Evidence map›Paper›PMID 24586700›Full record

SynthesisPloS one2014

NOD2 polymorphisms associated with cancer risk: a meta-analysis.

Jingwei Liu, Caiyun He, Qian Xu, Chengzhong Xing, Yuan Yuan

Open access · goldAbstract readMeta-Analysis
In one paragraph

Synthesis in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

45 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
  2. Role of Nod-like Receptors inMicroorganisms · 2026
    Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Role and molecular mechanism of NOD2 in chronic non-communicable diseases.Journal of molecular medicine (Berlin, Germany) · 2024
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
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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

5 authors at 1 institution in 1 country.

Jingwei LiuTumor Etiology and Screening Department of Cancer Institute and General Surgery, the First Affiliated Hospital of China Medical University, Shenyang, China ; Key Laboratory of Cancer Etiology and Prevention, China Medical University, Liaoning Provincial Education Department, Shenyang, China.
Caiyun HeTumor Etiology and Screening Department of Cancer Institute and General Surgery, the First Affiliated Hospital of China Medical University, Shenyang, China ; Key Laboratory of Cancer Etiology and Prevention, China Medical University, Liaoning Provincial Education Department, Shenyang, China.
Qian XuTumor Etiology and Screening Department of Cancer Institute and General Surgery, the First Affiliated Hospital of China Medical University, Shenyang, China ; Key Laboratory of Cancer Etiology and Prevention, China Medical University, Liaoning Provincial Education Department, Shenyang, China.
Chengzhong XingTumor Etiology and Screening Department of Cancer Institute and General Surgery, the First Affiliated Hospital of China Medical University, Shenyang, China ; Key Laboratory of Cancer Etiology and Prevention, China Medical University, Liaoning Provincial Education Department, Shenyang, China.
Yuan YuanTumor Etiology and Screening Department of Cancer Institute and General Surgery, the First Affiliated Hospital of China Medical University, Shenyang, China ; Key Laboratory of Cancer Etiology and Prevention, China Medical University, Liaoning Provincial Education Department, Shenyang, China.
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEmerging evidence indicated that common polymorphisms of NOD2 might impact individual susceptibility to cancer. However, the results from published studies were inconclusive. The aim of this meta-analysis was to elucidate whether NOD2 polymorphisms were associated with cancer risk.

methodsA systematically literature search was performed by using electronic databases including PubMed and Web of Science. ORs and their 95% CI were used to assess the strength of association between NOD2 gene polymorphisms and cancer risks.

resultsThirty case-control studies were included in this meta-analysis. The pooled analysis indicated that NOD2 rs2066842 C/T polymorphism was not significantly associated with cancer risk; for NOD2 rs2066844 C/T polymorphism, (TT+CT) genotype was associated with increased cancer risk compared with wild-type CC genotype (OR = 1.32, 95% CI = 1.01-1.72, P = 0.041); for NOD2 rs2066845 C/G polymorphism, individuals with (CC+CG) genotype were significantly associated with increased cancer risk compared with GG genotype (OR = 1.32, 95% CI = 1.01-1.72, P = 0.040); for NOD2 rs2066847 (3020insC) polymorphism, carriers of (insC/insC+insC/-) genotype were significantly associated with increased cancer risk compared with -/- carriers (OR = 1.23, 95% CI = 1.10-1.38, P<0.001). In the subgroup analysis of cancer type, (insC/insC+insC/-) genotype was significantly associated with increased risk of colorectal cancer, gastric cancer and MALT lymphoma, breast cancer, lung cancer, laryngeal cancer but not with urogenital cancer, pancreatic cancer, melanoma or non-Hodgkin lymphoma.

conclusionNOD2 rs2066844 C/T, rs2066845 C/G and rs2066847 (3020insC) polymorphisms might be associated with increased cancer risk. No significant association was observed between NOD2 rs2066842 C/T polymorphism and cancer risk. Further large-scale and well-designed studies are still needed to confirm the results of our meta-analysis.

Indexed as

Genetic Predisposition to DiseaseCase-Control StudiesHumansNeoplasmsNod2 Signaling Adaptor ProteinPolymorphism, GeneticPrognosisRisk AssessmentNOD2 protein, humanNod2 Signaling Adaptor Protein

Identifiers

PMID24586700
PMCPMC3930717
OpenAlexW2079550929

What OpenQuestion holds

Textmetadata
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.