Zaira Ianniello, PhD
Associate Research Scientist in Therapeutic RadiologyAbout
Research
Publications
2025
Harnessing exDNA for precision exatecan delivery in cancer: a novel antibody-drug conjugate approach
Ianniello Z, Lu H, Quijano E, Colón-Ríos D, Rackear M, Bommireddy V, Ludwig D, Shen Z, Glazer P. Harnessing exDNA for precision exatecan delivery in cancer: a novel antibody-drug conjugate approach. Molecular Cancer 2025, 24: 253. PMID: 41077566, PMCID: PMC12516839, DOI: 10.1186/s12943-025-02462-z.Peer-Reviewed Original ResearchTriple-negative breast cancerAntibody-drug conjugatesAnti-tumor activityBlood-brain barrierCancer cell linesSafety profileTumor selectivityTherapeutic efficacyXenograft modelXenograft models of triple-negative breast cancerModels of triple-negative breast cancerDose-escalation studyProlonged median survivalBone marrow toxicityBystander killing effectTumor-selective targetingNuclear drug deliveryAntibody-drug conjugate approachTumor-bearing miceTumor growth inhibitionCell linesDNA damage responseLong-term treatmentKidney function testsAnalysis of hematological parametersSystemic administration of an RNA binding and cell-penetrating antibody targets therapeutic RNA to multiple mouse models of cancer
Quijano E, Martinez-Saucedo D, Ianniello Z, Pinto-Medici N, Rackear M, Chen H, Lola-Pereira L, Liu Y, Hegan D, Shan X, Tseng R, Yugawa D, Chowdhury S, Khang M, Singh J, Abdullah R, Azhir P, Kashima S, Woods W, Gosstola N, Turner B, Squinto S, Ludwig D, Bindra R, Robert M, Braun D, Perez Pinera P, Saltzman W, Escobar-Hoyos L, Glazer P. Systemic administration of an RNA binding and cell-penetrating antibody targets therapeutic RNA to multiple mouse models of cancer. Science Translational Medicine 2025, 17: eadk1868. PMID: 40668891, PMCID: PMC12375925, DOI: 10.1126/scitranslmed.adk1868.Peer-Reviewed Original ResearchConceptsMouse modelAntitumor efficacyTumor cellsMouse model of pancreatic cancerActivation of cytotoxic T cellsOrthotopic pancreatic cancer modelImmune responseModel of pancreatic cancerAntitumor immune responseCytotoxic T cellsPancreatic cancer modelTreatment of patientsMultiple mouse modelsRIG-IPattern recognition receptorsInnate immune responseImmunocompetent miceTumor massT cellsMalignant cellsPancreatic cancerCancer modelsTumor targetingNonmalignant cellsTumor growth
2024
Next-generation cell-penetrating antibodies for tumor targeting and RAD51 inhibition
Rackear M, Quijano E, Ianniello Z, Colón-Ríos D, Krysztofiak A, Abdullah R, Liu Y, Rogers F, Ludwig D, Dwivedi R, Bleichert F, Glazer P. Next-generation cell-penetrating antibodies for tumor targeting and RAD51 inhibition. Oncotarget 2024, 15: 699-713. PMID: 39352803, PMCID: PMC11444335, DOI: 10.18632/oncotarget.28651.Peer-Reviewed Original ResearchConceptsTumor targetingMonoclonal antibody therapyTumor-specific targetingCell uptakeNucleic acid bindingCell surface antigensAntibody therapyHuman variantsClinical successCell-penetrating antibodiesAcid bindingSystemic administrationSurface antigensTumorRAD51 inhibitionAntibody platformMechanism of cell penetrationBind RAD51AntibodiesFull-lengthSpecific targetsCell penetrationDisease targetsCellsAutoantibodies
2023
circPVT1 and PVT1/AKT3 show a role in cell proliferation, apoptosis, and tumor subtype‐definition in small cell lung cancer
Tolomeo D, Traversa D, Venuto S, Ebbesen K, Rodríguez J, Tamma G, Ranieri M, Simonetti G, Ghetti M, Paganelli M, Visci G, Liso A, Kok K, Muscarella L, Fabrizio F, Frassanito M, Lamanuzzi A, Saltarella I, Solimando A, Fatica A, Ianniello Z, Marsano R, Palazzo A, Azzariti A, Longo V, Tommasi S, Galetta D, Catino A, Zito A, Mazza T, Napoli A, Martinelli G, Kjems J, Kristensen L, Vacca A, Storlazzi C. circPVT1 and PVT1/AKT3 show a role in cell proliferation, apoptosis, and tumor subtype‐definition in small cell lung cancer. Genes Chromosomes And Cancer 2023, 62: 377-391. PMID: 36562080, DOI: 10.1002/gcc.23121.Peer-Reviewed Original ResearchConceptsSmall cell lung cancerCell lung cancerPVT1 transcriptsAnti-apoptotic programMYC-driven SCLCLineage-specific factorsLung cancerSmall cell lung cancer in vitroMYC-amplified tumorsChimeric RNAsIncrease of apoptosisExpression of NeuroD1MYC oncogeneCell growthTranscriptionMYC amplificationFunctional rolePro-proliferativeMolecular subtypesDrug sensitivityHomogeneous diseaseCell proliferationHistological classesMetabolic profileMYC
