Table S2 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts

WES Summary</p

Figure S8 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts

Changes in chromatin accessibility in HCC827 and PC9 cells upon ASCL1 expression. Global changes in chromatin accessibility in mutant EGFR lung cancer cell lines following ASCL1 overexpression and osimertinib treatment.</p

Figure S5 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts

Characterization of mutant EGFR lung cancer PDXs at single-cell resolution. Workflow for scRNA-seq on PDXs and single cell data for an additional PDX.</p

Figure S2 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts

Drug tolerant residual tumors exhibit variable levels of proliferation and low levels of apoptosis. IHC Quantification and additional IHC results to profile cell proliferation.</p

Table S1 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts

Patient Information</p

Figure S4 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts

Expression of signature genes in residual disease in PDXs.</p

Figure S7 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts

ASCL1 expression activates an EMT transcriptional program in permissive cellular contexts. Expression of individual EMT marker genes in mutant EGFR lung cancer cell lines and PDXs with or without ASCL1 overexpression.</p

Table S3 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts

Marker Genes in Clusters from YU-006</p

Figure S6 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts

ASCL1 overexpression does not affect PC9 or H1975 cells. Drug response data in two additional lung cancer cell lines overexpressing ASCL1.</p

Figure S3 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts

Drug tolerant residual disease is characterized by profound gene expression, but not mutational, changes compared to untreated tumors. Pyrosequencing results and mapping of bulk RNA-seq reads to mouse and human genome.</p