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EGFR-TKIs show dramatic treatment benefits for advanced lung adenocarcinoma patients with activating  EGFR  mutations. Considering the essential role of autophagy in EGFR-TKIs treatments, we hypothesized that genetic variants in autophagy core genes might contribute to outcomes of advanced lung adenocarcinoma treated with gefitinib. We systematically examined 27 potentially functional genetic polymorphisms in 11 autophagy core genes among 108 gefitinib-treated advanced lung adenocarcinoma patients. We found that  ATG10  rs10036653,  ATG12  rs26538,  ATG16L1  rs2241880 and  ATG16L2  rs11235604 were significantly associated with survival of lung adenocarcinoma patients (all  P  < 0.05). Among  EGFR -mutant patients,  ATG5  rs688810,  ATG5  rs510432,  ATG7  rs8154,  ATG10  rs10036653,  ATG12  rs26538,  ATG16L1  rs2241880 and  ATG16L2  rs11235604 significantly contributed to disease prognosis. We also found that  ATG5  rs510432,  ATG5  rs688810,  ATG10  rs10036653 and  ATG10  rs1864182 were associated with primary or acquired resistance to gefitinib. Functional analyses of  ATG10  rs10036653 polymorphism suggested that  ATG10  A allele might increase transcription factor OCT4 binding affinity compared to the T allele in lung cancer cells. Our results indicate that autophagy core genetic variants show potential clinical implications in gefitinib treatment, especially among advanced lung adenocarcinoma patients, highlighting the possibility of patient-tailored decisions during EGFR-TKIs based on both germline and somatic variation detection.

Clinical Implications of the Autophagy Core Gene Variations in Advanced Lung Adenocarcinoma Treated with Gefitinib