A meta-analysis of the four studies that focused on AML was performed on data from 345 cases and 651 controls. The subjects in all four studies were Caucasians. A high degree of heterogeneity was observed under the recessive (I2=79%, P=0.003), dominant (I2=70%, P=0.02), allele contrast (I2=84%, P=0.0003), and homozygote contrast (I2=82%, P=0.0007) models. Therefore, random-effects modeling was performed for the four contrast models. The meta-analysis for these studies revealed no association between the XRCC1 Arg399Gln SNP and the risk of AML under the recessive model (OR 0.89, 95% CI 0.33–2.44, P=0.83), dominant (OR 0.97, 95% CI 0.58–1.63, P=0.91), allele contrast (OR 0.94, 95% CI 0.55–1.59, P=0.81), or homozygote contrast models (OR 0.86, 95% CI 0.27–2.78, P=0.81).

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In view of the high degree of heterogeneity, a sensitivity analysis was conducted, and the study by Banescu et al9 was found to be an outlier. Removal of their data from the analysis reduced the degree of heterogeneity under the recessive and dominant models, but not sufficiently so under the allele contrast (I2=65%, P=0.06; Figure 2A) and homozygote contrast models (I2=59%, P=0.09; Figure 2B). Fixed-effects modeling was thus performed for the recessive and dominant models, and finally, the SNP was associated with AML risk under the recessive model (OR 0.58, 95% CI 0.38–0.89,P=0.01; Figure 2C) but not under the dominant model (OR 0.79, 95% CI 0.58–1.07, P=0.13; Figure 2D). Therefore, the result for AML under the recessive model is sensitive to the study by Banescu et al.9

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Eleven of the 23 included studies investigated the distribution of XRCC1 SNP in childhood ALL cases and controls and provided sufficient data for analysis. A meta-analysis of these eleven studies was performed, and included data from 1,088 cases and 1,588 controls.

The forest plot revealed no heterogeneity under the recessive (P=0.65, I2=0%) and homozygote contrast (P=0.50, I2=0%) models, and I2<50% under the allele contrast (P=0.05, I2=46%) model. The fixed-effects model was therefore used for these three contrast models. The degree of heterogeneity was high (I2=62%, P=0.003) under the dominant model; therefore, a random-effects model was employed under that model. Finally, an association was found between the SNP and increased childhood ALL risk under the allele contrast (OR 1.21, 95% CI 1.06–1.37, P=0.003) and homozygote contrast (OR 1.41, 95% CI 1.06–1.88, P=0.02) models. The funnel plot did not reveal any obvious publication bias (Figure 3).

(To view a larger version of Figure 3, click here.)