Toma Tebaldi, PhD
Assistant Professor AdjunctDownloadHi-Res Photo
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Hematology
Primary
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About
Titles
Assistant Professor Adjunct
Biography
My research aims at understanding the RNA molecular mechanisms underlying dysregulation in human diseases, by combining experimental and computational approaches and with focus on alternative splicing events, binding of non-coding RNAs and mutant RNA binding proteins, RNA modifications (the epitranscriptome), translation dynamics and single cell expression data.
https://www.researchgate.net/profile/Toma_Tebaldi
https://orcid.org/0000-0002-0625-1631
Appointments
Hematology
Assistant Professor AdjunctPrimary
Other Departments & Organizations
Education & Training
- Visiting Professor
- University of Trento (2020)
- Visiting Professor
- University of Trento (2019)
- Postdoctoral fellowship
- University of Trento (2017)
- EMBO Short Fellowship
- University of Edinburgh (2015)
- International Internship
- University of Edinburgh (2013)
- Postdoctoral fellowship
- University of Trento (2013)
- Postdoctoral fellowship
- University of Trento (2012)
- PhD
- University of Trento, Information and Communication Technology (2010)
- International internship
- Harvard Medical School (2009)
- International internship
- University of Sheffield (2009)
- MSc
- University of Milano Bicocca, Biotechnologies - Bioinformatics (2006)
- BSc
- University of Milano Bicocca, Biotechnologies (2003)
Research
Overview
RNA biology
Medical Subject Headings (MeSH)
Computational Biology; Hematologic Neoplasms
ORCID
0000-0002-0625-1631
Research at a Glance
Yale Co-Authors
Frequent collaborators of Toma Tebaldi's published research.
Publications Timeline
A big-picture view of Toma Tebaldi's research output by year.
Giulia Biancon, PhD
Stephanie Halene, MD, Dr Med
Andrew Xiao, PhD
Bluma Lesch, MD, PhD
Diane Krause, MD, PhD
Emanuela Bruscia, PhD
18Publications
168Citations
Publications
2023
NOC1 is a direct MYC target, and its protein interactome dissects its activity in controlling nucleolar function
Manara V, Radoani M, Belli R, Peroni D, Destefanis F, Angheben L, Tome G, Tebaldi T, Bellosta P. NOC1 is a direct MYC target, and its protein interactome dissects its activity in controlling nucleolar function. Frontiers In Cell And Developmental Biology 2023, 11: 1293420. PMID: 38213308, PMCID: PMC10782387, DOI: 10.3389/fcell.2023.1293420.Peer-Reviewed Original ResearchAltmetricConceptsNucleolar homeostasisRRNA processingNucleolar structureDirect Myc targetsNuclear mRNA exportMYC transcription factorsProtein interactome analysisE-box sequenceCellular stress responseDirect functional linkN6-methyladenosine (m6A) methylationPotential involvementRibosome biogenesisMRNA exportSubnuclear compartmentsProtein interactomeRibosomal maturationFunctional MycRNA processingRibosomal biogenesisNucleolar proteinsRNA splicingNucleolar localizationInteractome analysisNucleolar functionALKBH5 modulates hematopoietic stem and progenitor cell energy metabolism through m6A modification-mediated RNA stability control
Gao Y, Zimmer J, Vasic R, Liu C, Gbyli R, Zheng S, Patel A, Liu W, Qi Z, Li Y, Nelakanti R, Song Y, Biancon G, Xiao A, Slavoff S, Kibbey R, Flavell R, Simon M, Tebaldi T, Li H, Halene S. ALKBH5 modulates hematopoietic stem and progenitor cell energy metabolism through m6A modification-mediated RNA stability control. Cell Reports 2023, 42: 113163. PMID: 37742191, PMCID: PMC10636609, DOI: 10.1016/j.celrep.2023.113163.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsAlkB homolog 5Post-transcriptional regulatory mechanismsHematopoietic stemNumerous cellular processesProgenitor cell fitnessEnergy metabolismMitochondrial ATP productionMethyladenosine (m<sup>6</sup>A) RNA modificationTricarboxylic acid cycleCell energy metabolismHuman hematopoietic cellsMitochondrial energy productionCell fitnessCellular processesRNA modificationsRNA methylationRegulatory mechanismsEnzyme transcriptsATP productionHomolog 5Acid cycleΑ-ketoglutarateHematopoietic cellsMessenger RNAΑ-KGThe Akt/mTOR and MNK/eIF4E pathways rewire the prostate cancer translatome to secrete HGF, SPP1 and BGN and recruit suppressive myeloid cells
