In addition, there is no significant correlation between GSTT1 null genotype and the risk of esophageal adenocarcinoma (OR = 0.98; 95% CI 0.71-1.35; <i>P</i> > 0.05).
The strong statistical association between smoking and risk for EADC in individuals with the active allele of either GSTM1 or GSTT1 may have potential clinical application in endoscopic surveillance programs to identify individuals with BE at increased risk for progression to EADC.
In ADC, our results suggest 3 distinct hypotheses: (1) activation of exogenous procarcinogens, such as small halogenated compounds by GSTT1; (2) contribution of GSTT1 to the inflammatory response of esophageal mucosa, which is known to be a strong risk factor for ADC, possibly through leukotriene synthesis; (3) higher sensitivity to the inflammatory process associated with intracellular depletion of glutathione.