2022
MALAT1-dependent hsa_circ_0076611 regulates translation rate in triple-negative breast cancer
Turco C, Esposito G, Iaiza A, Goeman F, Benedetti A, Gallo E, Daralioti T, Perracchio L, Sacconi A, Pasanisi P, Muti P, Pulito C, Strano S, Ianniello Z, Fatica A, Forcato M, Fazi F, Blandino G, Fontemaggi G. MALAT1-dependent hsa_circ_0076611 regulates translation rate in triple-negative breast cancer. Communications Biology 2022, 5: 598. PMID: 35710947, PMCID: PMC9203778, DOI: 10.1038/s42003-022-03539-x.Peer-Reviewed Original ResearchConceptsTriple-negative breast cancerVascular endothelial growth factor ATriple-negative breast cancer cellsBreast cancerTranslation initiation machineryVascular endothelial growth factor A isoformsIsoforms of vascular endothelial growth factor-ARegulation of VEGFA expressionSerum of breast cancer patientsMigration of TNBC cellsBreast cancer patientsEndothelial growth factor AVascular endothelial growth factor-A mRNAGrowth factor AInitiation machineryMRNA splicingAngiogenic growth factorsTranslation rateBack-splicingSolid tumorsExon 7Target mRNAsCancer patientsTNBC cellsCancer cells
2021
New insight into the catalytic -dependent and -independent roles of METTL3 in sustaining aberrant translation in chronic myeloid leukemia
Ianniello Z, Sorci M, Ceci Ginistrelli L, Iaiza A, Marchioni M, Tito C, Capuano E, Masciarelli S, Ottone T, Attrotto C, Rizzo M, Franceschini L, de Pretis S, Voso M, Pelizzola M, Fazi F, Fatica A. New insight into the catalytic -dependent and -independent roles of METTL3 in sustaining aberrant translation in chronic myeloid leukemia. Cell Death & Disease 2021, 12: 870. PMID: 34561421, PMCID: PMC8463696, DOI: 10.1038/s41419-021-04169-7.Peer-Reviewed Original ResearchMeSH KeywordsAdenosineCatalysisCell Line, TumorCell NucleusCell ProliferationCell SurvivalDrug Resistance, NeoplasmGene Knockdown TechniquesHumansImatinib MesylateLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMethyltransferasesModels, BiologicalProtein BiosynthesisProto-Oncogene Proteins c-mycRNA-Binding ProteinsRNA, MessengerUp-RegulationConceptsChronic myeloid leukemiaTyrosine kinase inhibitorsChronic myeloid leukemia patientsMyeloid leukemiaResistance to tyrosine kinase inhibitorsCytoplasmic localizationTyrosine kinase inhibitor imatinibBCR-ABL1 fusion proteinResistant chronic myeloid leukemiaFirst-choice treatmentGlobal translation efficiencyChronic myeloid leukemia cell linePrimary CML cellsDepletion of METTL3Myeloproliferative neoplasmsNascent transcriptsRibosome biogenesisMethyltransferase complexCML cellsKinase inhibitorsTranslational efficiencyDeregulated transcriptsAberrant translationMRNA translationFusion proteinMETTL3-dependent MALAT1 delocalization drives c-Myc induction in thymic epithelial tumors
Iaiza A, Tito C, Ianniello Z, Ganci F, Laquintana V, Gallo E, Sacconi A, Masciarelli S, De Angelis L, Aversa S, Diso D, Anile M, Petrozza V, Facciolo F, Melis E, Pescarmona E, Venuta F, Marino M, Blandino G, Fontemaggi G, Fatica A, Fazi F. METTL3-dependent MALAT1 delocalization drives c-Myc induction in thymic epithelial tumors. Clinical Epigenetics 2021, 13: 173. PMID: 34530916, PMCID: PMC8447796, DOI: 10.1186/s13148-021-01159-6.Peer-Reviewed Original ResearchConceptsThymic tumorsRare neoplasmsEpithelial tumorsC-MycExpression of c-Myc proteinBackgroundThymic epithelial tumorsEpithelial thymic cellsThymic epithelial tumorsAggressive malignant phenotypeInduction of c-myc expressionThymic carcinoma cellsC-myc expressionInduction of cell deathC-myc inductionInhibition of proliferationC-myc proteinExpression of METTL3Thymic cellsTumor phenotypeTumor tissuesMETTL3 depletionMethyltransferase complexRNA modificationsTreatment choiceTumorTranslational control of polyamine metabolism by CNBP is required for Drosophila locomotor function