Brina D, Ponzoni A, Troiani M, Calì B, Pasquini E, Attanasio G, Mosole S, Mirenda M, D’Ambrosio M, Colucci M, Guccini I, Revandkar A, Alajati A, Tebaldi T, Donzel D, Lauria F, Parhizgari N, Valdata A, Maddalena M, Calcinotto A, Bolis M, Rinaldi A, Barry S, Rüschoff J, Sabbadin M, Sumanasuriya S, Crespo M, Sharp A, Yuan W, Grinu M, Boyle A, Miller C, Trotman L, Delaleu N, Fassan M, Moch H, Viero G, de Bono J, Alimonti A. The Akt/mTOR and MNK/eIF4E pathways rewire the prostate cancer translatome to secrete HGF, SPP1 and BGN and recruit suppressive myeloid cells. Nature Cancer 2023, 4: 1102-1121. PMID: 37460872, PMCID: PMC11331482, DOI: 10.1038/s43018-023-00594-z.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsMyeloid-derived suppressor cellsProstate cancerAvailable immunotherapiesSuppressive myeloid cellsAKT inhibitor ipatasertibAkt/mTORProstate tumor cellsDifferent genetic alterationsMDSC infiltrationSuppressor cellsImmune surveillanceMDSC migrationTherapeutic strategiesMyeloid cellsTumor growthImmunotherapyCancerTumor cellsMNK1/2 inhibitorGenetic alterationsHGFSPP1Translational levelCellsCoordinated lossAlpha-1 Adrenergic Antagonists Sensitize Neuroblastoma to Therapeutic Differentiation.
Broso F, Gatto P, Sidarovich V, Ambrosini C, De Sanctis V, Bertorelli R, Zaccheroni E, Ricci B, Destefanis E, Longhi S, Sebastiani E, Tebaldi T, Adami V, Quattrone A. Alpha-1 Adrenergic Antagonists Sensitize Neuroblastoma to Therapeutic Differentiation. Cancer Research 2023, 83: 2733-2749. PMID: 37289021, DOI: 10.1158/0008-5472.can-22-1913.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsResidual diseaseAdrenergic antagonistsAdrenergic receptorsAlpha-1 adrenergic antagonistAdministration of doxazosinPost-consolidation therapyOverall survival probabilityPrevention of relapseHigh-risk casesMultimodal therapeutic approachPost-consolidation phaseDifferentiation of neuroblastomaNB cell viabilityAggressive childhood tumorRetinoids isotretinoinPediatric patientsΑ1B-adrenergic receptorPrevent relapseChildhood tumorsTherapeutic approachesSpecific blockadeNB cellsPharmacologic targetNeuroblastomaTumor growthVisualizing gene expression changes in time, space, and single cells with expressyouRcell
Paganin M, Tebaldi T, Lauria F, Viero G. Visualizing gene expression changes in time, space, and single cells with expressyouRcell. IScience 2023, 26: 106853. PMID: 37250782, PMCID: PMC10220493, DOI: 10.1016/j.isci.2023.106853.Peer-Reviewed Original ResearchAltmetricConceptsGene expressionSingle cellsGene expression variationBulk RNA sequencingGene expression changesProtein level changesHigh-throughput techniquesGene expression datasetsProteomic datasetsRNA sequencingExpression variationExpression changesExpression datasetsProtein levelsR packageCellsExpressionTranscriptsSequencingMassive advancementVariationComplex variationsTERRA stability is regulated by RALY and polyadenylation in a telomere-specific manner
Savoca V, Rivosecchi J, Gaiatto A, Rossi A, Mosca R, Gialdini I, Zubovic L, Tebaldi T, Macchi P, Cusanelli E. TERRA stability is regulated by RALY and polyadenylation in a telomere-specific manner. Cell Reports 2023, 42: 112406. PMID: 37060569, DOI: 10.1016/j.celrep.2023.112406.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and Concepts
2022
Hydrogen peroxide induced by nerve injury promotes axon regeneration via connective tissue growth factor
Negro S, Lauria F, Stazi M, Tebaldi T, D’Este G, Pirazzini M, Megighian A, Lessi F, Mazzanti C, Sales G, Romualdi C, Fillo S, Lista F, Sleigh J, Tosolini A, Schiavo G, Viero G, Rigoni M. Hydrogen peroxide induced by nerve injury promotes axon regeneration via connective tissue growth factor. Acta Neuropathologica Communications 2022, 10: 189. PMID: 36567321, PMCID: PMC9791753, DOI: 10.1186/s40478-022-01495-5.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsConnective tissue growth factorPerisynaptic Schwann cellsMotor axon terminalsTissue growth factorPro-regenerative factorsGrowth factorInjured sciatic nervePeripheral nerve injuryMotor nerve repairMonth old miceECM remodeling processDegeneration/regenerationNerve injuryCTGF levelsSciatic nerveNeuromuscular functionAxon terminalsNerve repairSchwann cellsNerve regenerationPro-regenerative signalsAxonal growthSC migrationMuscle fibersRemodeling processRecruited monocytes/macrophages drive pulmonary neutrophilic inflammation and irreversible lung tissue remodeling in cystic fibrosis
