Search

Table S1. Clinicopathological characteristics of the NSCLC cohort 1 from which tumor samples were analyzed by Immunohistochemistry. Table S2. Clinicopathological characteristics of the NSCLC cohort from which frozen tumor tissue was analyzed. Used for the study of methylation of MAP17 promoter and gene. Cohort number 2. Table S3. Clinicopathological characteristics of the erlotinib/gefitinib-treated NSCLC patient cohort. Cohort number 3. Table S4. Description of the driver molecular alterations and MAP17 mRNA expression of our lung cell line panel Figure S1. Related to Fig. 1. ADC=Adenocarcinoma, SCC=Squamous Cell Carcinoma, TN=“Triple Negative” (referring to the absence of alterations in KRAS, EGFR or ALK), I=Immortalized. Table S5. IC50 sensitivity values of adenocarcinoma cell lines to cisplatin, carboplatin, erlotinib and bortezomib. Table S6. clinicopathological characteristics of the platinum-treated lung adenocarcinoma TCGA cohort. Figure S1. MAP17 upregulation occurs during lung tumorogenesis and is preferentially detected in lung adenocarcinomas. (A-D) MAP17 mRNA expression in non-tumor and NSCLC samples of different histologic subtypes from different publicly available databases accessible at Oncomine (https://powertools.oncomine.com). NT lung = Lung non-tumoral tissue, LCLC = Large cell carcinoma. (E) MAP17 mRNA expression in lung epithelial immortalized non-tumoral (normal), adenocarcinoma (ADC) and squamous cell carcinoma (SCC) cell lines. Figure S2. Analysis of the survival probability according to MAP17 expression in differeng grades or stage of Lung cancer tumors in the Lung Metabase database (n=1053). Figure S3. Relationship between MAP17 mRNA levels and EGFR mutations (based on Table S5). (DOCX 411 kb)