Meta-analysis of studies on the association between the NF-κB1-94ins/del ATTG promoter polymorphism and cancer

Nian, Xuewu; Zhang, Wei; Liu, Limin; Sun, Yan; Sun, E; Han, Rong

doi:10.1007/s13277-014-2470-3

Cited by 7 publications

(6 citation statements)

References 38 publications

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“…Consequently, -94 del allele carriers may be genetically with a higher inflammatory response. Interestingly, the results were contrary to the results of two previous meta-analyses 33 34 that no significant association was seen between NFKB1 -94 ins/del ATTG polymorphism and the risk of cancer in Caucasians. The contradictory results are interpreted by the following reasons: (1) the small sample was included in the previous two meta-analyses.…”

Section: Discussioncontrasting

confidence: 99%

“… 33 and Nian et al . 34 reported that the -94 ins/del ATTG polymorphism was significantly associated with decreased cancer risk in Asian populations, but not in Caucasian populations. Unfortunately, the two previous meta-analyses included some studies, in which the genotype distributions of control groups were not consistent with Hardy–Weinberg equilibrium (HWE).…”

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confidence: 99%

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Genetic association between NFKB1 −94 ins/del ATTG Promoter Polymorphism and cancer risk: a meta-analysis of 42 case-control studies

Xie

Wang

et al. 2016

Sci Rep

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Accumulating evidences have indicated that the functional -94 ins/del ATTG polymorphism in the promoter region of human nuclear factor-kappa B1 (NFKB1) gene may be associated with cancer risk. However, some studies yielded conflicting results. To clarify precise association, we performed a comprehensive meta-analysis of 42 case-control studies involving 43,000 subjects (18,222 cases and 24,778 controls). The overall results suggested that the -94 ins/del ATTG polymorphism had a decreased risk for cancer, reaching significant levels in five genetic models (dominant model: OR = 0.86, 95% CI = 0.79–0.95, P = 0.002; recessive model: OR = 0.84, 95% CI = 0.74–0.94, P = 0.003; homozygous model: OR = 0.77, 95% CI = 0.66–0.90, P = 0.001; heterozygous model: OR = 0.90, 95% CI = 0.83–0.98, P = 0.011; allelic model: OR = 0.89, 95% CI = 0.83–0.96, P = 0.002). Furthermore, the -94 ins/del ATTG polymorphism could confer a decreased or increased risk for cancer development among Asians and Caucasians, respectively. Additionally, the stratification analysis revealed a significant association between the variant and decreased risk of oral, ovarian, and nasopharyngeal cancer in Asians. After we adjusted p values using the Benjamini-Hochberg false discovery rate method to account for multiple comparisons, these associations remained.

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Section: Discussioncontrasting

confidence: 99%

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confidence: 99%

Genetic association between NFKB1 −94 ins/del ATTG Promoter Polymorphism and cancer risk: a meta-analysis of 42 case-control studies

Xie

Wang

et al. 2016

Sci Rep

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“…Stratified analysis revealed that the polymorphism was associated with increased risk for oral squamous cell carcinoma and ovarian cancer, but not for colorectal cancer, bladder cancer, or renal cell cancer. In another meta-analysis involving 7,281 cases and 10,039 controls from 25 case-control studies, Nian et al [30] found that the -94ins/delATTG polymorphism was significantly associated with decreased susceptibility to cancer in overall population under homozygous, recessive, dominant, and allele contrast models. Subgroups analysis based on ethnicity revealed that the polymorphism conferred decreased cancer susceptibility in the Asian population.…”

Section: Discussionmentioning

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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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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“…The deletion of 4 bases (ATTG) reduces or prevents binding to nuclear proteins, and leads to lower transcript levels of the NF-κB1 gene, thereby changing mRNA stability and regulating translation efficiency. 20 Neither numerous case-control studies [23][24][25][26][27] nor several meta-analyses [28][29][30][31][32][33][34] have resolved the controversy of a potential association between the NF-κB1 -94 ins/del ATTG promoter polymorphism and cancer risk.…”

Section: Nf-κb1 -94ins/delattg (Rs28362491)mentioning

confidence: 99%

NF-κB1 -94del/del ATTG polymorphic variant maintains CLL at an early, mildest stage

et al. 2021

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Background. NF-κB is an essential player in cancer biology, especially in tumor development, due to its constitutive activation, and because a four-base deletion (ATTG) in the NF-κB1 promoter region at site -94, alters mRNA stability and regulates translation efficiency. This polymorphism is a good candidate risk marker and modulator of clinical course in chronic lymphocytic leukemia (CLL). As the effect of this NF-κB1 gene polymorphism has not been studied in patients with CLL so far, the present study was undertaken to find out whether the NF-κB1 promoter -94 ins/del ATTG polymorphism might be an essential genetic risk factor and/or modulatory disease player associated with CLL.Objectives. The NF-κB1 -94 ins/del ATTG (rs28362491) polymorphism was investigated as a potential CLL susceptibility and progression factor, along with demonstration of potential modulation of the stage of clinical disease based on Rai classification. Materials and methods.The associations of NF-κB1 -94 ins/del ATTG polymorphism with CLL and its clinical manifestation in 282 Polish individuals, including 156 CLL patients, were analyzed using polymerase chain reaction (PCR) with primers including a labeled forward primer, followed by capillary electrophoresis.Results. A higher occurrence of the del/del homozygosity was observed among patients when compared to controls, resulting in an increase in CLL risk of more than twofold in patients carrying this homozygous genotype (OR = 2.23, p = 0.02, 95% CI = 1. 14-4.37). Moreover, the del/del-positive patients more frequently presented the less aggressive disease phenotype (Rai 0), suggesting a low probability of progression to more advanced disease. Conclusions.The NF-κB1 -94 del/del genetic variant, although associated with increased risk of CLL disease, may be associated with maintenance of disease severity in the early, mildest stage. The likelihood of disease progression may increase as the frequency of wild-type (insertion) alleles for this polymorphism increases.

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Meta-analysis of studies on the association between the NF-κB1-94ins/del ATTG promoter polymorphism and cancer

Cited by 7 publications

References 38 publications

Genetic association between NFKB1 −94 ins/del ATTG Promoter Polymorphism and cancer risk: a meta-analysis of 42 case-control studies

Genetic association between NFKB1 −94 ins/del ATTG Promoter Polymorphism and cancer risk: a meta-analysis of 42 case-control studies

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

NF-κB1 -94del/del ATTG polymorphic variant maintains CLL at an early, mildest stage

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