Jing Du, MD, PhD, MHS
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Featured Publications
A Phase II Adjuvant Trial Evaluating the Impact of Omitting Chemotherapy Based on Patient's Selection for Moderate to High-Anatomical Risk, Low-Genomic Risk, ER-positive, HER2-negative Breast Cancer with a Combination Regimen of Ribociclib and Optimized Endocrine Therapy - SELECT Trial
Clin Cancer ResPeer-Reviewed Original Research
2025
Interobserver agreement and histologic analysis of atypical ductal hyperplasia bordering on ductal carcinoma in situ: A multi-institutional study
Korie U, Ai D, Podany P, Zhang H, Zhan H, Kahila M, Colon-Cartagena L, Wei S, Sun H, Du J, Krishnamurti U, Liang Y. Interobserver agreement and histologic analysis of atypical ductal hyperplasia bordering on ductal carcinoma in situ: A multi-institutional study. American Journal Of Clinical Pathology 2025, 164: 704-711. PMID: 40994034, DOI: 10.1093/ajcp/aqaf088.Peer-Reviewed Original ResearchConceptsDuctal carcinoma in situAtypical ductal hyperplasiaCarcinoma in situSpindle-shaped nucleiAssociated with carcinomaIndividual histologic featuresHistological featuresInterobserver agreementDuctal hyperplasiaBreast pathologistsBiopsy casesCases of atypical ductal hyperplasiaLow-grade ductal carcinoma in situEpithelial cellsClinical follow-up dataLesion extentHistological analysisDiagnostic gray zoneMulti-institutional studyVariable interobserver agreementFollow-up dataModerate to substantial agreementDuct involvementHistologic reviewRadiological findingsEpigenomic Heterogeneity of Non-Functional Pancreatic Neuroendocrine Tumors Uncovered by Single nucleus and Spatial ATAC Profiling.
Wang D, Di X, Gao F, Li G, Lin L, He S, Zhang D, Jin JY, Liang Y, Cecchini M, Lacy J, Kunstman J, Kunz P, Du J, Liu Y. Epigenomic Heterogeneity of Non-Functional Pancreatic Neuroendocrine Tumors Uncovered by Single nucleus and Spatial ATAC Profiling. BioRxiv 2025 PMID: 41000913, DOI: 10.1101/2025.09.11.675640.Peer-Reviewed Original ResearchQuantifying the clinical impact of tissue reflex testing for liquid biopsy ESR1 mutation–negative cases with low ctDNA tumor fraction (TF) in HR(+)HER2(-) breast cancer.
Journal of Clinical OncologyPeer-Reviewed Original Research
2022
Platelet-derived TLT-1 promotes tumor progression by suppressing CD8+ T cells
Tyagi T, Jain K, Yarovinsky TO, Chiorazzi M, Du J, Castro C, Griffin J, Korde A, Martin KA, Takyar SS, Flavell RA, Patel AA, Hwa J. Platelet-derived TLT-1 promotes tumor progression by suppressing CD8+ T cells. Journal Of Experimental Medicine 2022, 220: e20212218. PMID: 36305874, PMCID: PMC9814191, DOI: 10.1084/jem.20212218.Peer-Reviewed Original ResearchConceptsCD8 T cellsT cellsTLT-1Non-small cell lung cancer patientsCell lung cancer patientsTREM-like transcript-1Tumor immunosuppressive mechanismsT cell suppressionLung cancer patientsPatient T cellsNF-ÎşB pathwayPatient-derived tumorsDistinct activation phenotypesNSCLC patientsImmunosuppressive mechanismsSyngeneic tumorsHumanized miceImmunoregulatory rolePrognostic significanceImmunocompetent miceCancer patientsCell suppressionActivation phenotypeReduced tumorTumor growthUnfolded Protein Response Differentially Modulates the Platelet Phenotype
Jain K, Tyagi T, Du J, Hu X, Patell K, Martin KA, Hwa J. Unfolded Protein Response Differentially Modulates the Platelet Phenotype. Circulation Research 2022, 131: 290-307. PMID: 35862006, PMCID: PMC9357223, DOI: 10.1161/circresaha.121.320530.Peer-Reviewed Original ResearchConceptsUPR pathwayProtein responseMouse plateletsUnfolded protein responseActivation of UPRPlatelet phenotypeTranscriptional regulationGenomic regulationProtein misfoldingAnucleate plateletsProtein aggregationUPR activationPhosphorylation of PLCγ2Chemical chaperonesXBP1 pathwayP38 MAPKPERK pathwayUPRPKCδ activationPlatelet physiologyActivation pathwayPathwayPhenotypeIRE1α inhibitionSelective induction
