Jing Du, MD, PhD
she/her/hers
Assistant Professor of Medicine (Medical Oncology/Hematology)Cards
About
Research
Publications
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
2017
Opposing Actions of AKT (Protein Kinase B) Isoforms in Vascular Smooth Muscle Injury and Therapeutic Response
Jin Y, Xie Y, Ostriker AC, Zhang X, Liu R, Lee MY, Leslie KL, Tang W, Du J, Lee SH, Wang Y, Sessa WC, Hwa J, Yu J, Martin KA. Opposing Actions of AKT (Protein Kinase B) Isoforms in Vascular Smooth Muscle Injury and Therapeutic Response. Arteriosclerosis Thrombosis And Vascular Biology 2017, 37: 2311-2321. PMID: 29025710, PMCID: PMC5699966, DOI: 10.1161/atvbaha.117.310053.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBinding SitesCell Cycle ProteinsCell DifferentiationCell MovementCell ProliferationCells, CulturedDisease Models, AnimalForkhead Transcription FactorsGene Expression RegulationGenetic Predisposition to DiseaseHumansMice, KnockoutMuscle, Smooth, VascularMyocytes, Smooth MuscleNeointimaNuclear ProteinsPhenotypePromoter Regions, GeneticProto-Oncogene Proteins c-aktRNA InterferenceRNA, MessengerSignal TransductionSirolimusTime FactorsTrans-ActivatorsTranscription FactorsTransfectionVascular System InjuriesConceptsIntimal hyperplasiaTherapeutic inhibitionVascular smooth muscle injurySmooth muscle-specific deletionSmooth muscle cell proliferationSystemic vascular diseaseSevere intimal hyperplasiaSmooth muscle injuryNew treatment strategiesWild-type miceAkt isoformsMuscle cell proliferationMuscle-specific deletionMechanism of actionVascular smooth muscle cell differentiationCoronary revascularizationSmooth muscle cell differentiationDiabetes mellitusDiabetic patientsControl miceRapamycin therapyVascular diseaseMuscle injuryTherapeutic responseSevere thrombosis
Clinical Trials
Current Trials
Phase Ib Randomized Open-label Trial of Sacituzumab Govitecan Plus Nivolumab or Sacituzumab Govitecan Plus Nivolumab and Relatlimab as Second-line Therapy for PD-L1 Positive Metastatic Triple Negative Breast Cancer
HIC ID2000037105RoleSub InvestigatorPrimary Completion Date12/31/2030Recruiting ParticipantsA Single Arm Phase II Trial of Circulating Tumor DNA-guided Adjuvant Therapy With Elacestrant in Hormone Receptor Positive HER2 Negative Breast Cancers at Risk for Late Recurrence (CATE)
HIC ID2000039112RoleSub InvestigatorPrimary Completion Date09/30/2027Recruiting ParticipantsA Single-Arm, Phase II Study of Sequential Therapy With Curative Intent in de Novo HER2+ Metastatic Breast Cancer: The SAPPHO Study
HIC ID2000039526RoleSub InvestigatorPrimary Completion Date03/30/2030Recruiting ParticipantsSELECT: 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
HIC ID2000038734RolePrincipal InvestigatorPrimary Completion Date09/30/2030Recruiting ParticipantsStudy to Assess Clinical Activity of Zelenectide Pevedotin in Participants With Advanced Breast Cancer
HIC ID2000039480RoleSub InvestigatorPrimary Completion Date06/30/2028Recruiting 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.
Clinical Specialties
Breast Oncology; Medical Oncology
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