Qin Yan, PhD
Professor of PathologyCards
Additional Titles
Co-Leader, Genomics, Genetics and Epigenetics Research Program, Yale Cancer Center
Director, Center for Epigenetics and Biomarkers, Pathology
Scientific Co-Director, Center for Breast Cancer, Yale Cancer Center
Featured Publication
Contact Info
Additional Titles
Co-Leader, Genomics, Genetics and Epigenetics Research Program, Yale Cancer Center
Director, Center for Epigenetics and Biomarkers, Pathology
Scientific Co-Director, Center for Breast Cancer, Yale Cancer Center
Featured Publication
Contact Info
Additional Titles
Co-Leader, Genomics, Genetics and Epigenetics Research Program, Yale Cancer Center
Director, Center for Epigenetics and Biomarkers, Pathology
Scientific Co-Director, Center for Breast Cancer, Yale Cancer Center
Featured Publication
Contact Info
About
Titles
Professor of Pathology
Co-Leader, Genomics, Genetics and Epigenetics Research Program, Yale Cancer Center; Director, Center for Epigenetics and Biomarkers, Pathology; Scientific Co-Director, Center for Breast Cancer, Yale Cancer Center
Biography
Dr. Qin Yan (严钦) is a Professor of Pathology at Yale Medical School and a member of Yale Comprehensive Cancer Center, Yale Stem Cell Center, Yale Center for Immuno-Oncology, and Yale Center for Research on Aging. He directs a research laboratory to elucidate the roles of epigenetic mechanisms that drive tumor initiation and progression and to translate their findings to the clinic. His laboratory has made significant contributions to the understanding of the KDM5 H3K4me3/2 histone demethylases and epigenetic regulators of immune evasion and cancer metastasis. Dr. Yan received his B.S. degree from the University of Science and Technology of China. After his Ph.D. training on regulation of transcription and ubiquitination with Drs. Joan and Ronald Conaway at the Oklahoma Medical Research Foundation and Stowers Institute for Medical Research, he completed his postdoctoral training on cancer biology with Nobel laureate Dr. William Kaelin at the Dana-Farber Cancer Institute and Harvard Medical School. He has received a number of awards including the ASIP Outstanding Investigator Award, Era of Hope Scholar Award from DoD Breast Cancer Research Program, Stewart Fellow Award and V Scholar Award.
Appointments
Pathology
ProfessorPrimary
Other Departments & Organizations
- Discovery to Cure Internship
- Genomics, Genetics, and Epigenetics
- Molecular Medicine, Pharmacology, and Physiology
- Pathology
- Pathology and Molecular Medicine
- Pathology Research
- SPORE in Skin Cancer
- Yale Cancer Center
- Yale Center for Immuno-Oncology
- Yale Center for Research on Aging (Y-Age)
- Yale Combined Program in the Biological and Biomedical Sciences (BBS)
- Yale Stem Cell Center
- Yale Ventures
- Yan Lab
Education & Training
- Postdoctoral Associate
- Dana-Farber Cancer Institute and Howard Hughes Medical Institute (2007)
- PhD
- University of Oklahoma College of Medicine, Biochemistry and Molecular Biology (2002)
- BS
- University of Science and Technology of China, Molecular Biology (1996)
Research
Overview
Medical Subject Headings (MeSH)
ORCID
0000-0003-4077-453X- View Lab Website
Yan lab
Research at a Glance
Yale Co-Authors
Publications Timeline
Research Interests
Marcus Bosenberg, MD, PhD
Yao Li, MD
Akiko Iwasaki, PhD
Don Nguyen, PhD
Goran Micevic, MD, PhD
Ruth Halaban, PhD
Immunotherapy
Melanoma
Jumonji Domain-Containing Histone Demethylases
Retroelements
Epigenomics
Neoplasm Metastasis
Publications
Featured Publications
KDM5B promotes immune evasion by recruiting SETDB1 to silence retroelements