2020
Parkin Coordinates Platelet Stress Response in Diabetes Mellitus: A Big Role in a Small Cell
Lee SH, Du J, Hwa J, Kim WH. Parkin Coordinates Platelet Stress Response in Diabetes Mellitus: A Big Role in a Small Cell. International Journal Of Molecular Sciences 2020, 21: 5869. PMID: 32824240, PMCID: PMC7461561, DOI: 10.3390/ijms21165869.Peer-Reviewed Original ResearchMeSH Keywords14-3-3 ProteinsAnimalsBlood PlateletsCells, CulturedDiabetes MellitusHumansLysosomal Membrane ProteinsMiceMice, Inbred C57BLMitochondriaMitochondrial Trifunctional Protein, alpha SubunitMitophagyPlatelet ActivationProtein BindingProtein Serine-Threonine KinasesStress, PhysiologicalUbiquitin-Protein LigasesValosin Containing ProteinConceptsDiabetes mellitusDiabetic plateletsPlatelet activationNew potential therapeutic targetsEndogenous protective rolePotential therapeutic targetHealthy controlsMitochondrial β-oxidationPlatelet mitochondrial dysfunctionHealthy plateletsTherapeutic targetProtective rolePlatelet aggregationMitochondrial protectionMitochondrial dysfunctionMellitusPlateletsΒ-oxidationStress responseActivationParkinParkin-dependent mitophagyCellsDysfunctionTargeting lysosomes
2019
Mitochondrial MsrB2 serves as a switch and transducer for mitophagy
Lee SH, Lee S, Du J, Jain K, Ding M, Kadado AJ, Atteya G, Jaji Z, Tyagi T, Kim W, Herzog RI, Patel A, Ionescu CN, Martin KA, Hwa J. Mitochondrial MsrB2 serves as a switch and transducer for mitophagy. EMBO Molecular Medicine 2019, 11: emmm201910409. PMID: 31282614, PMCID: PMC6685081, DOI: 10.15252/emmm.201910409.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlood PlateletsCell LineDiabetes MellitusFemaleHumansMethionine Sulfoxide ReductasesMice, Inbred C57BLMice, KnockoutMicrofilament ProteinsMicrotubule-Associated ProteinsMitochondriaMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMitophagyMutationOxidation-ReductionOxidative StressParkinson DiseaseSignal TransductionUbiquitin-Protein LigasesUbiquitinationConceptsReduced mitophagyOxidative stress-induced mitophagyNovel regulatory mechanismStress-induced mitophagyLC3 interactionMitochondrial matrixDamaged mitochondriaMsrB2Reactive oxygen speciesRegulatory mechanismsMethionine oxidationMitophagyMitochondriaPlatelet apoptosisOxygen speciesPlatelet-specific knockoutApoptosisPathophysiological importanceExpressionImportant roleUbiquitinationParkin mutationsParkinSpeciesLC3Age associated non-linear regulation of redox homeostasis in the anucleate platelet: Implications for CVD risk patients
Jain K, Tyagi T, Patell K, Xie Y, Kadado AJ, Lee SH, Yarovinsky T, Du J, Hwang J, Martin KA, Testani J, Ionescu CN, Hwa J. Age associated non-linear regulation of redox homeostasis in the anucleate platelet: Implications for CVD risk patients. EBioMedicine 2019, 44: 28-40. PMID: 31130473, PMCID: PMC6604369, DOI: 10.1016/j.ebiom.2019.05.022.Peer-Reviewed Original ResearchMeSH KeywordsAdaptation, PhysiologicalAge FactorsAgedAged, 80 and overAgingAnimalsAntioxidantsApoptosisBiomarkersBlood PlateletsCardiovascular DiseasesComorbidityDisease Models, AnimalFemaleHomeostasisHumansMaleMiceMiddle AgedOxidation-ReductionOxidative StressPlatelet ActivationPlatelet AdhesivenessReactive Oxygen SpeciesRisk AssessmentRisk FactorsConceptsRisk patientsMouse studiesPlatelet phenotypeMajor adverse cardiovascular eventsHigh cardiovascular risk patientsAdaptive increaseAdverse cardiovascular eventsCentral pathophysiological roleCVD risk patientsCardiovascular risk patientsAggressive antiplatelet therapyEffect of comorbidityAge group 40Young healthy subjectsAntiplatelet therapyCardiovascular eventsYear age cohortAdvanced ageCVD patientsGroup 40Healthy subjectsPathophysiological roleElderly populationCardiovascular pathologyPatients
2018
