Evidence map›Paper›PMID 25945024›Full record

SynthesisWorld journal of gastroenterology2015

Relationship between apurinic endonuclease 1 Asp148Glu polymorphism and gastrointestinal cancer risk: An updated meta-analysis.

Zhi-Jun Dai, Yong-Ping Shao, Hua-Feng Kang, Wei Tang, Dan Xu, Yang Zhao, Di Liu, Meng Wang, Peng-Tao Yang, Xi-Jing Wang

Open access · bronzeAbstract readMeta-AnalysisReview
In one paragraph

Synthesis in World journal of gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

  1. The Link Between Human Alkyladenine DNA Glycosylase and Cancer Development.International journal of molecular sciences · 2025
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  3. Cancers · 2024
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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

10 authors at 1 institution in 1 country.

Zhi-Jun DaiZhi-Jun Dai, Hua-Feng Kang, Yang Zhao, Di Liu, Meng Wang, Peng-Tao Yang, Xi-Jing Wang, Department of Oncology, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China.
Yong-Ping ShaoZhi-Jun Dai, Hua-Feng Kang, Yang Zhao, Di Liu, Meng Wang, Peng-Tao Yang, Xi-Jing Wang, Department of Oncology, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China.
Hua-Feng KangZhi-Jun Dai, Hua-Feng Kang, Yang Zhao, Di Liu, Meng Wang, Peng-Tao Yang, Xi-Jing Wang, Department of Oncology, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China.
Wei TangZhi-Jun Dai, Hua-Feng Kang, Yang Zhao, Di Liu, Meng Wang, Peng-Tao Yang, Xi-Jing Wang, Department of Oncology, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China.
Dan XuZhi-Jun Dai, Hua-Feng Kang, Yang Zhao, Di Liu, Meng Wang, Peng-Tao Yang, Xi-Jing Wang, Department of Oncology, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China.
Yang ZhaoZhi-Jun Dai, Hua-Feng Kang, Yang Zhao, Di Liu, Meng Wang, Peng-Tao Yang, Xi-Jing Wang, Department of Oncology, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China.
Di LiuZhi-Jun Dai, Hua-Feng Kang, Yang Zhao, Di Liu, Meng Wang, Peng-Tao Yang, Xi-Jing Wang, Department of Oncology, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China.
Meng WangZhi-Jun Dai, Hua-Feng Kang, Yang Zhao, Di Liu, Meng Wang, Peng-Tao Yang, Xi-Jing Wang, Department of Oncology, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China.
Peng-Tao YangZhi-Jun Dai, Hua-Feng Kang, Yang Zhao, Di Liu, Meng Wang, Peng-Tao Yang, Xi-Jing Wang, Department of Oncology, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China.
Xi-Jing WangZhi-Jun Dai, Hua-Feng Kang, Yang Zhao, Di Liu, Meng Wang, Peng-Tao Yang, Xi-Jing Wang, Department of Oncology, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China.
Second Affiliated Hospital of Xi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo evaluate the relationship between apurinic endonuclease 1 (APE1) Asp148Glu polymorphism and the susceptibility to gastrointestinal (GI) cancers.

methodsWe searched PubMed, ISI Web of Knowledge, and Chinese National Knowledge Infrastructure (CNKI) databases updated on July 15, 2014 for relevant studies. Only case-control studies comparing APE1 Asp148Glu polymorphism and GI cancer risk were included. We excluded studies reporting only standardized incidence ratios without control groups and those without detailed genotyping data. Meta-analysis was performed on 17 studies involving 4856 cancer patients and 6136 cancer-free controls. Review Manager version 5.1 was used to perform the meta-analysis. The pooled odds ratios (ORs) and 95% confidence intervals (CIs) were estimated under the allele contrast, homozygous, heterozygous, dominant and recessive genetic models. We also conducted subgroup analyses stratified by ethnicity and cancer type. Publication bias was evaluated using Begg's test.

resultsThe meta-analysis showed a significant association between APE1 Asp148Glu polymorphism and GI cancer risk in three genetic models in the overall population (G vs T: OR = 1.18; 95%CI: 1.05-1.32; TG vs TT: OR = 1.28; 95%CI: 1.08-1.52; TG + GG vs TT: OR = 1.32; 95%CI: 1.10-1.57). Stratified analysis by ethnicity revealed a statistically increased GI cancer risk in Asians (G vs T: OR = 1.27; 95%CI: 1.07-1.51; GG vs TT: OR = 1.58; 95%CI: 1.05-2.38; TG vs TT: OR = 1.30; 95%CI, 1.01- 1.67; and TG + GG vs TT: OR = 1.38; 95%CI: 1.07-1.78), but not in Caucasians. Further subgroup analysis by cancer type indicated that APE1 Asp148Glu polymorphism may contribute to gastric cancer risk. However, Asp148Glu has no significant association with colorectal or esophageal cancer risk in any genetic model.

conclusionThis meta-analysis suggests that the APE1 Asp148Glu polymorphism G allele is associated with an increased GI cancer risk, especially in gastric cancer.

Indexed as

Polymorphism, GeneticAsian PeopleChi-Square DistributionDNA-(Apurinic or Apyrimidinic Site) LyaseGastrointestinal NeoplasmsGene FrequencyGenetic Predisposition to DiseaseHumansLinear ModelsOdds RatioPhenotypeRisk AssessmentRisk FactorsStomach NeoplasmsAPEX1 protein, humanDNA-(Apurinic or Apyrimidinic Site) LyaseApurinic endonuclease 1Cancer riskGastrointestinal cancersMeta-analysisSingle nucleotide polymorphism

Identifiers

PMID25945024
PMCPMC4408483
OpenAlexW2001510956

What OpenQuestion holds

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Registered trials

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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.