Nadya Dimitrova, PhD
Associate Professor on Term of Molecular, Cellular and Developmental BiologyDownloadHi-Res Photo
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Genetics
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Associate Professor on Term of Molecular, Cellular and Developmental Biology
Biography
Nadya Dimitrova is an Assistant Professor in the Department of Molecular, Cellular, and Developmental Biology at Yale University. Her research focuses on the functional characterization of tumor suppressor and oncogenic long non-coding RNAs and their roles in the regulation of the cancer transcriptome. Originally from Sofia, Bulgaria, Nadya graduated with an Sc.B. in Biochemistry from Brown University in 2002. She joined the graduate program at The Rockefeller University and in 2009 received a Ph.D. for her work on the signaling and repair of dysfunctional telomeres in the laboratory of Dr. Titia de Lange. For her graduate work, Nadya was awarded the Harold M. Weintraub Graduate Student Award. As a postdoctoral fellow, Nadya joined the laboratory of Dr. Tyler Jacks at the Koch Institute for Integrative Cancer Research at MIT where she developed genetic mouse models to study long non-coding RNAs in cancer biology. Nadya is the recipient of the HHMI Predoctoral Fellowship, the Damon Runyon Postdoctoral Fellowship Award, the Lung Cancer Research Foundation 2016 Scientific Merit Award, the V Scholar Award, and the Pew-Stewart Scholar for Cancer Research Award.
Appointments
Genetics
Associate Professor on TermSecondary
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Education & Training
- PhD
- The Rockefeller University (2009)
Research
Overview
Medical Research Interests
Genetics; Genomics; Molecular Biology; RNA, Untranslated
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Nadya Dimitrova Lab
Research at a Glance
Yale Co-Authors
Frequent collaborators of Nadya Dimitrova's published research.
Publications Timeline
A big-picture view of Nadya Dimitrova's research output by year.
Clara Liao, BA
Katerina Politi, PhD
10Publications
745Citations
Publications
2024
Challenges in LncRNA Biology: Views and Opinions
Adjeroh D, Zhou X, Paschoal A, Dimitrova N, Derevyanchuk E, Shkurat T, Loeb J, Martinez I, Lipovich L. Challenges in LncRNA Biology: Views and Opinions. Non-Coding RNA 2024, 10: 43. PMID: 39195572, PMCID: PMC11357347, DOI: 10.3390/ncrna10040043.Peer-Reviewed Original ResearchAltmetricOverexpression of Malat1 drives metastasis through inflammatory reprogramming of the tumor microenvironment
Martinez-Terroba E, Plasek-Hegde L, Chiotakakos I, Li V, de Miguel F, Robles-Oteiza C, Tyagi A, Politi K, Zamudio J, Dimitrova N. Overexpression of Malat1 drives metastasis through inflammatory reprogramming of the tumor microenvironment. Science Immunology 2024, 9: eadh5462. PMID: 38875320, DOI: 10.1126/sciimmunol.adh5462.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsTumor microenvironmentLung adenocarcinomaMetastatic diseasePromoting metastatic diseaseGlobal chromatin accessibilityMetastasis-associated lung adenocarcinoma transcript 1Overexpression of MALAT1Lung adenocarcinoma transcript 1Lung adenocarcinoma metastasisCCL2 blockadeInflammatory reprogrammingEnhanced cell mobilityMacrophage depletionMechanism of actionTumor typesTumor progressionMouse modelCell mobilizationTumorLong noncoding RNAsParacrine secretionMetastasisCell linesTranscript 1MicroenvironmentTherapeutic Inhibition of LincRNA-p21 Protects Against Cardiac Hypertrophy
Wang Y, Zhang M, Wang R, Lin J, Ma Q, Guo H, Huang H, Liang Z, Cao Y, Zhang X, Lu Y, Liu J, Xiao F, Yan H, Dimitrova N, Huang Z, Mably J, Pu W, Wang D. Therapeutic Inhibition of LincRNA-p21 Protects Against Cardiac Hypertrophy. Circulation Research 2024, 135: 434-449. PMID: 38864216, PMCID: PMC11257812, DOI: 10.1161/circresaha.123.323356.Peer-Reviewed Original ResearchCitationsAltmetricConceptsCardiac hypertrophyHeart failureGenome-wide transcriptome analysisCardiac functionDeterioration of cardiac functionResponse to pressure overloadAssociated heart failureTherapeutic potentialLoss-of-function miceDilated cardiomyopathy patientsPressure-overload conditionsInhibit cardiac hypertrophyTranscriptome analysisCardiac-specific knockoutMaladaptive cardiac remodelingLong noncoding RNAsVentricular wall thickeningNoncoding RNAsTranscriptional network analysisCardiomyopathy patientsMarker elevationPressure overloadCardiac remodelingPathological hypertrophyAdverse remodelingTranscription regulation by long non-coding RNAs: mechanisms and disease relevance
Ferrer J, Dimitrova N. Transcription regulation by long non-coding RNAs: mechanisms and disease relevance. Nature Reviews Molecular Cell Biology 2024, 25: 396-415. PMID: 38242953, PMCID: PMC11045326, DOI: 10.1038/s41580-023-00694-9.Peer-Reviewed Original ResearchCitationsAltmetricConceptsCis-regulatory functionLong non-coding RNAsGene transcriptionNon-coding RNAsTranscription factorsControl of gene transcriptionProtein-coding transcriptsActivation of gene transcriptionDosage-sensitive genesEncode transcription factorsX-chromosome inactivationTranscription unitTranscription elongationGenetic experimentsTranscriptional regulationTranscript stabilityCharacterized lncRNATranscriptionHuman diseasesFindings of lncRNAsImprinted lncRNAsLncRNA involvementLincRNA-p21Severe phenotypeLncRNAs
