Edward Stites, MD, PhD
Associate Professor of Laboratory Medicine and PathologyCards
Appointments
Stites Lab
Contact Info
Appointments
Stites Lab
Contact Info
Appointments
Stites Lab
Contact Info
About
Titles
Associate Professor of Laboratory Medicine and Pathology
Biography
Ed Stites, MD, PhD, is an Associate Professor in the Department of Laboratory Medicine. His experimental and computational research laboratory brings ideas from mathematics to the study of disease and its treatment, with a focus on cancer. After undergraduate studies in Mathematics (University of Kentucky), he pursued dual-degree MD, PhD training (University of Virginia). His doctoral research focused on the RAS proteins that play prominent roles in many different forms of cancer. By developing a mathematical model of the processes that regulate RAS signaling, he was able to identify new aspects to how RAS functions to promote cancer. While completing his medical degree, he was recruited to the Translational Genomics Research Institute (TGen) for an independent postdoctoral fellowship as the Randy Pausch Scholar. This position enabled him to work on early personalized medicine clinical trials and cancer genomics while also maintaining a research program on RAS-pathway systems biology. He completed his clinical training with a Clinical Pathology residency at Washington University School of Medicine. He began his faculty career in 2017 at the Salk Institute for Biological Studies, where his lab combined experimental and computational methods to study clinically important problems involving RAS proteins, extended its modeling approach to additional cancer promoting proteins, and performed integrative genomic analyses that better characterize the mutations that promote cancer. His laboratory relocated to Yale University in 2022 to further expand its interdisciplinary research program.
Appointments
Laboratory Medicine
Associate Professor on TermPrimaryPathology
Associate Professor on TermSecondary
Other Departments & Organizations
Education & Training
- Postdoctoral Fellow
- Washington University School of Medicine (2016)
- Resident
- Washington University School of Medicine (2015)
- Randy Pausch Scholar
- Translational Genomics Research Institution (2012)
- MD
- University of Virginia (2010)
- PhD
- University of Virginia, Biophysics (2008)
- BS
- University of Kentucky, Mathematics (1998)
Research
The Stites Lab is broadly interested in the use of systems approaches to understand disease.
Overview
Medical Subject Headings (MeSH)
ORCID
0000-0002-3783-7336- View Lab Website
Stites Lab
Research at a Glance
Research Interests
Signal Transduction
Ras Proteins
Computational Biology
Systems Biology
Proto-Oncogene Proteins
Publications
2024
Systems modeling of oncogenic G-protein and GPCR signaling reveals unexpected differences in downstream pathway activation
Trogdon M, Abbott K, Arang N, Lande K, Kaur N, Tong M, Bakhoum M, Gutkind J, Stites E. Systems modeling of oncogenic G-protein and GPCR signaling reveals unexpected differences in downstream pathway activation. Npj Systems Biology And Applications 2024, 10: 75. PMID: 39013872, PMCID: PMC11252164, DOI: 10.1038/s41540-024-00400-1.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsSignaling networksMathematical models of biochemical reaction networksModels of biochemical reaction networksG-proteinCell signaling networksDisease-causing mutationsComputational systems biologyBiochemical reaction networksDownstream pathway activationSignaling phenotypeSystems biologyBioinformatics analysisGPCR signalingMutationsCo-occurring mutationsOncogenic mutationsPathway activationDiscovery toolPathwayReaction networkSignalCYSLTR2 mutationsDiscoveryPhenotypeMutually-exclusiveCancer 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 ResearchConceptsCancer 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 ResearchMeSH Keywords and ConceptsDecreasing alloimmunization‐specific mortality in sickle cell disease in the United States: Cost‐effectiveness of a shared transfusion resource
