AIM: Inconsistency of reported associations of the G/A polymorphism (rs2301756) in the PTPN11 gene and gastric atrophy prompted us to undertake a meta-analysis. MATERIALS AND METHODS: We searched PubMed for published literature up to July 2013. Individual data from studies with case-control design were evaluated for the PTPN11 G/A polymorphism in Helicobacter pylori (-) (seronegative) and (+) (seropositive) subjects (four studies each, totaling 3,597 cases and 4,865 controls). RESULTS: Associations of PTPN11 polymorphism with gastric atrophy in H. pylori (-) and (+) subjects are more readily interpreted in the homozygous and recessive models given that the dominant codominant effects skirted null associations. Thus, homozygous and recessive effects indicated reduced risk [odds ratio (OR) 0.92-0.96, p = 0.51-0.74], which is significant among H. pylori (+) subjects (OR 0.66-0.68, p = 0.04-0.05). Confined to the Japanese, reduced risk effects were unaltered in both groups, less protective among seronegative subjects (OR 0.85-0.86, p = 0.71-0.73) than seropositive subjects with significance in the recessive model (OR 0.67, p = 0.05). Sensitivity analysis demonstrated robustness of the seropositive findings, but probably not the seronegative results where homozygous and recessive pooled ORs were altered from protection to increased risk. CONCLUSIONS: Evidence of overall and subgroup decreased risks, strong in seropositive subjects, demonstrates protective effects of the PTPN11 G/A polymorphism from gastric atrophy.
AIM: Inconsistency of reported associations of the G/A polymorphism (rs2301756) in the PTPN11 gene and gastric atrophy prompted us to undertake a meta-analysis. MATERIALS AND METHODS: We searched PubMed for published literature up to July 2013. Individual data from studies with case-control design were evaluated for the PTPN11 G/A polymorphism in Helicobacter pylori (-) (seronegative) and (+) (seropositive) subjects (four studies each, totaling 3,597 cases and 4,865 controls). RESULTS: Associations of PTPN11 polymorphism with gastric atrophy in H. pylori (-) and (+) subjects are more readily interpreted in the homozygous and recessive models given that the dominant codominant effects skirted null associations. Thus, homozygous and recessive effects indicated reduced risk [odds ratio (OR) 0.92-0.96, p = 0.51-0.74], which is significant among H. pylori (+) subjects (OR 0.66-0.68, p = 0.04-0.05). Confined to the Japanese, reduced risk effects were unaltered in both groups, less protective among seronegative subjects (OR 0.85-0.86, p = 0.71-0.73) than seropositive subjects with significance in the recessive model (OR 0.67, p = 0.05). Sensitivity analysis demonstrated robustness of the seropositive findings, but probably not the seronegative results where homozygous and recessive pooled ORs were altered from protection to increased risk. CONCLUSIONS: Evidence of overall and subgroup decreased risks, strong in seropositive subjects, demonstrates protective effects of the PTPN11 G/A polymorphism from gastric atrophy.
Authors: M J Blaser; G I Perez-Perez; H Kleanthous; T L Cover; R M Peek; P H Chyou; G N Stemmermann; A Nomura Journal: Cancer Res Date: 1995-05-15 Impact factor: 12.701