Evidence map›Paper›PMID 26161396›Full record

ArticleBioMed research international2015

Polymorphisms of NFκB1 and IκBα and Their Synergistic Effect on Nasopharyngeal Carcinoma Susceptibility.

Yehua Liu, Fuman Qiu, Lei Yang, Rongrong Yang, Xiaorong Yang, Dongsheng Huang, Wenxiang Fang, Lisha Zhang, Qingping Jiang, Lan Zhang and 2 more

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 4 pooled it
0.8field-weighted citation impact, top 30% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 4 syntheses or guidelines pooled it, 9 citations in OpenAlex.

  1. Genetic Association betweenDisease markers · 2019
    Pooled it
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 1 country.

Yehua LiuThe State Key Lab of Respiratory Disease, Collaborative Innovation Center for Environmental Toxicity, The Institute for Chemical Carcinogenesis, Guangzhou Medical University, 195 Dongfengxi Road, Guangzhou 510182, China.
Fuman QiuThe State Key Lab of Respiratory Disease, Collaborative Innovation Center for Environmental Toxicity, The Institute for Chemical Carcinogenesis, Guangzhou Medical University, 195 Dongfengxi Road, Guangzhou 510182, China.
Lei YangThe State Key Lab of Respiratory Disease, Collaborative Innovation Center for Environmental Toxicity, The Institute for Chemical Carcinogenesis, Guangzhou Medical University, 195 Dongfengxi Road, Guangzhou 510182, China.
Rongrong YangThe State Key Lab of Respiratory Disease, Collaborative Innovation Center for Environmental Toxicity, The Institute for Chemical Carcinogenesis, Guangzhou Medical University, 195 Dongfengxi Road, Guangzhou 510182, China.
Xiaorong YangThe State Key Lab of Respiratory Disease, Collaborative Innovation Center for Environmental Toxicity, The Institute for Chemical Carcinogenesis, Guangzhou Medical University, 195 Dongfengxi Road, Guangzhou 510182, China.
Dongsheng HuangThe State Key Lab of Respiratory Disease, Collaborative Innovation Center for Environmental Toxicity, The Institute for Chemical Carcinogenesis, Guangzhou Medical University, 195 Dongfengxi Road, Guangzhou 510182, China.
Wenxiang FangThe State Key Lab of Respiratory Disease, Collaborative Innovation Center for Environmental Toxicity, The Institute for Chemical Carcinogenesis, Guangzhou Medical University, 195 Dongfengxi Road, Guangzhou 510182, China.
Lisha ZhangThe State Key Lab of Respiratory Disease, Collaborative Innovation Center for Environmental Toxicity, The Institute for Chemical Carcinogenesis, Guangzhou Medical University, 195 Dongfengxi Road, Guangzhou 510182, China.
Qingping JiangThe State Key Lab of Respiratory Disease, Collaborative Innovation Center for Environmental Toxicity, The Institute for Chemical Carcinogenesis, Guangzhou Medical University, 195 Dongfengxi Road, Guangzhou 510182, China.
Lan ZhangThe State Key Lab of Respiratory Disease, Collaborative Innovation Center for Environmental Toxicity, The Institute for Chemical Carcinogenesis, Guangzhou Medical University, 195 Dongfengxi Road, Guangzhou 510182, China.
Yifeng ZhouDepartment of Genetics, Collaborative Innovation Center for Environmental Toxicity, Medical College of Soochow University, 199 Renai Road, Suzhou 215123, China.
Jiachun LuThe State Key Lab of Respiratory Disease, Collaborative Innovation Center for Environmental Toxicity, The Institute for Chemical Carcinogenesis, Guangzhou Medical University, 195 Dongfengxi Road, Guangzhou 510182, China.
Guangzhou Medical University · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nasopharyngeal carcinoma (NPC) is a multifactoral and polygenic disease with high prevalence in Southeast Asia and Southern China. Environmental factors and genetic susceptibility play important roles in NPC pathogenesis. In the present study, we tested the hypothesis that single nucleotide polymorphisms (SNPs) in nuclear factor-kappa B (NFκB) and its inhibitor (IκBα) conferred consistent risks for NPC. Four putatively functional SNPs (NFκB1: rs28362491del>ins ATTG; NFκB2: rs12769316G>A; IκBα: rs2233406C>T and rs696G>A) were analyzed to evaluate their associations with NPC risk in total 1590 NPC cases and 1979 cancer-free controls. We found that the rs28362491 insATTG variants (ins/del + ins/ins) in NFκB1 conferred an increased risk of NPC (odds ratio [OR] = 1.30, 95% confidence interval [CI] = 1.09-1.55, and P = 2.80 × 10(-3)) compared with the del/del homozygous genotype. The rs696AA variant in IκBα had an increased risk of NPC (OR = 1.41, 95% CI = 1.20-1.66, and P = 2.28 × 10(-5)) by decreasing IκBα expression due to the modulation of microRNA hsa-miR-449a. Furthermore, both adverse genotypes of NFκB/IκBα and their interaction also exerted an increased risk on NPC. Taken together, Our findings indicated that genetic variants in NFκB1 (rs28362491del>ins ATTG) and IκBα (rs696G>A) and their synergistic effect might contribute to NPC predisposition.

Indexed as

Genetic Predisposition to DiseaseBase SequenceCarcinomaCase-Control StudiesEnzyme AssaysFemaleHumansI-kappa B ProteinsLuciferasesMaleMiddle AgedMolecular Sequence DataNasopharyngeal CarcinomaNasopharyngeal NeoplasmsNF-KappaB Inhibitor alphaNF-kappa B p50 SubunitI-kappa B ProteinsLuciferasesNF-KappaB Inhibitor alphaNF-kappa B p50 SubunitNFKBIA protein, human

Identifiers

PMID26161396
PMCPMC4486297
OpenAlexW1553509455

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.