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 vulnerabilitiesCancerKMT2CPopulationMutationsHealthGeneticsKMT2DMathematical Modeling to Study KRAS Mutant-Specific Responses to Pathway Inhibition
Stites E. Mathematical Modeling to Study KRAS Mutant-Specific Responses to Pathway Inhibition. Methods In Molecular Biology 2021, 2262: 311-321. PMID: 33977486, PMCID: PMC8639139, DOI: 10.1007/978-1-0716-1190-6_19.Peer-Reviewed Original ResearchMeSH KeywordsColorectal NeoplasmsErbB ReceptorsHumansModels, TheoreticalMolecular Targeted TherapyMutationProtein Kinase InhibitorsProto-Oncogene Proteins p21(ras)ConceptsRegulates Ras signalingMutant Ras proteinsKRAS G13D mutationRas proteinsRAS communityRas mutantsRas signalingRas pathwayBiochemical reactionsWild-typeRasMutationsPathway inhibitionG13D mutationDose-response experimentsMutantsKnowledge of reaction mechanismsInhibitionEGFR inhibitionKRAS mutationsProteinKRASKRAS‐Mutated, Estrogen Receptor‐Positive Low‐Grade Serous Ovarian Cancer: Unraveling an Exceptional Response Mystery
Kato S, McFall T, Takahashi K, Bamel K, Ikeda S, Eskander R, Plaxe S, Parker B, Stites E, Kurzrock R. KRAS‐Mutated, Estrogen Receptor‐Positive Low‐Grade Serous Ovarian Cancer: Unraveling an Exceptional Response Mystery. The Oncologist 2021, 26: e530-e536. PMID: 33528846, PMCID: PMC8018312, DOI: 10.1002/onco.13702.Peer-Reviewed Original ResearchMeSH KeywordsAromatase InhibitorsFemaleHumansNitrilesOvarian NeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins p21(ras)Receptors, EstrogenTamoxifenTriazolesConceptsMEK inhibitorsMechanism of actionOvarian cancerAromatase inhibitorsEstrogen modulationKRAS-mutantLow-grade serous ovarian cancerCombination of trametinibEstrogen receptor-positiveSerous ovarian cancerPrecision medicine strategiesPI3K inhibitorsReceptor-positiveCombination therapyEstrogen depletionTamoxifenTrametinibAgonist effectsIn vitro investigationLetrozoleEstrogenIn vitro experimentsMedicine strategiesMEKExceptional response
2020
Discernment between candidate mechanisms for KRAS G13D colorectal cancer sensitivity to EGFR inhibitors
McFall T, Schomburg N, Rossman K, Stites E. Discernment between candidate mechanisms for KRAS G13D colorectal cancer sensitivity to EGFR inhibitors. Cell Communication And Signaling 2020, 18: 179. PMID: 33153459, PMCID: PMC7643456, DOI: 10.1186/s12964-020-00645-3.Peer-Reviewed Original ResearchConceptsKRAS mutationsKRAS G13DEGFR inhibitorsColorectal cancerSensitivity to EGFR inhibitorsRas-GTP levelsSensitivity to cetuximabClinical trial evidenceWild-type RasGTPase activityKRAS G13D mutationBind NF1Tumor suppressor NF1EGFR inhibitionG13D mutationKRASCetuximabBiophysical studiesTrial evidenceG13DWild-typeNF1MutationsCellular modelEGFR
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
2018
Quantitative Systems Pharmacology Analysis of KRAS G12C Covalent Inhibitors
Stites E, Shaw A. Quantitative Systems Pharmacology Analysis of KRAS G12C Covalent Inhibitors. CPT Pharmacometrics & Systems Pharmacology 2018, 7: 342-351. PMID: 29484842, PMCID: PMC5980551, DOI: 10.1002/psp4.12291.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic AgentsCell Line, TumorComputer SimulationDrug DiscoveryHumansLung NeoplasmsMutationProto-Oncogene Proteins p21(ras)Signal TransductionSystems BiologyConceptsRegulates Ras activitySystems biology approachBiology approachRas activationProtein turnoverKRAS-G12C covalent inhibitorsKRAS G12C inhibitorsSystems pharmacology analysisRasKRAS mutantDrug developmentG12C inhibitorsCovalent inhibitorsInhibitorsKRASMutantsPharmacological analysisMutationsKRAS G12C
2012
Genome-Wide Characterization of Pancreatic Adenocarcinoma Patients Using Next Generation Sequencing
Liang W, Craig D, Carpten J, Borad M, Demeure M, Weiss G, Izatt T, Sinari S, Christoforides A, Aldrich J, Kurdoglu A, Barrett M, Phillips L, Benson H, Tembe W, Braggio E, Kiefer J, Legendre C, Posner R, Hostetter G, Baker A, Egan J, Han H, Lake D, Stites E, Ramanathan R, Fonseca R, Stewart A, Von Hoff D. Genome-Wide Characterization of Pancreatic Adenocarcinoma Patients Using Next Generation Sequencing. PLOS ONE 2012, 7: e43192. PMID: 23071490, PMCID: PMC3468610, DOI: 10.1371/journal.pone.0043192.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaBase SequenceBRCA2 ProteinDNA RepairFemaleGene DosageGenome, HumanHigh-Throughput Nucleotide SequencingHumansMaleMetabolic Networks and PathwaysPancreatic NeoplasmsProto-Oncogene ProteinsProto-Oncogene Proteins c-mycProto-Oncogene Proteins p21(ras)Ras ProteinsSequence Analysis, RNATranscriptomeTumor Suppressor Protein p53ConceptsPancreatic adenocarcinoma patientsNext generation sequencingPancreatic adenocarcinomaGeneration sequencingSomatic eventsGenome-wide characterizationChromosomal copy number variantsCopy number variantsImproved therapeutic selectivityTumor suppressive pathwaysPancreatic adenocarcinoma tumorigenesisTumor-stroma interactionsKRAS signaling pathwaySequence dataTranscriptomic informationTumor/normal samplesEvaluate expression changesTranslocation eventsMultiple genesPoint mutationsRNA sequencingMapped readsPatient tumorsAdenocarcinoma patientsPathway analysis