Background
- KRAS-mutant NSCLC with co-occurring loss-of-function mutations in STK11 and KEAP1 are remarkably aggressive, have poor prognosis (Figure. 1) and unresponsive to chemo- and immunotherapy.
- Novel therapeutic strategies are urgently needed to improve outcomes for patients with KRAS/STK11/KEAP1 (KSK) co-mutant NSCLC.
- We interrogated the transcriptomic landscape using a large real-world (RW) dataset of NSCLC to identify therapeutic vulnerabilities that may help guide treatment selections in KSK.