2021
The p53 transcriptional response across tumor types reveals core and senescence-specific signatures modulated by long noncoding RNAs
Tesfaye E, Martinez-Terroba E, Bendor J, Winkler L, Olivero C, Chen K, Feldser DM, Zamudio JR, Dimitrova N. The p53 transcriptional response across tumor types reveals core and senescence-specific signatures modulated by long noncoding RNAs. Proceedings Of The National Academy Of Sciences Of The United States Of America 2021, 118: e2025539118. PMID: 34326251, PMCID: PMC8346867, DOI: 10.1073/pnas.2025539118.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsCarcinogenesisCell Line, TumorCell ProliferationCellular SenescenceDNA DamageE2F Transcription FactorsGene Expression Regulation, NeoplasticGenome-Wide Association StudyMiceNeoplasmsProto-Oncogene Proteins c-mycRNA, Long NoncodingSignal TransductionStress, PhysiologicalTumor Suppressor Protein p53ConceptsOncogenic contextPermanent cell cycle arrestP53-induced lncRNAsP53 transcriptional responseMYC target genesTumor suppressor mechanismRepression of E2FP53-binding siteP53-dependent senescenceTumor-type specificCell cycle arrestTranscriptional responseProliferative arrestTarget genesMurine cancer cell linesTranscriptional signatureRegulatory axisTumor typesCycle arrestP53 functionDistinct tumor typesFunctional investigationDownstream mediatorP53 pathwayCancer cell lines
2020
Identification and characterization of functional long noncoding RNAs in cancer
Olivero CE, Dimitrova N. Identification and characterization of functional long noncoding RNAs in cancer. The FASEB Journal 2020, 34: 15630-15646. PMID: 33058262, PMCID: PMC7756267, DOI: 10.1096/fj.202001951r.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and Conceptsp53 Activates the Long Noncoding RNA Pvt1b to Inhibit Myc and Suppress Tumorigenesis
Olivero CE, MartÃnez-Terroba E, Zimmer J, Liao C, Tesfaye E, Hooshdaran N, Schofield JA, Bendor J, Fang D, Simon MD, Zamudio JR, Dimitrova N. p53 Activates the Long Noncoding RNA Pvt1b to Inhibit Myc and Suppress Tumorigenesis. Molecular Cell 2020, 77: 761-774.e8. PMID: 31973890, PMCID: PMC7184554, DOI: 10.1016/j.molcel.2019.12.014.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsCarcinogenesisCell LineCell ProliferationCells, CulturedChromatinEnhancer Elements, GeneticGene Expression RegulationHumansLung NeoplasmsMiceMice, Inbred C57BLPromoter Regions, GeneticProto-Oncogene MasProto-Oncogene Proteins c-mycRNA, Long NoncodingStress, PhysiologicalTumor Suppressor Protein p53ConceptsMYC transcriptional networkLong noncoding RNA PVT1Cellular proliferationTumor suppressor p53Chromatin organizationTranscriptional networksTarget genesMYC transcriptionTranscriptional activityKb downstreamMYC levelsOncogenic signalingSuppressor p53Suppress tumorigenesisDNA damageRNA PVT1Autochthonous mouse modelMYCTranscriptionP53Anti-proliferative activityTumor progressionTumor growthLung cancerMouse model
2018
Chapter 16 Genetic Variations of Long Noncoding RNAs in Cancer
Dimitrova N. Chapter 16 Genetic Variations of Long Noncoding RNAs in Cancer. 2018, 289-308. DOI: 10.1016/b978-0-12-811022-5.00016-4.Peer-Reviewed Original ResearchConceptsComprehensive genome analysisFunction of lncRNAsLong noncoding RNALncRNA lociCancer susceptibility variantsGenome analysisGenetic variationRegulatory regionsNoncoding RNAsGenomic dataSomatic variationExpression patternsFocal amplificationCancer predispositionPhysiological roleLncRNAsFunctional consequencesHuman cancersNucleotide polymorphismsExpression levelsRNAMechanism of actionNovel classIntriguing associationStrong linkage
2016
Stromal Expression of miR-143/145 Promotes Neoangiogenesis in Lung Cancer Development
Dimitrova N, Gocheva V, Bhutkar A, Resnick R, Jong RM, Miller KM, Bendor J, Jacks T. Stromal Expression of miR-143/145 Promotes Neoangiogenesis in Lung Cancer Development. Cancer Discovery 2016, 6: 188-201. PMID: 26586766, PMCID: PMC4744583, DOI: 10.1158/2159-8290.cd-15-0854.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and Concepts
2014
LincRNA-p21 Activates p21 In cis to Promote Polycomb Target Gene Expression and to Enforce the G1/S Checkpoint
Dimitrova N, Zamudio JR, Jong RM, Soukup D, Resnick R, Sarma K, Ward AJ, Raj A, Lee JT, Sharp PA, Jacks T. LincRNA-p21 Activates p21 In cis to Promote Polycomb Target Gene Expression and to Enforce the G1/S Checkpoint. Molecular Cell 2014, 54: 777-790. PMID: 24857549, PMCID: PMC4103188, DOI: 10.1016/j.molcel.2014.04.025.Peer-Reviewed Original ResearchMeSH Keywords and ConceptsConceptsG1/S checkpointGene expressionS checkpointPolycomb target genesGlobal gene expressionP53 transcriptional networkTarget gene expressionTumor suppressor pathwayConditional knockout mouse modelP53 tumor suppressor pathwayChromatin stateTranscriptional networksKnockout mouse modelNeighboring genesMRNA translationProtein stabilityTarget genesP21 transcriptionSuppressor pathwayAdditional phenotypesGenesP21 levelsLincRNA-p21P21 expressionCoactivator
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