{"paper_id":"d7b62c96-a7e3-4516-9ebe-6d7eb7055307","body_text":"Additional file 1.  Materials and methods.  Table S1  Demographic data of lung adenocarcinoma patients.  Fig. S1  Examination of the role of AKR1C3 in regulating tumor-initiating cell (T-IC) phenotypes and the correlation of AKR1C3 and resistance development time.  Fig. S2  In vitro effect of erlotinib (ER) and AKR1C3 inhibitor 3-{[4-(trifluoromethyl)phenyl]amino}benzoic acid (BA) co-treatment on apoptosis.  Fig. S3  Therapeutic potential of erlotinib (ER) combined with AKR1C3 inhibitor 3-{[4- (trifluoromethyl)phenyl]amino}benzoic acid (BA) in ER-resistant lung adenocarcinoma cell line-derived xenograft (CDX) models.\nAdditional file 1.  Materials and methods.  Table S1  Demographic data of lung adenocarcinoma patients.  Fig. S1  Examination of the role of AKR1C3 in regulating tumor-initiating cell (T-IC) phenotypes and the correlation of AKR1C3 and resistance development time.  Fig. S2  In vitro effect of erlotinib (ER) and AKR1C3 inhibitor 3-{[4-(trifluoromethyl)phenyl]amino}benzoic acid (BA) co-treatment on apoptosis.  Fig. S3  Therapeutic potential of erlotinib (ER) combined with AKR1C3 inhibitor 3-{[4- (trifluoromethyl)phenyl]amino}benzoic acid (BA) in ER-resistant lung adenocarcinoma cell line-derived xenograft (CDX) models.","source_license":"CC-BY-4.0","license_restricted":false}