Coni S, Falconio F, Marzullo M, Munafò M, Zuliani B, Mosti F, Fatica A, Ianniello Z, Bordone R, Macone A, Agostinelli E, Perna A, Matkovic T, Sigrist S, Silvestri G, Canettieri G, Ciapponi L. Translational control of polyamine metabolism by CNBP is required for Drosophila locomotor function. ELife 2021, 10: e69269. PMID: 34517941, PMCID: PMC8439652, DOI: 10.7554/elife.69269.Peer-Reviewed Original ResearchConceptsLocomotor defectsMicrosatellite expansionsTranslational controlCellular nucleic acid binding proteinNucleic Acid Binding ProteinsZinc finger RNA binding proteinAssociated with myotonic dystrophy type 2RNA-binding proteinsAccumulation of toxic RNAPolyamine metabolismOrnithine decarboxylaseMammalian developmentToxic RNACCTG repeatsMyotonic dystrophy type 2Levels of ornithine decarboxylasePolyamine supplementationCNBPMetabolismProteinPathophysiological conditionsPolyaminesMicrosatelliteVertebratesDystrophic phenotypeADAR1 is a new target of METTL3 and plays a pro-oncogenic role in glioblastoma by an editing-independent mechanism
Tassinari V, Cesarini V, Tomaselli S, Ianniello Z, Silvestris D, Ginistrelli L, Martini M, De Angelis B, De Luca G, Vitiani L, Fatica A, Locatelli F, Gallo A. ADAR1 is a new target of METTL3 and plays a pro-oncogenic role in glioblastoma by an editing-independent mechanism. Genome Biology 2021, 22: 51. PMID: 33509238, PMCID: PMC7842030, DOI: 10.1186/s13059-021-02271-9.Peer-Reviewed Original ResearchConceptsRNA-binding proteinsPost-transcriptional eventsGlioblastoma growth in vivoCancer progressionPro-oncogenic roleMRNA fateRNA editingRNA modificationsModification eventsADAR1 mRNATarget of METTL3BackgroundN6-methyladenosineADAR1 knockdownADAR1Cell homeostasisCancer-promoting roleGrowth in vivoPro-tumorigenic mechanismsDeaminase activityMETTL3M6AProtein levelsMRNACDK2 mRNAProtein
2020
Blockade of EIF5A hypusination limits colorectal cancer growth by inhibiting MYC elongation
Coni S, Serrao S, Yurtsever Z, Di Magno L, Bordone R, Bertani C, Licursi V, Ianniello Z, Infante P, Moretti M, Petroni M, Guerrieri F, Fatica A, Macone A, De Smaele E, Di Marcotullio L, Giannini G, Maroder M, Agostinelli E, Canettieri G. Blockade of EIF5A hypusination limits colorectal cancer growth by inhibiting MYC elongation. Cell Death & Disease 2020, 11: 1045. PMID: 33303756, PMCID: PMC7729396, DOI: 10.1038/s41419-020-03174-6.Peer-Reviewed Original ResearchMeSH KeywordsAdenomatous Polyposis ColiAmino Acid MotifsAmino Acid SequenceAnimalsCell Line, TumorCell ProliferationColorectal NeoplasmsDown-RegulationEukaryotic Translation Initiation Factor 5AGene Expression ProfilingGene Expression Regulation, NeoplasticHumansLysineMice, NudeOpen Reading FramesOxidoreductases Acting on CH-NH Group DonorsPeptide Initiation FactorsPeptidesPolyaminesProtein BiosynthesisProto-Oncogene Proteins c-mycRNA-Binding ProteinsConceptsHypusinated eIF5APause motifDeoxyhypusine hydroxylaseEIF5A hypusinationInhibition of eIF5A hypusinationTranslation initiation factor 5ALentiviral-mediated knockdownTumor-promoting propertiesInhibition of hypusinationInitiation factor 5AGene expression analysisRibosome stallingExpression of transcriptsMultiplex gene expression analysisPosttranslational modificationsCellular processesGrowth inhibitory effectEIF5AHypusineTranslation factorsProtein stabilityInhibitor GC7Colorectal cancer cellsPolyamine homeostasisExpression analysis
Academic Achievements & Community Involvement
News
News
- July 16, 2025
Yale Researchers Develop Novel Antibody-RNA Therapy for Resistant Cancers
- May 01, 2025
New Research Presented from Yale Cancer Center at #AACR25
- April 21, 2025
Yale Cancer Center Research Breakthroughs Unveiled at AACR Annual Meeting
- April 12, 2024
Yale Cancer Center Faculty and Trainees Present at AACR Annual Meeting