Zhang SM, Cai WL, Liu X, Thakral D, Luo J, Chan LH, McGeary MK, Song E, Blenman KRM, Micevic G, Jessel S, Zhang Y, Yin M, Booth CJ, Jilaveanu LB, Damsky W, Sznol M, Kluger HM, Iwasaki A, Bosenberg MW, Yan Q. KDM5B promotes immune evasion by recruiting SETDB1 to silence retroelements. Nature 2021, 598: 682-687. PMID: 34671158, PMCID: PMC8555464, DOI: 10.1038/s41586-021-03994-2.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsCell Line, TumorDNA-Binding ProteinsEpigenesis, GeneticGene SilencingHeterochromatinHistone-Lysine N-MethyltransferaseHumansInterferon Type IJumonji Domain-Containing Histone DemethylasesMaleMelanomaMiceMice, Inbred C57BLMice, KnockoutNuclear ProteinsRepressor ProteinsRetroelementsTumor EscapeConceptsImmune checkpoint blockadeImmune evasionCheckpoint blockadeImmune responseAnti-tumor immune responseRobust adaptive immune responseTumor immune evasionAnti-tumor immunityAdaptive immune responsesType I interferon responseDNA-sensing pathwayMouse melanoma modelImmunotherapy resistanceMost patientsCurrent immunotherapiesTumor immunogenicityImmune memoryMelanoma modelCytosolic RNA sensingRole of KDM5BConsiderable efficacyInterferon responseImmunotherapyEpigenetic therapyBlockadeCECR2 drives breast cancer metastasis by promoting NF-κB signaling and macrophage-mediated immune suppression
Zhang M, Liu ZZ, Aoshima K, Cai WL, Sun H, Xu T, Zhang Y, An Y, Chen JF, Chan LH, Aoshima A, Lang SM, Tang Z, Che X, Li Y, Rutter SJ, Bossuyt V, Chen X, Morrow JS, Pusztai L, Rimm DL, Yin M, Yan Q. CECR2 drives breast cancer metastasis by promoting NF-κB signaling and macrophage-mediated immune suppression. Science Translational Medicine 2022, 14: eabf5473. PMID: 35108062, PMCID: PMC9003667, DOI: 10.1126/scitranslmed.abf5473.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsBreast cancer metastasisReticuloendotheliosis viral oncogene homolog ACancer metastasisImmune suppressionM2 macrophagesWorse metastasis-free survivalMetastatic breast cancerMetastasis-free survivalV-rel avian reticuloendotheliosis viral oncogene homolog ACancer-related deathPrimary breast tumorsMultiple mouse modelsNF-κB signalingImmunocompetent settingNuclear factor-κB family membersMetastasis-promoting genesDistant metastasisMetastatic sitesPrimary tumorEffective therapyBreast cancerMetastasis treatmentMouse modelBreast tumorsMetastasisHuman WDR5 promotes breast cancer growth and metastasis via KMT2-independent translation regulation
Cai WL, Chen JF, Chen H, Wingrove E, Kurley SJ, Chan LH, Zhang M, Arnal-Estape A, Zhao M, Balabaki A, Li W, Yu X, Krop ED, Dou Y, Liu Y, Jin J, Westbrook TF, Nguyen DX, Yan Q. Human WDR5 promotes breast cancer growth and metastasis via KMT2-independent translation regulation. ELife 2022, 11: e78163. PMID: 36043466, PMCID: PMC9584608, DOI: 10.7554/elife.78163.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsBreast cancer cellsMetastatic breast cancerBreast cancerRibosomal gene expressionCancer cellsKnockdown of WDR5Vivo genetic screenReversible epigenetic mechanismsGenetic screenTranslation regulationTriple-negative breast cancerEpigenetic regulatorsEpigenetic mechanismsBreast cancer growthCancer-related deathTranslation efficiencyWDR5Novel therapeutic strategiesTranslation rateGene expressionCell growthAdvanced diseaseEffective therapyMetastatic capabilityPotent suppressionCancer Epigenetics, Tumor Immunity, and Immunotherapy
Cao J, Yan Q. Cancer Epigenetics, Tumor Immunity, and Immunotherapy. Trends In Cancer 2020, 6: 580-592. PMID: 32610068, PMCID: PMC7330177, DOI: 10.1016/j.trecan.2020.02.003.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsCitationsAltmetricMeSH Keywords and ConceptsConceptsImmune responseAntitumor immune responseCancer-immunity cycleAnticancer immune responseEpigenetic targeting agentsImpaired immunosurveillanceCurrent immunotherapiesTumor immunityImmunomodulatory drugsImmune cellsImmune restrictionTargeting agentEpigenetic mechanismsEpigenetic regulatorsImmunotherapyPharmaceutical modulationEpigenetic therapyTumorsImmunosurveillanceTherapyCurrent advancesDNA methylationImmunityResponseThe Crossroads of Cancer Epigenetics and Immune Checkpoint Therapy.
