Abstract 37: Computational analysis of the KRAS G13D colorectal cancer response to EGFR inhibition with an alternatively parameterized model
McFall T, Stites E. Abstract 37: Computational analysis of the KRAS G13D colorectal cancer response to EGFR inhibition with an alternatively parameterized model. Clinical Cancer Research 2020, 26: 37-37. DOI: 10.1158/1557-3265.advprecmed20-37.Peer-Reviewed Original ResearchColon cancer cellsMultiple colon cancer cell linesBiochemical rate constantsCancer cellsColon cancer cell linesCell linesResponse to EGFR inhibitionKRAS mutantRAS biologyCancer cell linesRas signalingEGFR inhibitionMedicinal drug developmentSignaling regulationComputational analysisPersonalized cancer medicineMutantsG13D mutantWild-typeCombination of computational modelingEGFR inhibitor cetuximabColorectal cancer patientsDrug developmentCellsCancer medicineA 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