Supplemental Figure legends from EGFR Mutations and Resistance to Irreversible Pyrimidine-Based EGFR Inhibitors

Supplemental Figure legends. This file contains the detailed descriptions of the supplementaal figures.</p

Supplemental Figures 1 - 7 from EGFR Mutations and Resistance to Irreversible Pyrimidine-Based EGFR Inhibitors

Supplemental Figures 1 - 7. Figure S1. Sequence tracings from WZ4002 resistant Ba/F3 cells demonstrating EGFR L718Q, C797S and L844V mutations. Figure S2. EGFR Del19 Ba/F3 cells alone or expressing EGFR L718Q were treated with EGF. Figure S3. Structure of TX 2-30. Figure S4. Impact of EGFR L718Q and L844V on sensitivity to WZ4002 and quinazoline based EGFR inhibitors Figure S5. Impact of EGFR Q791R mutation. Figure S6. EGFR L718Q and L844V cause resistance in trans in EGFR mutant NSCLC cell lines. Figure S7. Evaluation of cetuximab on EGFR dimerization and growth in EGFR C797S expressing cells.</p

Supplemental figure 1 from Clinical and Molecular Characteristics of <i>NF1</i>-Mutant Lung Cancer

Gene mutations evaluated in 275 gene panel referenced in the manuscript.</p

Supplemental Tables 1-4 from EGFR Mutations and Resistance to Irreversible Pyrimidine-Based EGFR Inhibitors

Supplemental Tables 1-4. Table S1. Secondary EGFR mutations recovered in the presence of WZ4002. Table S2. Efficacy (IC50 values) of EGFR kinase inhibitors in EGFR mutant Ba/F3 cells Table S3. Efficacy (IC50 values) of covalent EGFR kinase inhibitors in EGFR mutant Ba/F3 cells or lung cancer cell lines. Table S4. Frequency and type of EGFR secondary mutation following ENU mutagenesis screen using irreversible pyrimidine EGFR inhibitors.</p

Supplemental Tables 1-3, Supplementary Figure Legends from Clinical and Molecular Characteristics of <i>NF1</i>-Mutant Lung Cancer

Supplemental Table 1: Identified NF1 variants; Supplemental Table 2: Tumors with multiple NF1 mutations include splice site, missense, nonsense, and frameshift mutations; Supplemental Table 3: KRAS mutations identified by next-generation sequencing.</p

Supplementary Figure 1 from Identification of Existing Drugs That Effectively Target <i>NTRK1</i> and <i>ROS1</i> Rearrangements in Lung Cancer

Pathways targeted by the Dana-Farber Targeted Therapy Collection and clinical development status</p

Supplementary Figure 7 from Combined EGFR/MEK Inhibition Prevents the Emergence of Resistance in <i>EGFR</i>-Mutant Lung Cancer

Supplementary Figure S7. Effect of Torin2 on PC9 and PC9 derived WZ4002 + trametinib resistant cell lines. (A) Inhibition of S6 was assessed at the indicated concentration by immunoblot. (B) Viability was assessed by MTS assay after 72 hours of the indicated concentration of Torin2 (mean +/- SD, n = 6 technical replicates). (C) PC9 W+T resistant clone was treated with WZ4002 + trametinib for 72 hours and viability was assessed by MTS (mean +/- SD, n = 6 technical replicates).</p

Supplementary figure legends from Identification of Existing Drugs That Effectively Target <i>NTRK1</i> and <i>ROS1</i> Rearrangements in Lung Cancer

Legends to the supplementary figures</p

Supplementary Figure 3 from Combined EGFR/MEK Inhibition Prevents the Emergence of Resistance in <i>EGFR</i>-Mutant Lung Cancer

Supplementary Figure S3. Biochemical analysis of WZ4002 + trametinib (W+T) resistant and sensitive cell lines. Each cell line was treated with 100 nM WZ4002 (W) or 30 nM trametinib (T) or a combination (C) thereof for 8 hours and total or phospho-EGFR, ERK1/2, AKT and S6 were assessed by western blot. Sensitivity to six week W+T treatment is indicated below the image. Hsp90 was used as a loading control.</p

Supplementary Figure 4 from Identification of Existing Drugs That Effectively Target <i>NTRK1</i> and <i>ROS1</i> Rearrangements in Lung Cancer

Chemical structures of lead compounds</p