Micevic G, Bosenberg M, Yan Q. The Crossroads of Cancer Epigenetics and Immune Checkpoint Therapy. Clinical Cancer Research 2022, 29: 1173-1182. PMID: 36449280, PMCID: PMC10073242, DOI: 10.1158/1078-0432.ccr-22-0784.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsCitationsAltmetricMeSH Keywords and ConceptsConceptsImmune checkpoint inhibitorsImmune checkpoint therapyT cell exhaustionCheckpoint therapyAntitumor immune responseT cell populationsCell-intrinsic immunityTypes of cancerViral mimicry responseLow response rateCheckpoint inhibitorsCurrent immunotherapiesPancreatic cancerSustained responsePreclinical modelsTreatment outcomesImmune responseEndogenous antigensResponse rateTumor typesMultiple epigenetic regulatorsCritical mediatorLow immunogenicityTherapyCancerPotent BRD4 inhibitor suppresses cancer cell-macrophage interaction
Yin M, Guo Y, Hu R, Cai WL, Li Y, Pei S, Sun H, Peng C, Li J, Ye R, Yang Q, Wang N, Tao Y, Chen X, Yan Q. Potent BRD4 inhibitor suppresses cancer cell-macrophage interaction. Nature Communications 2020, 11: 1833. PMID: 32286255, PMCID: PMC7156724, DOI: 10.1038/s41467-020-15290-0.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAdministration, OralAnimalsCell CommunicationCell Cycle ProteinsCell Line, TumorCell ProliferationDisease Models, AnimalDown-RegulationDrug DesignFemaleHumansHypoxia-Inducible Factor 1, alpha SubunitMacrophage Colony-Stimulating FactorMacrophagesMice, Inbred BALB CMice, NudeNeoplasmsPhosphorylationProto-Oncogene Proteins c-mycReceptors, Granulocyte-Macrophage Colony-Stimulating FactorSignal TransductionTranscription FactorsTreatment OutcomeConceptsTumor growthMajor clinical stagesBET inhibitorsProliferation of tumorsExtraterminal domain (BET) family proteinsTumor cell proliferationClinical stageTumor shrinkageSyngeneic modelPotent BRD4 inhibitorsSmall molecule inhibitorsSolid tumorsBRD4 inhibitionTumor cellsOral bioavailabilityCancer treatmentCell proliferationBRD4 inhibitorsMolecule inhibitorsMultiple mechanismsC-MycTumorsInhibitorsKDM5 histone demethylases repress immune response via suppression of STING
Wu L, Cao J, Cai WL, Lang SM, Horton JR, Jansen DJ, Liu ZZ, Chen JF, Zhang M, Mott BT, Pohida K, Rai G, Kales SC, Henderson MJ, Hu X, Jadhav A, Maloney DJ, Simeonov A, Zhu S, Iwasaki A, Hall MD, Cheng X, Shadel GS, Yan Q. KDM5 histone demethylases repress immune response via suppression of STING. PLOS Biology 2018, 16: e2006134. PMID: 30080846, PMCID: PMC6095604, DOI: 10.1371/journal.pbio.2006134.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsImmune responseSTING expressionCyclic GMP-AMP synthase stimulatorSuppression of STINGCancer cellsCancer immunotherapy agentsHuman papilloma virusAdaptive immune responsesMultiple clinical trialsExpression of STINGBreast cancer cellsInnate immune defenseRobust interferon responseMultiple cancer typesIntratumoral CD8Immunotherapy agentsAnticancer immunotherapyPatient survivalNeck cancerPapilloma virusClinical trialsT cellsSTING agonistsKDM5 histonePositive headEpigenetic markers and therapeutic targets for metastasis
Kravitz C, Yan Q, Nguyen D. Epigenetic markers and therapeutic targets for metastasis. Cancer And Metastasis Reviews 2023, 42: 427-443. PMID: 37286865, PMCID: PMC10595046, DOI: 10.1007/s10555-023-10109-y.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsCitationsAltmetricMeSH Keywords and ConceptsConceptsEpigenomic alterationsLineage integrityTherapeutic targetEpigenetic markersCancer cellsGenetic aberrationsCurrent knowledgeHuman tumorsMalignant cell cloneTumor progressionDNANumber of discoveriesCell clonesDisseminated diseaseCertain organsPrimary tumorTherapeutic responseMetastatic cancerEpigenomeChromatinHistonesLiquid biopsyAlterationsClonesTarget