Ito S, Pandya A, Hauser R, Krishnamurti L, Stites E, Tormey C, Krumholz H, Hendrickson J, Goshua G. Decreasing alloimmunization‐specific mortality in sickle cell disease in the United States: Cost‐effectiveness of a shared transfusion resource. American Journal Of Hematology 2024, 99: 570-576. PMID: 38279581, DOI: 10.1002/ajh.27211.Peer-Reviewed Original ResearchAltmetricConceptsSickle cell diseaseDelayed hemolytic transfusion reactionQuality-adjusted life expectancyAlloimmunized patientsPatient populationRed blood cell alloimmunizationCell diseaseCost-effective interventionMedical expenditure of patientsHealth system perspectiveExpenditure of patientsIncremental cost-effectiveness ratioHemolytic transfusion reactionsUnited StatesMarkov cohort simulationCost-effectiveAverage patient populationCost-effectiveness ratioBirth cohortAnalytical time horizonAntibody historyCohort simulationTransfusionTransfusion reactionsLife expectancy
2023
Theoretical analysis reveals a role for RAF conformational autoinhibition in paradoxical activation
Mendiratta G, Stites E. Theoretical analysis reveals a role for RAF conformational autoinhibition in paradoxical activation. ELife 2023, 12: e82739. PMID: 37823369, PMCID: PMC10627510, DOI: 10.7554/elife.82739.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsMaking inroads to precision medicine for the treatment of autoimmune diseases: Harnessing genomic studies to better diagnose and treat complex disorders
Baglaenko Y, Wagner C, Bhoj V, Brodin P, Gershwin M, Graham D, Invernizzi P, Kidd K, Korsunsky I, Levy M, Mammen A, Nizet V, Ramirez-Valle F, Stites E, Williams M, Wilson M, Rose N, Ladd V, Sirota M. Making inroads to precision medicine for the treatment of autoimmune diseases: Harnessing genomic studies to better diagnose and treat complex disorders. Cambridge Prisms Precision Medicine 2023, 1: e25. PMID: 38550937, PMCID: PMC10953750, DOI: 10.1017/pcm.2023.14.Peer-Reviewed Original ResearchCitationsAltmetricConceptsAutoimmune diseasesPrecision medicinePathogenic autoantigenPatient subtypesDisease heterogeneityComplex etiologyMolecular profilingDiseaseAccount individual variabilityDisease mechanismsForeign cellsMolecular pathwaysNatural defense systemComplex disorderDisease treatmentHealthy tissueIndividual variabilityOwn cellsTreatmentMedicineTherapeuticsDefense systemCurrent understandingCellsAutoantigensComputational Random Mutagenesis to Investigate RAS Mutant Signaling
Stites E. Computational Random Mutagenesis to Investigate RAS Mutant Signaling. Methods In Molecular Biology 2023, 2634: 329-335. PMID: 37074586, PMCID: PMC10530643, DOI: 10.1007/978-1-0716-3008-2_15.Peer-Reviewed Original Research
2022
Co-targeting KRAS G12C and EGFR reduces both mutant and wild-type RAS-GTP
McFall T, Trogdon M, Guizar A, Langenheim J, Sisk-Hackworth L, Stites E. Co-targeting KRAS G12C and EGFR reduces both mutant and wild-type RAS-GTP. Npj Precision Oncology 2022, 6: 86. PMID: 36418474, PMCID: PMC9684405, DOI: 10.1038/s41698-022-00329-w.Peer-Reviewed Original ResearchCitationsAltmetricTherapeutic Targeting of RAS Mutant Cancers
Stites E, Paskvan K, Kato S. Therapeutic Targeting of RAS Mutant Cancers. 2022 DOI: 10.1017/9781009064828.Peer-Reviewed Original ResearchCitationsAltmetricHow 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 ResearchCitationsAltmetric
Academic Achievements & Community Involvement
activity Forbeck Foundation Scientific Advisory Board
Advisory BoardsMemberDetailsForbeck Foundation10/12/2024 - Presenthonor New Innovator Award (DP2)
National AwardNational Institutes of Health Director's Common FundDetails08/15/2020honor Career Development Award
National AwardDepartment of DefenseDetails08/01/2020honor Lung Cancer Discovery Award
National AwardAmerican Lung AssociationDetails07/01/2020honor Young Investigator Award
National AwardMelanoma Research AllianceDetails06/01/2018
Clinical Care
Overview
Clinical Specialties
Board Certifications
Clinical Pathology
- Certification Organization
- AB of Pathology
- Original Certification Date
- 2019
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