Inflammatory Gene Polymorphisms in Lung Cancer Susceptibility

Eaton, Keith D.; Romine, Perrin E.; Goodman, Gary E.; Thornquist, Mark; Barnett, Matt J.; Petersdorf, Effie W.

doi:10.1016/j.jtho.2018.01.022

Cited by 38 publications

(29 citation statements)

References 48 publications

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“…TNF‐α is a powerful pro‐inflammatory factor involved in several biological processes such as macrophage activation, recruitment of inflammatory cells and amplification of pro‐inflammatory cytokines . Polymorphisms in the promoter of TNF may increase its transcription level and thus cytokine production . Many studies have reported the associations of −238 G/A and/or −308 G/A polymorphisms in TNF with susceptibility to HCC, but the results are conflicting .…”

Section: Discussionmentioning

confidence: 99%

“…26 Polymorphisms in the promoter of TNF may increase its transcription level and thus cytokine production. 27 Many studies have reported the associations of −238 G/A and/or −308 G/A polymorphisms in TNF with susceptibility to HCC, but the results are conflicting. [28][29][30] Our findings indicated that TNF −238 GG genotype was associated with increased risk of HCC.…”

Section: Discussionmentioning

confidence: 99%

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Association of CTLA‐4, TNF alpha and IL 10 polymorphisms with susceptibility to hepatocellular carcinoma

Wang

Tai-chang

2019

Scand J Immunol

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Our aim was to evaluate the association of genetic polymorphisms of immunoregulatory molecules with susceptibility to hepatocellular carcinoma (HCC). The polymorphisms in CTLA‐4 (−318 T/C, CT60 G/A), TNF (−238 G/A, −308 G/A) and IL10 (−592 C/A, −819 C/T) were genotyped by PCR and DNA sequencing. The functional relevance of the polymorphisms was examined by ELISAs, in vitro lymphocyte proliferation assay and cytotoxic assay. The CTLA‐4 −318 TC/TT, CTLA‐4 CT60 GG, IL10 −592 CA and −819 CT/TT variants, CTLA‐4 −318 T and IL 10 −819 T alleles were positively associated with HCC risk (P < .05). While TNF −238 AA variant, TNF −238 A allele were associated with decreased risk of HCC (P < .05). Furthermore, combinations of CTLA‐4 −318 TC/TT and TNF −238 GG/GA; CTLA‐4 −318 TC/TT and IL 10 −819 CC; CTLA‐4 −318 CC and IL 10 −819 CT/TT in patients with HCC were statistically significant (P < .05). Peripheral blood mononuclear cells (PBMCs) carrying −318 TC/TT genotypes exhibited significantly lower proliferation rates, decreased IL‐2, IL‐4 levels, fewer cytolytic activities and elevated TGF‐β levels. For IL 10 −819 C/T, the CC genotype was significantly associated with higher proliferation rate, decreased TGF‐β, IL‐10 levels and higher cytolytic activities (P < .05). For TNF −238 G/A, the AA genotype only had association with serum IL‐2, IL‐4 (P < .05). In addition, we also found that CTLA‐4 −318 T/C, IL‐10 −819 T/C variants, combinations of CTLA‐4 −318 CC with IL 10 −819 CT or TT, CTLA‐4 −318 TC or TT with IL 10 −819 CT or TT were associated with the severity of HCC. These findings suggest that CTLA‐4 −318 TC/TT and IL 10 −819 CT/TT could promote the pathogenesis of HCC, which might be related with down‐regulation of Th1/Th2‐type cytokines and/or up‐regulation of Th3‐type cytokines.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Association of CTLA‐4, TNF alpha and IL 10 polymorphisms with susceptibility to hepatocellular carcinoma

Wang

Tai-chang

2019

Scand J Immunol

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“…Studying both pro-and anti-inflammatory cytokine genes is essential for PCA [21]. TNF-α, as a main mediator of inflammation, has a vital role in PCA development [10]. By considering the capacity of TNF-α promoter SNPs (rs1800629 and rs361525), and the influence of their gene expression [13,14], these two SNPs have been identified as potential functional variants and as novel biomarkers for the early detection for PCA susceptibility.…”

