2020
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 medicine
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