Genetic polymorphisms in oxidative stress pathway genes and modification of BMI and risk of non-Hodgkin lymphoma
Menée aux Etats-Unis, cette étude cas-témoins en population évalue l'association entre des polymorphismes de gènes impliqués dans le stress oxydant, l'indice de masse corporelle et le risque de lymphome non hodgkinien
Background: Being overweight and obese increases oxidative stress in the body. To test the hypothesis that genetic variations in oxidative stress pathway genes modifies the relationship between body mass index (BMI) and risk of non-Hodgkin lymphoma (NHL), we conducted a population-based case-control study in Connecticut women. Methods: Individuals who were overweight/obese (BMI > 25) were compared to normal and underweight individuals (BMI < 25) and their risk of NHL stratified assuming a dominant allele model for each oxidative stress pathway SNP. Results: Polymorphisms in AKR1A1, AKR1C1, AKR1C3, CYBA, GPX1, MPO, NCF2, NCF4, NOS1, NOS2A NOS3, OGG1, ATG9B, SOD1, SOD2, SOD3, RAC1 and RAC2 genes after false discovery rate (FDR) adjustment did not modify the association between BMI and risk of NHL overall and histological subtypes. Conclusions: The results suggest that common genetic variations in oxidative stress genes do not modify the relationship between BMI and risk of NHL. Impact: Studies of BMI and oxidative stress independently may elevate NHL risk, but this study suggests no interaction of the two risk factors. Future studies with larger study populations may reveal interactions.