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Background  It is well known that genetic alternation of epidermal growth factor receptor ( EGFR ) plays critical roles in tumorgenesis of lung cancer and can predict outcome of non-small-cell lung cancer treatment, especially the EGFR tyrosine-kinase inhibitors (EGFR-TKIs) therapy. However, it is unclear whether epigenetic changes such as DNA methylation involve in the response to the EGFR-TKI therapy.    Methods  Tumor samples from 155 patients with stages IIIB to IV NSCLC who received EGFR-TKI therapy were analyzed for DNA methylation status of Wnt antagonist genes, including  SFRP1 ,  SFRP2 ,  SFRP5 ,  DKK3 ,  WIF1 , and  APC , using methylation specific PCR (MSP) method. EGFR mutations detections were performed in the same tissues samples using Denaturing High Performance Liquid Chromatography (DHPLC).    Results  We found that Wnt antagonists tend to methylate simultaneously. Methylation of sFRP1 and sFRP5 are reversely correlated with EGFR mutation (P = 0.005, P = 0.011). However, no correlations of methylations of other Wnt antagonist genes with EGFR mutation were found. The patients with methylated  SFRP5  have a significant shorter progression free survival than those with unmethylated  SFRP5  in response to EGFR-TKI treatment (P = 0.002), which is independent of  EGFR  genotype.    Conclusions  Patients with unmethylated  SFRP5  are more likely to benefit from EGFR-TKI therapy.

DNA Methylation status of Wnt antagonist SFRP5 can predict the response to the EGFR-tyrosine kinase inhibitor therapy in non-small cell lung cancer