2024
Cancer research is not correlated with driver gene mutation burdens
Mendiratta G, Liarakos D, Tong M, Ito S, Ke E, Goshua G, Stites E. Cancer research is not correlated with driver gene mutation burdens. Med 2024, 5: 832-838.e4. PMID: 38908369, DOI: 10.1016/j.medj.2024.05.013.Peer-Reviewed Original ResearchCancer patient populationCancer researchCancer research effortsResearch allocation decisionsNational InstitutePatient populationResearch fundingBurdenBurden of mutationsFunding decisionsCancerGenetic driversGene mutation burdenFunding amountFundingGenetic drivers of cancerAllocation decisionsCancer-associated genesEpidemiologyDrivers of cancerMutational burdenBaselineEffortsFactorsBalance of prioritiesThe 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
2022
How often is each gene mutated within the cancer patient population?
Mendiratta G, Jones M, Stites E. How often is each gene mutated within the cancer patient population? Molecular & Cellular Oncology 2022, 9: 2065176. PMID: 35529901, PMCID: PMC9067461, DOI: 10.1080/23723556.2022.2065176.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
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 ResearchConceptsBiochemical 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
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
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 ResearchConceptsCell signaling networksSignaling networksCancer phenotypeMutant Ras signalingAcquisition of mutationsRas signalingCell signalingBiochemistry of proteinsLevel of signalMutated genesExpression levelsBiochemical reaction mechanismsPhenotypeMechanistic modelInvestigated signalSignalGenesMutationsRasProteinCancerIndividual reactionsExpression