Extended Data Fig. 5: Exploratory analyses of immune mechanisms underlying sotorasib response and resistance.
From: Molecular determinants of sotorasib clinical efficacy in KRASG12C-mutated non-small-cell lung cancer

(a) Prevalence of KC, KL, and KP tumor types (left panel) or TP53, STK11, and KEAP1 mutation status (right panels) based on PD-L1 expression among patients treated with sotorasib in the combined dataset. (b) Kaplan-Meier curve of PFS based on PD-L1 TPS for patients treated with sotorasib in the combined dataset. (c) Prevalence of immune subtypes based on PD-L1 TPS for patients with RNA-seq and PD-L1 expression data among patients treated with sotorasib from the combined dataset. (d) Kaplan-Meier curve of PFS based on immune subtypes for patients treated with sotorasib in CB100 (left panel) and CB200 (right panel). (e) Prevalence of patients with fast progression or long-term benefit across immune subtypes for patients treated with sotorasib from the combined dataset. (f) Kaplan-Meier curve of PFS for patients with inflammatory subtype treated with sotorasib in the combined dataset. CB100, CodeBreaK 100; CB200, CodeBreaK 200; IFN-ɣ, interferon gamma; KRAS, Kirsten rat sarcoma virus; MUT, mutant; PD-L1, programmed death-ligand 1; PFS, progression-free survival; TGF-β, transforming growth factor beta; RNA-seq, RNA-sequencing; TP53, tumor protein p53; TPS, tumor proportion score; WT, wild-type.