<p>The purpose of this study was to identify mechanisms of resistance and associated mutational signatures in non-small cell lung cancers (NSCLCs) treated with targeted therapies. Whole genome sequencing (WGS) and whole exome sequencing (WES) were performed on tumor tissue or cell lines derived from oncogene-driven NSCLCs before and after treatments with tyrosine kinase inhibitors. Somatic mutations were called and mutational signature analysis was performed, revealing enrichment of APOBEC mutational signatures mutational signatures in post-treatment tumors after the development to resistance to targeted therapies. The cohort includes WGS and WES data of tumor and normal tissues from patients with oncogene-driven NSCLCs harboring <a href="https://www.ncbi.nlm.nih.gov/gene/1956">EGFR</a> mutations, <a href="https://www.ncbi.nlm.nih.gov/gene/238">ALK</a> fusions or <a href="https://www.ncbi.nlm.nih.gov/gene/4914">NTRK1</a> fusions, who were treated with molecularly targeted therapies that target these oncogenes.</p>

Therapy-Induced APOBEC3A Drives Evolution of Resistance to Targeted    Therapies in Non-Small Cell Lung Cancer

15 variables across Demographics, Race and Ethnicity

Therapy-Induced APOBEC3A Drives Evolution of Resistance to Targeted Therapies in Non-Small Cell Lung Cancer

Demographics (2)

Race and Ethnicity (1)

Other (12)