2024
The Abundance of KRAS and RAS Gene Mutations in Cancer
Stites E. The Abundance of KRAS and RAS Gene Mutations in Cancer. Methods In Molecular Biology 2024, 2797: 13-22. PMID: 38570449, DOI: 10.1007/978-1-0716-3822-4_2.Peer-Reviewed Original Research
2021
Cancer gene mutation frequencies for the U.S. population
Mendiratta G, Ke E, Aziz M, Liarakos D, Tong M, Stites E. Cancer gene mutation frequencies for the U.S. population. Nature Communications 2021, 12: 5961. PMID: 34645806, PMCID: PMC8514428, DOI: 10.1038/s41467-021-26213-y.Peer-Reviewed Original ResearchMeSH KeywordsComputational BiologyDNA-Binding ProteinsEpigenesis, GeneticGene Expression Regulation, NeoplasticGenetics, PopulationHumansIncidenceMutation RateNeoplasm ProteinsNeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)Terminology as TopicTranscription FactorsTumor Suppressor Protein p53United StatesConceptsMutated driver genesMutant formsCancer driversCancer geneticsCancer casesDriver genesGene mutation frequencyMutated genesU.S. populationEpigenetic dysregulationMutation frequencyDevelopment of cancerGenesPublic healthEpidemiological dataCancer typesTargetable vulnerabilitiesCancerKMT2CPopulationMutationsHealthGeneticsKMT2D
2020
Real-world data from a molecular tumor board demonstrates improved outcomes with a precision N-of-One strategy
Kato S, Kim K, Lim H, Boichard A, Nikanjam M, Weihe E, Kuo D, Eskander R, Goodman A, Galanina N, Fanta P, Schwab R, Shatsky R, Plaxe S, Sharabi A, Stites E, Adashek J, Okamura R, Lee S, Lippman S, Sicklick J, Kurzrock R. Real-world data from a molecular tumor board demonstrates improved outcomes with a precision N-of-One strategy. Nature Communications 2020, 11: 4965. PMID: 33009371, PMCID: PMC7532150, DOI: 10.1038/s41467-020-18613-3.Peer-Reviewed Original ResearchConceptsMolecular tumor boardOverall survivalTumor boardNext-generation sequencingReviewed patient characteristicsResistant to monotherapyProgression-freeOncological outcomesRemission rateChoice regimenGenomic alterationsPatient characteristicsRecommended drugsMolecular findingsPatientsTherapyMaster protocolCancer targetPhysician-directedPFSPrecision strategySurvivalDrugMedication accessOutcomes
2018
Proceedings of the fifth international RASopathies symposium: When development and cancer intersect
Rauen K, Schoyer L, Schill L, Stronach B, Albeck J, Andresen B, Cavé H, Ellis M, Fruchtman S, Gelb B, Gibson C, Gripp K, Hefner E, Huang W, Itkin M, Kerr B, Linardic C, McMahon M, Oberlander B, Perlstein E, Ratner N, Rogers L, Schenck A, Shankar S, Shvartsman S, Stevenson D, Stites E, Stork P, Sun C, Therrien M, Ullian E, Widemann B, Yeh E, Zampino G, Zenker M, Timmer W, McCormick F. Proceedings of the fifth international RASopathies symposium: When development and cancer intersect. American Journal Of Medical Genetics Part A 2018, 176: 2924-2929. PMID: 30302932, PMCID: PMC6312476, DOI: 10.1002/ajmg.a.40632.Peer-Reviewed Original ResearchConceptsGerm line mutationsPredisposition to cancerSomatic malignancyOcular abnormalitiesCraniofacial dysmorphologyMalformation syndromePathogenetic etiologyRas/mitogen-activated protein kinasePathogenetic mechanismsEffects of dysregulationSomatic cancersOncogenic pathwaysCancerPhenotypic featuresRASopathiesMAPK pathwayRas pathwayNormal functionEncode componentsProtein kinaseNeurocognitive issuesExcellent modelPathwayMalignancy
2013
Chemical kinetic mechanistic models to investigate cancer biology and impact cancer medicine
Stites E. Chemical kinetic mechanistic models to investigate cancer biology and impact cancer medicine. Physical Biology 2013, 10: 026004. PMID: 23406820, DOI: 10.1088/1478-3975/10/2/026004.Peer-Reviewed Original ResearchMeSH KeywordsComputer SimulationHumansModels, BiologicalMutationNeoplasmsSignal TransductionSystems BiologyConceptsBiochemical networksCancer biologyInvestigate cancer biologyDisrupt cellular processesAcquisition of mutationsCellular processesClinical management of cancer patientsMutated genesCancer medicineMolecular biologyExperimental biologyFeatures of cancerBiologyMutationsMechanistic modelExperimental approachGenesMolecular reactionsPace of progressKinetic mechanistic modelsCancerManagement of cancer patients
2011
Mechanistic modeling to investigate signaling by oncogenic Ras mutants
Stites E, Ravichandran K. Mechanistic modeling to investigate signaling by oncogenic Ras mutants. WIREs Mechanisms Of Disease 2011, 4: 117-127. PMID: 21766467, DOI: 10.1002/wsbm.156.Peer-Reviewed Original ResearchMeSH KeywordsCell CommunicationHumansModels, GeneticMutationNeoplasmsOncogenesRas ProteinsSignal TransductionConceptsCell signaling networksSignaling networksCancer phenotypeMutant Ras signalingAcquisition of mutationsRas signalingCell signalingBiochemistry of proteinsLevel of signalMutated genesExpression levelsBiochemical reaction mechanismsPhenotypeMechanistic modelInvestigated signalSignalGenesMutationsRasProteinCancerIndividual reactionsExpression
2009
A Systems Perspective of Ras Signaling in Cancer
Stites E, Ravichandran K. A Systems Perspective of Ras Signaling in Cancer. Clinical Cancer Research 2009, 15: 1510-1513. PMID: 19208795, DOI: 10.1158/1078-0432.ccr-08-2753.Peer-Reviewed Original Research
2007
Network Analysis of Oncogenic Ras Activation in Cancer
Stites E, Trampont P, Ma Z, Ravichandran K. Network Analysis of Oncogenic Ras Activation in Cancer. Science 2007, 318: 463-467. PMID: 17947584, DOI: 10.1126/science.1144642.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic AgentsCell LineCell Line, TumorCell Transformation, NeoplasticComputer SimulationExtracellular Signal-Regulated MAP KinasesGenes, rasGTP PhosphohydrolasesGTPase-Activating ProteinsGuanosine DiphosphateGuanosine TriphosphateHumansMathematicsMetabolic Networks and PathwaysModels, BiologicalNeoplasmsPhosphorylationPoint MutationRas ProteinsSignal Transduction