Diabetes Exacerbates Myocardial Ischemia/Reperfusion Injury by Down-Regulation of MicroRNA and Up-Regulation of O-GlcNAcylation
Wang D, Hu X, Lee SH, Chen F, Jiang K, Tu Z, Liu Z, Du J, Wang L, Yin C, Liao Y, Shang H, Martin KA, Herzog RI, Young LH, Qian L, Hwa J, Xiang Y. Diabetes Exacerbates Myocardial Ischemia/Reperfusion Injury by Down-Regulation of MicroRNA and Up-Regulation of O-GlcNAcylation. JACC Basic To Translational Science 2018, 3: 350-362. PMID: 30062222, PMCID: PMC6058960, DOI: 10.1016/j.jacbts.2018.01.005.Peer-Reviewed Original ResearchR injuryInfarct sizeMyocardial ischemia/reperfusion injuryIschemia/reperfusion injuryMyocardial ischemia/reperfusionMiR-24Ischemia/reperfusionMyocardial infarct sizePromising therapeutic candidateReperfusion injuryDiabetic heartMyocardial infarctionPoor survivalMouse modelTherapeutic candidateO-GlcNAcylationGenetic overexpressionUp-RegulationInjuryDown regulationMultiple key proteinsKey proteinsHeartReperfusionHyperglycemia
Clinical Trials
Current Trials
An Interventional, Open-Label, Randomized, Multicenter, Phase 3 Study of PF-07248144 Plus Fulvestrant Compared to Investigator's Choice of Therapy in Adult Participants With Hormone Receptor-Positive, HER2-Negative Advanced/Metastatic Breast Cancer Whose Disease Progressed After Prior CDK4/6 Inhibitor-based Therapy
IRB ID2000040647RoleSub InvestigatorPrimary Completion Date07/22/2027Recruiting ParticipantsA Phase 1b/2, Open-Label, Multicohort Study of Disitamab Vedotin in Adults With HER2 Expressing Advanced Breast Cancer
IRB ID2000040649RoleSub InvestigatorPrimary Completion Date10/25/2027Recruiting ParticipantsA Phase 1/2, Open-label, First-in-human Study of the Safety, Tolerability, Pharmacokinetics, and Preliminary Efficacy of ETX-636, a Pan-mutant-selective PI3Kα Inhibitor, as Monotherapy and in Combination With Other Anticancer Therapies in Participants With Advanced Solid Tumors
IRB ID2000040945RoleSub InvestigatorPrimary Completion Date06/30/2027Recruiting ParticipantsShortStop-HER2: Shortened Duration of Adjuvant Therapy in Patients With Early-Stage HER2+ Breast Cancer Who Achieve pCR After Neoadjuvant Chemotherapy With HER2 Blockade
IRB ID2000040993RolePrincipal InvestigatorPrimary Completion Date03/13/2028Recruiting ParticipantsA Phase 3 Open-Label Randomized Study Assessing the Efficacy and Safety of RLY-2608 + Fulvestrant Versus Capivasertib + Fulvestrant as Treatment for PIK3CA-mutant Hormone Receptor Positive, Human Epidermal Growth Factor Receptor 2 Negative (HR+/HER2-) Locally Advanced or Metastatic Breast Cancer Following Recurrence or Progression On or After Treatment With a CDK4/6 Inhibitor
IRB ID2000040635RoleSub InvestigatorPrimary Completion Date04/30/2028Recruiting Participants
Clinical Care
Overview
Jing Du, MD, PhD, is a medical oncologist who specializes in the care of adults with breast cancer. She delivers compassionate, personalized care, tailoring treatments to meet each patient’s unique medical and personal needs.
As an assistant professor of medicine (medical oncology/hematology) at Yale School of Medicine, Dr. Du designs and leads clinical trials to investigate novel therapies with the goal of reducing treatment-related toxicities and improving patient outcomes. Her research interests focus on the tumor microenvironment and its role in cancer progression and treatment resistance. Utilizing cutting-edge techniques, she aims to identify new biomarkers to enhance cancer diagnosis and guide more effective, personalized treatment strategies.
Dr. Du received her medical degree from Shanghai Jiao Tong University School of Medicine and her doctoral degree in biochemistry from the University of South Carolina. Dr. Du pursued a Kirschstein-NRSA Training Fellowship at Yale School of Medicine and completed her residency and oncology-hematology fellowship at Yale New Haven Health.
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