Öz H, Cheng E, Di Pietro C, Tebaldi T, Biancon G, Zeiss C, Zhang P, Huang P, Esquibies S, Britto C, Schupp J, Murray T, Halene S, Krause D, Egan M, Bruscia E. Recruited monocytes/macrophages drive pulmonary neutrophilic inflammation and irreversible lung tissue remodeling in cystic fibrosis. Cell Reports 2022, 41: 111797. PMID: 36516754, PMCID: PMC9833830, DOI: 10.1016/j.celrep.2022.111797.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsC motif chemokine receptor 2Monocytes/macrophagesLung tissue damageCystic fibrosisTissue damageCF lungPulmonary neutrophilic inflammationPro-inflammatory environmentChemokine receptor 2CF lung diseaseNumber of monocytesSpecific therapeutic agentsGrowth factor βCF transmembrane conductance regulatorLung hyperinflammationLung neutrophiliaNeutrophilic inflammationNeutrophil inflammationInflammation contributesLung damageNeutrophil recruitmentLung diseaseLung tissueReceptor 2Therapeutic targetDeconvolution of in vivo protein-RNA contacts using fractionated eCLIP-seq
Biancon G, Busarello E, Joshi P, Lesch B, Halene S, Tebaldi T. Deconvolution of in vivo protein-RNA contacts using fractionated eCLIP-seq. STAR Protocols 2022, 3: 101823. PMID: 36595959, PMCID: PMC9676202, DOI: 10.1016/j.xpro.2022.101823.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsProtein-RNA interactionsIndividual RNA-binding proteinsTranscriptome-wide analysisThousands of RNAsProtein-RNA contactsRNA-binding proteinSingle nucleotide levelComputational analysis pipelineRNA processingMulticomponent complexesRNA immunoprecipitationRead countsComplete detailsAnalysis pipelineAdditional levelProteinImmunoprecipitationRNAInteractionComplexesMODL-22. Establishment of a novel system to specifically trace and ablate quiescent/slow cycling cells in high-grade glioma
Antonica F, Santomaso L, Pernici D, Petrucci L, Aiello G, Cutarelli A, Conti L, Romanel A, Miele E, Tebaldi T, Tiberi L. MODL-22. Establishment of a novel system to specifically trace and ablate quiescent/slow cycling cells in high-grade glioma. Neuro-Oncology 2022, 24: i173-i173. DOI: 10.1093/neuonc/noac079.645.Peer-Reviewed Original ResearchConceptsSlow-cycling cellsHigh-grade gliomasBrain cancerCancer organoidsTumor infiltrationHigh-grade brain cancerAdult high-grade gliomasTumor cellsHigh-grade glioma patientsCommon malignant brain tumorCycling tumor cellsPediatric high-grade glioma patientsMalignant brain tumorsSlow cycling stem cellsCycling cellsHuman tumor samplesPoor prognosisSurgical removalMalignant featuresTumor relapseGlioma patientsMouse modelBrain tumorsTemozolomide treatmentMalignant cells
Academic Achievements & Community Involvement
activity Frontiers in Genetics - Computational Biology
Journal ServiceAssociate EditorDetails2021 - Presentactivity PRIN 2020 MIUR
Peer Review Groups and Grant Study SectionsReviewerDetails2021 - Presentactivity Yale Center for Biomedical Data Science
Professional OrganizationsMemberDetails2018 - Presentactivity Yale Cancer Center
Professional OrganizationsMemberDetails2020 - Presentactivity Italian Society of Yale Students and Affiliates
Professional OrganizationsBoard MemberDetails2017 - Present
News & Links
News
- December 12, 2022Source: Yale News
Driver of cystic fibrosis lung inflammation yields target for treatment
- March 31, 2022Source: Yale Daily News
New Yale Study Shows Potential Target for Treating Blood Cancers
- March 17, 2022
Yale Scientists Discover a New Pathogenic Mechanism in Hematological Malignancies
- November 15, 2020Source: Yale SEAS News
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