LAUSR

9059 Background: Immune checkpoint inhibitors (ICIs) have demonstrated limited efficacy in patients (pts) with actionable oncogenic drivers. As a result, pts with the prototypic oncogenic drivers (EGFR and ALK) have purposefully been excluded from many NSCLC ICI trials although ICI is commonly used in combination with chemotherapy for these pts. Data from one randomized trial that included pts with known EGFR and ALK alterations did not show a survival benefit with an ICI plus a platinum doublet. We sought to gain further insight into the role of chemotherapy plus ICI in pts with oncogenic driven tumors. Methods: We conducted a retrospective analysis of pts with oncogenic drivers (EGFR, ALK, ROS1, BRAF, MET, RET, HER2 and KRAS) who were treated with chemotherapy (C) or chemotherapy plus ICI (C+ICI) between 2018 and 2019 at the five University of California (UC) NCI Designated Cancer Centers (UC Irvine, UC Davis, UC Los Angeles, UC San Diego and UC San Francisco). Descriptive statistics were used. Kaplan-Meier plots and confidence intervals summarize PFS and OS in the overall cohort and oncogenic subgroups. Results: 125 pts were identified. Median age 64.1 years; M/F (45%/55%); White/Asian (59%/33%); Current/Former/Never Smokers (4%/39%/57%); PS 0/1/2(22%/68%/10%); prior number of tyrosine kinase inhibitors 0/1/2/ > 3 (46%/23%/19%/11%); Oncogenic driver: EGFR mutations (60%), KRAS mutations (23%), ALK fusions (8%), MET mutations (2.4%), RET fusions (1.6%), ROS1 fusions (1.6%), HER2 mutations (1.6%), and BRAF mutations (0.8%). The table below displays the efficacy outcomes. Conclusions: There was no survival benefit for pts with oncogenic drivers treated with chemotherapy plus an immune checkpoint inhibitor in the overall cohort or any of the subsets. Pts with KRAS mutations treated with C+ICI had a numerically longer median PFS than their counterparts treated with C. Updated data and additional analyses including PD-L1, TMB, co-mutations and toxicity will be presented.[Table: see text]