c-Raf, but Not B-Raf, Is Essential for Development of K-Ras Oncogene-Driven Non-Small Cell Lung Carcinoma
Open Access
- 21 April 2011
- journal article
- research article
- Published by Elsevier in Cancer Cell
- Vol. 19 (5), 652-663
- https://doi.org/10.1016/j.ccr.2011.04.002
Abstract
No abstract availableKeywords
This publication has 51 references indexed in Scilit:
- Acquired Resistance to BRAF Inhibitors Mediated by a RAF Kinase Switch in Melanoma Can Be Overcome by Cotargeting MEK and IGF-1R/PI3KCancer Cell, 2010
- Association of KRAS p.G13D Mutation With Outcome in Patients With Chemotherapy-Refractory Metastatic Colorectal Cancer Treated With CetuximabJAMA, 2010
- A Synthetic Lethal Interaction between K-Ras Oncogenes and Cdk4 Unveils a Therapeutic Strategy for Non-small Cell Lung CarcinomaCancer Cell, 2010
- RAF inhibitors transactivate RAF dimers and ERK signalling in cells with wild-type BRAFNature, 2010
- Kinase-Dead BRAF and Oncogenic RAS Cooperate to Drive Tumor Progression through CRAFCell, 2010
- Requirement for NF-κB signalling in a mouse model of lung adenocarcinomaNature, 2009
- Systematic RNA interference reveals that oncogenic KRAS-driven cancers require TBK1Nature, 2009
- A Gene Expression Signature Associated with “K-Ras Addiction” Reveals Regulators of EMT and Tumor Cell SurvivalCancer Cell, 2009
- A Genome-wide RNAi Screen Identifies Multiple Synthetic Lethal Interactions with the Ras OncogeneCell, 2009
- RASSF1A Elicits Apoptosis through an MST2 Pathway Directing Proapoptotic Transcription by the p73 Tumor Suppressor ProteinMolecular Cell, 2007