299 cases and 23,484 controls were selected. Crude odds ratios (ORs) and 95% confidence intervals (CIs) were used to determine the strength of the association. The NFKB1 -94ins/delATTG polymorphism was associated with a decreased risk of overall cancer in the homozygote model (DD vs. II): OR = 0.75, 95% CI = 0.64-0.87); heterozygote model (ID vs. II): OR = 0.91, 95% CI = 0.83-0.99; recessive model (DD vs. ID/II): OR = 0.81, 95% CI = 0.71-0.91; dominant model (ID/DD vs. II): OR = 0.86, 95% CI = 0.78-0.95; and allele contrast model (D vs. I): OR = 0.88, 95% CI = 0.81-0.95). Subgroup and stratified analyses revealed decreased risks for lung cancer, nasopharyngeal carcinoma, prostate cancer, ovarian cancer, and oral squamous cell carcinoma, and this association held true also for Asians (especially Chinese subjects) in hospital-based studies, and in studies with quality scores less than nine. Well-designed, large-scale case-control studies are needed to confirm these results.

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Section: Discussionmentioning

confidence: 99%

“…Numerous studies have demonstrated that inflammation is critically implicated in the development of some cancers [4, 5]. In view of this, it is plausible that genetic polymorphisms in inflammation-related genes could modify cancer susceptibility [6–8]. …”

Section: Introductionmentioning

confidence: 99%

NFKB1-94insertion/deletion ATTG polymorphism and cancer risk: Evidence from 50 case-control studies

Zhang

Chen

et al. 2016

Oncotarget

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“…Finally, a meta-analysis was conducted to evaluate the association between mTOR rs2295080 SNP and cancer risk. Briefly, the search terms, inclusion, and exclusion criteria were defined in previous publications 38 39 . Relevant studies were searched from the MEDLINE, EMBASE and Scopus databases (Last Updated: July 25, 2014).…”

Section: Methodsmentioning

confidence: 99%

Associations of PI3KR1 and mTOR Polymorphisms with Esophageal Squamous Cell Carcinoma Risk and Gene-Environment Interactions in Eastern Chinese Populations

Zhu

Wang

Zhu

et al. 2015

Sci Rep

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Single nucleotide polymorphisms (SNPs) in the PI3K/PTEN/AKT/mTOR signaling pathway may contribute to carcinogenesis. We genotyped five potentially functional PIK3R1 and mTOR SNPs in 1116 esophageal squamous cell cancer (ESCC) patients and 1117 cancer-free controls to assess their associations with ESCC risk. We observed no association with ESCC risk for any of the selected SNPs. However, the combined analysis of these SNPs revealed that subjects with one-to-three risk genotypes had an increased ESCC risk. Stratified analysis by body mass index (BMI) found that ESCC risk was significantly associated with each of three mTOR SNPs among subjects with BMI < 25.0. Specifically, we found that subjects carrying ≥ 1 risk genotypes had significantly increased ESCC risk, particularly for males, ever-smokers, ever-drinkers, and those with age > 60, or BMI < 25.0. Moreover, three mTOR haplotypes were associated with an increase in ESCC risk. Our meta-analysis of mTOR rs2295080 and cancer risk provided further evidence that mTOR SNPs might modulate cancer susceptibility. In this population, such risk effects might be modified by other risk factors, highlighting the importance of gene-environment interaction in esophageal carcinogenesis. Additional, larger studies are warranted to validate our findings.

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“…Finally, we performed mini meta‐analyses to evaluate the association of AKT1 rs2494750 and AKT2 rs7254617 SNPs with ESCC risk. Briefly, relevant studies were searched with defined search terms from the common public database (MEDLINE and EMBASE) and screened with inclusion and exclusion criteria in accordance with previous procedure . Chi‐square‐based Q ‐test was performed to test heterogeneity assumption.…”

Section: Methodsmentioning

confidence: 99%

Polymorphisms in the AKT1 and AKT2 genes and oesophageal squamous cell carcinoma risk in an Eastern Chinese population

Zhu

Wang

et al. 2016

J Cellular Molecular Medi

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Ethnic Han Chinese are at high risk of developing oesophageal squamous cell carcinoma (ESCC). Aberrant activation of the AKT signalling pathway is involved in many cancers, including ESCC. Some single nucleotide polymorphisms (SNPs) in genes involved in this pathway may contribute to ESCC susceptibility. We selected five potentially functional SNPs in AKT1 (rs2494750, rs2494752 and rs10138277) and AKT2 (rs7254617 and rs2304186) genes and investigated their associations with ESCC risk in 1117 ESCC cases and 1096 controls in an Eastern Chinese population. None of individual SNPs exhibited an association with ESCC risk. However, the combined analysis of three AKT1 SNPs suggested that individuals carrying one of AKT1 variant genotypes had a decreased ESCC risk [adjusted odds ratio (OR) = 0.60, 95% CI = 0.42–0.87]. Further stratified analysis found that AKT1 rs2294750 SNP was associated with significantly decreased ESCC risk among women (adjusted OR = 0.63, 95% CI = 0.43–0.94) and non‐drinkers (OR = 0.79, 95% CI = 0.64–0.99). Similar protective effects on women (adjusted OR = 0.56, 95% CI = 0.37–0.83) and non‐drinker (adjusted OR = 0.75, 95% CI = 0.60–0.94) were also observed for the combined genotypes of AKT1 SNPs. Consistently, logistic regression analysis indicated significant gene–gene interactions among three AKT1 SNPs (P < 0.015). A three‐AKT1 SNP haplotype (C‐A‐C) showed a significant association with a decreased ESCC risk (adjusted OR = 0.70, 95% CI = 0.52–0.94). Multifactor dimensionality reduction analysis confirmed a high‐order gene–environment interaction in ESCC risk. Overall, we found that three AKT1 SNPs might confer protection against ESCC risk; nevertheless, these effects may be dependent on other risk factors. Our results provided evidence of important gene–environment interplay in ESCC carcinogenesis.

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The association between the polymorphisms of TNF-α and non-Hodgkin lymphoma: a meta-analysis

Cited by 14 publications

References 67 publications

NFKB1-94insertion/deletion ATTG polymorphism and cancer risk: Evidence from 50 case-control studies

NFKB1-94insertion/deletion ATTG polymorphism and cancer risk: Evidence from 50 case-control studies

Associations of PI3KR1 and mTOR Polymorphisms with Esophageal Squamous Cell Carcinoma Risk and Gene-Environment Interactions in Eastern Chinese Populations

Polymorphisms in the AKT1 and AKT2 genes and oesophageal squamous cell carcinoma risk in an Eastern Chinese population

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