Discernment between candidate mechanisms for KRAS G13D colorectal cancer sensitivity to EGFR inhibitors
McFall T, Schomburg N, Rossman K, Stites E. Discernment between candidate mechanisms for KRAS G13D colorectal cancer sensitivity to EGFR inhibitors. Cell Communication And Signaling 2020, 18: 179. PMID: 33153459, PMCID: PMC7643456, DOI: 10.1186/s12964-020-00645-3.Peer-Reviewed Original ResearchConceptsKRAS mutationsKRAS G13DEGFR inhibitorsColorectal cancerSensitivity to EGFR inhibitorsRas-GTP levelsSensitivity to cetuximabClinical trial evidenceWild-type RasGTPase activityKRAS G13D mutationBind NF1Tumor suppressor NF1EGFR inhibitionG13D mutationKRASCetuximabBiophysical studiesTrial evidenceG13DWild-typeNF1MutationsCellular modelEGFRA mechanism for the response of KRASG13D expressing colorectal cancers to EGFR inhibitors
McFall T, Stites E. A mechanism for the response of KRASG13D expressing colorectal cancers to EGFR inhibitors. Molecular & Cellular Oncology 2020, 7: 1701914. PMID: 32158916, PMCID: PMC7051129, DOI: 10.1080/23723556.2019.1701914.Peer-Reviewed Original ResearchEpidermal growth factor receptorKRAS mutationsColorectal cancer patients treated with cetuximabPhase 3 clinical trial dataResistance to epidermal growth factor receptorPatients treated with cetuximabCancer personalized medicineColorectal cancer patientsGrowth factor receptorFactor receptorCancer patientsKRASCancer cellsAspartic acid mutationAmino acid 13NRAS signalingTrial dataPatientsCetuximabPersonalized medicineTumor suppressorMutationsImpaired bindingAcid mutationsExperimental biology