Peroxisome proliferator-activated receptors (PPARs) are nuclear transcription factors that play a role in lipid metabolism, cell proliferation, terminal differentiation, apoptosis, and inflammation. Although several cancer models have been suggested to explain PPARs' involvement in tumorigenesis, however, their role is still unclear. In this review, we examined associations of the different PPARs, polymorphisms and various types of cancer with a focus on gene-environment interactions. Reviewed evidence suggests that functional genetic variants of the different PPARs may modulate the relationship between environmental exposure and cancer risk. In addition, this report unveils the scarcity of reliable quantitative environmental exposure data when examining these interactions, and the current gaps in studying gene-environment interactions in many types of cancer, particularly colorectal, prostate, and bladder cancers.
Keywords: Peroxisome proliferator-activated receptor (PPAR); cancer risk; genetic polymorphism; gene–environment interaction (GxE); tumorigenesis.