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Association of APE1 Gene Asp148Glu Variant with Digestive Cancer: A Meta-Analysis.

Li H, Zou J, Mi J, Wei X, Zhao D, Zhang S, Tian G - Med. Sci. Monit. (2015)

Bottom Line: Random-effects model was utilized to pool effect estimates.In subgroup analyses by cancer sites, this variant was significantly associated with the increased risk for hepatocellular cancer under allelic (OR=1.50; 95% CI: 1.25-1.80; P<0.001) and homozygous genotypic (OR=1.55; 95% CI: 1.02-2.29; P=0.028) models.Further large and well-designed studies are required.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastric and Intestine, Yantai Affiliated Hospital of Binzhou Medical University, Yantai, Shandong, China (mainland).

ABSTRACT

Background: Apurinic/apyrimidinic endonuclease-1 (APE1) is a rate-limiting enzyme in DNA base excision repair and has been implicated in carcinogenesis. In this study, we summarize available data to examine the susceptibility of APE1 gene Asp148Glu variant to digestive cancer via a meta-analysis.

Material and methods: Study selection and data abstraction were conducted independently by 2 authors. Random-effects model was utilized to pool effect estimates. Heterogeneity and publication bias were addressed.

Results: Sixteen articles involving 4916 digestive cancer patients and 7748 controls were qualified for this meta-analysis. Overall association showed an indicative association between Asp148Glu variant and digestive cancer under allelic (odds ratio or OR=1.11; 95% confidence interval or CI: 0.99-1.25; P=0.074) and dominant (OR=1.18; 95% CI: 1.00-1.40; P=0.056) models, with strong evidence of heterogeneity. Deviation from Hardy-Weinberg equilibrium was an obvious source of heterogeneity. In subgroup analyses by cancer sites, this variant was significantly associated with the increased risk for hepatocellular cancer under allelic (OR=1.50; 95% CI: 1.25-1.80; P<0.001) and homozygous genotypic (OR=1.55; 95% CI: 1.02-2.29; P=0.028) models. There were low probabilities of publication bias for the above comparisons.

Conclusions: The results of this meta-analysis collectively suggest that APE1 gene Asp148Glu variant is not a risk-conferring factor for digestive cancer. Further large and well-designed studies are required.

No MeSH data available.


Related in: MedlinePlus

Begg’s funnel plots of APX1 gene Asp148Glu variant with digestive cancer risk under 3 genetic models.
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f2-medscimonit-21-2456: Begg’s funnel plots of APX1 gene Asp148Glu variant with digestive cancer risk under 3 genetic models.

Mentions: When all qualified studies were analyzed together, significance was indicative for the association between Asp148Glu variant and digestive cancer risk under allelic (OR=1.11; 95% CI: 0.99–1.25; P=0.074) and dominant (OR=1.18; 95% CI: 1.00–1.40; P=0.056) models (Figure 1). There was strong evidence of heterogeneity for all 3 genetic models (I2=76.3%, 61.5% and 74.3% for allelic, homozygous genotypic and dominant models, respectively), while low probabilities of publication bias were observed (Figure 2). In addition, as reflected by the trim and fill method, 1 study for allelic model and 2 studies for dominant model were required to make filled funnel plots symmetrical (Supplementary Figure 1). Adjusting for the missing studies still failed to attain statistical significance for both genetic models of inheritance (data not shown).


Association of APE1 Gene Asp148Glu Variant with Digestive Cancer: A Meta-Analysis.

Li H, Zou J, Mi J, Wei X, Zhao D, Zhang S, Tian G - Med. Sci. Monit. (2015)

Begg’s funnel plots of APX1 gene Asp148Glu variant with digestive cancer risk under 3 genetic models.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4548740&req=5

f2-medscimonit-21-2456: Begg’s funnel plots of APX1 gene Asp148Glu variant with digestive cancer risk under 3 genetic models.
Mentions: When all qualified studies were analyzed together, significance was indicative for the association between Asp148Glu variant and digestive cancer risk under allelic (OR=1.11; 95% CI: 0.99–1.25; P=0.074) and dominant (OR=1.18; 95% CI: 1.00–1.40; P=0.056) models (Figure 1). There was strong evidence of heterogeneity for all 3 genetic models (I2=76.3%, 61.5% and 74.3% for allelic, homozygous genotypic and dominant models, respectively), while low probabilities of publication bias were observed (Figure 2). In addition, as reflected by the trim and fill method, 1 study for allelic model and 2 studies for dominant model were required to make filled funnel plots symmetrical (Supplementary Figure 1). Adjusting for the missing studies still failed to attain statistical significance for both genetic models of inheritance (data not shown).

Bottom Line: Random-effects model was utilized to pool effect estimates.In subgroup analyses by cancer sites, this variant was significantly associated with the increased risk for hepatocellular cancer under allelic (OR=1.50; 95% CI: 1.25-1.80; P<0.001) and homozygous genotypic (OR=1.55; 95% CI: 1.02-2.29; P=0.028) models.Further large and well-designed studies are required.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastric and Intestine, Yantai Affiliated Hospital of Binzhou Medical University, Yantai, Shandong, China (mainland).

ABSTRACT

Background: Apurinic/apyrimidinic endonuclease-1 (APE1) is a rate-limiting enzyme in DNA base excision repair and has been implicated in carcinogenesis. In this study, we summarize available data to examine the susceptibility of APE1 gene Asp148Glu variant to digestive cancer via a meta-analysis.

Material and methods: Study selection and data abstraction were conducted independently by 2 authors. Random-effects model was utilized to pool effect estimates. Heterogeneity and publication bias were addressed.

Results: Sixteen articles involving 4916 digestive cancer patients and 7748 controls were qualified for this meta-analysis. Overall association showed an indicative association between Asp148Glu variant and digestive cancer under allelic (odds ratio or OR=1.11; 95% confidence interval or CI: 0.99-1.25; P=0.074) and dominant (OR=1.18; 95% CI: 1.00-1.40; P=0.056) models, with strong evidence of heterogeneity. Deviation from Hardy-Weinberg equilibrium was an obvious source of heterogeneity. In subgroup analyses by cancer sites, this variant was significantly associated with the increased risk for hepatocellular cancer under allelic (OR=1.50; 95% CI: 1.25-1.80; P<0.001) and homozygous genotypic (OR=1.55; 95% CI: 1.02-2.29; P=0.028) models. There were low probabilities of publication bias for the above comparisons.

Conclusions: The results of this meta-analysis collectively suggest that APE1 gene Asp148Glu variant is not a risk-conferring factor for digestive cancer. Further large and well-designed studies are required.

No MeSH data available.


Related in: MedlinePlus