2020
A 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
2019
A systems mechanism for KRAS mutant allele–specific responses to targeted therapy
McFall T, Diedrich J, Mengistu M, Littlechild S, Paskvan K, Sisk-Hackworth L, Moresco J, Shaw A, Stites E. A systems mechanism for KRAS mutant allele–specific responses to targeted therapy. Science Signaling 2019, 12 PMID: 31551296, PMCID: PMC6864030, DOI: 10.1126/scisignal.aaw8288.Peer-Reviewed Original ResearchConceptsEpidermal growth factor receptorWild-type Ras activationColorectal cancerSensitivity to EGFR inhibitionEpidermal growth factor receptor inhibitionKRAS mutantEGFR-independent mannerAllele-specific responsesRas activationGrowth factor receptorTumor suppressor neurofibrominPatient tumorsAntibody cetuximabTargeted therapyMechanisms of EGFR signalingCRC patientsEGFR inhibitionCancer treatment decisionsRAS mutationsFactor receptorKRASTherapeutic strategiesTreatment decisionsEGFR signalingPatients
2015
Use of Mechanistic Models to Integrate and Analyze Multiple Proteomic Datasets
Stites E, Aziz M, Creamer M, Von Hoff D, Posner R, Hlavacek W. Use of Mechanistic Models to Integrate and Analyze Multiple Proteomic Datasets. Biophysical Journal 2015, 108: 1819-1829. PMID: 25863072, PMCID: PMC4390817, DOI: 10.1016/j.bpj.2015.02.030.Peer-Reviewed Original ResearchConceptsEpidermal growth factor receptorExperimentally detected interactionsPhosphotyrosine-binding domainSrc homology 2Recruitment of proteinsCell line-specific modelsProtein copy numbersProtein-protein interactionsCell signaling networksEpidermal growth factor receptor signalingCell linesWell-characterized roleCell line-specific differencesLow-affinity interactionsLine-specific differencesActivation of EGFR signalingMultiple cell linesLigand-stimulated activationAutophosphorylation sitesSignaling networksProteomic datasetsCopy numberHomolog 2EGFR signalingMap interactions
2012
The Response of Cancers to BRAF Inhibition Underscores the Importance of Cancer Systems Biology
Stites E. The Response of Cancers to BRAF Inhibition Underscores the Importance of Cancer Systems Biology. Science Signaling 2012, 5: pe46. PMID: 23074264, DOI: 10.1126/scisignal.2003354.Peer-Reviewed Original ResearchConceptsEpidermal growth factor receptorBRAF(V600E) mutationAmount of epidermal growth factor receptorEpidermal growth factor receptor inhibitorsBRAF inhibitor vemurafenibColon cancer patientsGrowth factor receptorCancer systems biologyFunctional genomics approachDecreased negative feedbackMelanoma patientsClinical responseBRAF inhibitionInhibitor vemurafenibTreatment optionsColon cancerClinical evaluationFactor receptorCancer patientsCombined treatmentBRAF(V600EVemurafenibGenomic approachesSystems biologyCancer