Loss of wild type KRAS in KRAS lung adenocarcinoma is associated with cancer mortality and confers sensitivity to FASN inhibitors

The small molecule BI-2852 induces a nonfunctional dimer of KRAS

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Tissue-Specific Oncogenic Activity of KRASA146T

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The clinical KRAS(G12C) inhibitor AMG 510 drives anti-tumour immunity

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The KRASG12C Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients

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Genomic and Functional Approaches to Understanding Cancer Aneuploidy

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KRAS Dimerization Impacts MEK Inhibitor Sensitivity and Oncogenic Activity of Mutant KRAS

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De novo lipogenesis represents a therapeutic target in mutant Kras non-small cell lung cancer

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Scalable Open Science Approach for Mutation Calling of Tumor Exomes Using Multiple Genomic Pipelines

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Evolutionary routes and KRAS dosage define pancreatic cancer phenotypes

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Rationale for RAS mutation-tailored therapies

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Oncogene KRAS activates fatty acid synthase, resulting in specific ERK and lipid signatures associated with lung adenocarcinoma

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The K-Ras, N-Ras, and H-Ras Isoforms: Unique Conformational Preferences and Implications for Targeting Oncogenic Mutants

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Estimating Survival in Patients With Lung Cancer and Brain Metastases

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Recent advances in targeting the fatty acid biosynthetic pathway using fatty acid synthase inhibitors

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Ras Dimer Formation as a New Signaling Mechanism and Potential Cancer Therapeutic Target

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Inhibition of RAS function through targeting an allosteric regulatory site

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Selective Inhibition of Oncogenic KRAS Output with Small Molecules Targeting the Inactive State

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Fatty Acid Oxidation Mediated by Acyl-CoA Synthetase Long Chain 3 Is Required for Mutant KRAS Lung Tumorigenesis

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Biochemical and Structural Analysis of Common Cancer-Associated KRAS Mutations

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Ras-GTP dimers activate the Mitogen-Activated Protein Kinase (MAPK) pathway

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Comprehensive molecular profiling of lung adenocarcinoma

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A Comprehensive Survey of Ras Mutations in Cancer

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Integrated genomic analyses of ovarian carcinoma

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Amplification of the Driving Oncogene, KRAS or BRAF, Underpins Acquired Resistance to MEK1/2 Inhibitors in Colorectal Cancer Cells

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