Section: Discussionmentioning

confidence: 99%

“…The TNF-α gene, also termed DIF/TNFSF2/TNLG1F, is located in the class III region of the major histocompatibility complex (MHC III) and mapped to chromosome 6p21.33 with 4 exons [8,9]. Several single nucleotide polymorphisms (SNPs) in this gene have been widely reported and have been associated with the risk of several cancers, such as PCA, breast cancer, and lung cancer [10][11][12]. Rs1800629 is one of the most common SNPs, with a G to A transition at the − 308 nucleotide in the promoter of the transcription initiation site, which may affect the serum expression of TNF-α [13].…”

Section: Introductionmentioning

confidence: 99%

No association between three polymorphisms (rs1800629, rs361525 and rs1799724) in the tumor necrosis factor-α gene and susceptibility to prostate cancer: a comprehensive meta-analysis

et al. 2020

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Background: Inflammation is one of the factors associated with prostate cancer. The cytokine tumor necrosis factor-alpha (TNF-α) plays an important role in inflammation. Several studies have focused on the association between TNF-α polymorphisms and prostate cancer development. Our meta-analysis aimed to estimate the association between TNF-α rs1800629 (− 308 G/A), rs361525 (− 238 G/A) and rs1799724 polymorphisms and prostate cancer risk. Methods: Eligible studies were identified from electronic databases (PubMed, Embase, Wanfang and CNKI) using keywords: TNF-α, polymorphism, prostate cancer, until Nov 15, 2019. Odds ratios (ORs) with 95% confidence intervals (CIs) were applied to determine the association from a quantitative point-of-view. Publication bias and sensitivity analysis were also applied to evaluate the power of current study. All statistical analyses were done with Stata 11.0 software. Results: Twenty-two different articles were included (22 studies about rs1800629; 8 studies for rs361525 and 5 studies related to rs1799724). Overall, no significant association was found between rs1800629 and rs1799724 polymorphisms and the risk of prostate cancer in the whole (such as: OR = 1.03, 95% CI = 0.92-1.16, P = 0.580 in the allele for rs1800629; OR = 0.95, 95% CI = 0.84-1.07, P = 0.381 in the allele for rs1799724). The rs361525 polymorphism also had no association with prostate cancer in the cases (OR = 0.93, 95% CI = 0.66-1.32, P = 0.684 in the allele) and ethnicity subgroup. The stratified subgroup of genotype method, however, revealed that the rs361525 variant significantly decreased the risk of prostate cancer in the Others (OR = 0.65, 95% CI = 0.47-0.89, P = 0.008, A-allele vs G-allele) and PCR-RFLP (OR = 2.68, 95% CI = 1.00-7.20, P = 0.050, AG vs GG or AA+AG vs GG) methods.

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“…Further, analyzing these patients in a nested case-control study from a large cohort reduces selection bias inherent in institution-based sampling. With time, the utilization of similar trial cohorts and lung cancer screening studies to evaluate genetic variation may increase; however, as recognized by Eaton et al, 7 replication in appropriately similar data sets is currently an issue. Stricter eligibility criteria for cases and controls may help define more biologically homogenous groups for comparison and patients with lung cancer with similar somatic profiles, such that it may offset smaller sample sizes through decreased variability in risk from nongermline factors.…”

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confidence: 99%

Heritable Germline Variation and Lung Cancer Susceptibility: One Size Does not Fit All

Herman

Warkentin

Shepshelovich

et al. 2018

Journal of Thoracic Oncology

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Inflammatory Gene Polymorphisms in Lung Cancer Susceptibility

Abstract: This study provides further evidence that IL1B promoter polymorphisms may modulate the risk for development of lung cancer.

Cited by 38 publications

References 48 publications

Association of CTLA‐4, TNF alpha and IL 10 polymorphisms with susceptibility to hepatocellular carcinoma

Association of CTLA‐4, TNF alpha and IL 10 polymorphisms with susceptibility to hepatocellular carcinoma

No association between three polymorphisms (rs1800629, rs361525 and rs1799724) in the tumor necrosis factor-α gene and susceptibility to prostate cancer: a comprehensive meta-analysis

Heritable Germline Variation and Lung Cancer Susceptibility: One Size Does not Fit All

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