2024
Ultra-sensitive molecular residual disease detection through whole genome sequencing with single-read error correction
Li X, Liu T, Bacchiocchi A, Li M, Cheng W, Wittkop T, Mendez F, Wang Y, Tang P, Yao Q, Bosenberg M, Sznol M, Yan Q, Faham M, Weng L, Halaban R, Jin H, Hu Z. Ultra-sensitive molecular residual disease detection through whole genome sequencing with single-read error correction. EMBO Molecular Medicine 2024, 16: 2188-2209. PMID: 39164471, PMCID: PMC11393307, DOI: 10.1038/s44321-024-00115-0.Peer-Reviewed Original ResearchConceptsMolecular residual diseaseCirculating tumor DNAWhole-genome sequencingCell-free DNAGenome sequenceDetection of molecular residual diseaseCirculating tumor DNA detectionResidual disease detectionConsistent with clinical outcomesVariant allele frequencyResidual diseaseMelanoma patientsMonitoring immunotherapyTumor DNAEsophageal cancerClinical outcomesColorectal cancerWGS technologiesAllele frequenciesCancerDNAAnalytical sensitivitySequenceImmunotherapyRelapseCombined BET and MEK Inhibition synergistically suppresses melanoma by targeting YAP1
Hu R, Hou H, Li Y, Zhang M, Li X, Chen Y, Guo Y, Sun H, Zhao S, Liao M, Cao D, Yan Q, Chen X, Yin M. Combined BET and MEK Inhibition synergistically suppresses melanoma by targeting YAP1. Theranostics 2024, 14: 593-607. PMID: 38169595, PMCID: PMC10758063, DOI: 10.7150/thno.85437.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsMEK inhibitor resistanceMEK inhibitor trametinibTrametinib treatmentInhibitor resistanceInhibitor trametinibMelanoma patientsYAP1 expressionMEK inhibitionBRAF-mutant melanoma patientsResistance to MEK inhibitionYAP1 inhibitionResistance to trametinibMelanoma growth <i>inInhibition of BRD4Trametinib resistanceAntitumor effectMelanoma growthTrametinibNHWD-870YAP1 inhibitorDrug resistanceMelanomaMelanoma samplesMelanoma cellsBRD4 depletion
Academic Achievements & Community Involvement
activity Breast Cancer Alliance
Peer Review Groups and Grant Study SectionsMemberDetailsMember, Reviewer Committee2014 - Presentactivity American Society for Investigative Pathology
Professional OrganizationsMemberDetailsCo-chair, Gene Expression Scientific Interest Group11/19/2014 - Presentactivity Department of Defense Breast Cancer Research Program
Peer Review Groups and Grant Study SectionsMemberDetailsAd hoc reviewer, FY17-FY23 Programmatic Panel; Member, FY12 study section09/30/2012 - Presentactivity NIH
Peer Review Groups and Grant Study SectionsReviewerDetailsAd hoc member, Cancer Genetics (CG), Cancer Molecular Pathobiology (CAMP), Mechanisms of Cancer Therapeutics-1 (MCT1), NCI SPORE (P50), and F09A Fellowships Oncology Study Section2017 - Presentactivity Cancer and Metastasis Reviews
Journal ServiceAssociate EditorDetails12/01/2023 - Present
News & Links
News
- July 16, 2024
YCC 2024 Trainee Colloquium
- March 20, 2024
Breast cancer research
- February 28, 2024
Grants Awarded at YCC • 2024
- November 28, 2023
Yale Cancer Center Experts Present New Research at Leading Breast Cancer Symposium
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Brady Memorial Laboratory
Lab
310 Cedar Street, Rm BML338
New Haven, CT 06510
Fax
203.785.2443Appointments
203.785.6496Department of Pathology
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Brady Memorial Laboratory
310 Cedar Street, Rm BML348C
New Haven, CT 06510
Fax
203.785.2443Appointments
203.785.6672