Abstract
Background: Mutations in KRAS account for ∼25% of lung cancer cases and are refractory to therapy. Tumors with KRAS mutations encounter increased levels of genotoxic, proteotoxic and metabolic stress, which disrupt proliferation and homeostasis. The Integrated Stress Response (ISR) plays a key role in adaptation to stress via phosphorylation of eukaryotic initiation factor 2 (p-eIF2). When ISR is activated, p-eIF2 mediates translational and transcriptional reprogramming of genes with roles in survival and adaptation. Here we demonstrate the importance of ISR in the development of KRAS lung adenocarcinoma (LUAD), the most common histological type of lung cancer and a leading cause of cancer death worldwide.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
