2025
Predicting adenine base editing efficiencies in different cellular contexts by deep learning
Kissling L, Mollaysa A, Janjuha S, Mathis N, Marquart K, Weber Y, Moon W, Lin P, Fan S, Muramatsu H, Vadovics M, Allam A, Pardi N, Tam Y, Krauthammer M, Schwank G. Predicting adenine base editing efficiencies in different cellular contexts by deep learning. Genome Biology 2025, 26: 115. PMID: 40340964, PMCID: PMC12060317, DOI: 10.1186/s13059-025-03586-7.Peer-Reviewed Original ResearchConceptsBase editing efficiencyEditing efficiencyCell linesPathogenic mutationsBase editingPrimary cells in vivoBase editing screensBase editing outcomesCells in vivoHEK293T cellsAdenine base editingIn vivo settingTarget lociT cellsLipid nanoparticlesCellular contextTarget sequenceMRNA deliveryBase pairsOn-target editingBystander effectEditing outcomesBase editorsIn vitro datasetsMurine liverPreclinical Activity of Datopotamab Deruxtecan, an Antibody-Drug Conjugate Targeting Trophoblast Cell-Surface Antigen 2, in Uterine Serous Carcinoma.
Greenman M, Demirkiran C, Bellone S, Hartwich T, McNamara B, Ettorre V, Santin N, Sethi N, Yang-Hartwich Y, Papatla K, Ratner E, Santin A. Preclinical Activity of Datopotamab Deruxtecan, an Antibody-Drug Conjugate Targeting Trophoblast Cell-Surface Antigen 2, in Uterine Serous Carcinoma. Cancer Research Communications 2025, 5: 774-782. PMID: 40299780, PMCID: PMC12062949, DOI: 10.1158/2767-9764.crc-25-0057.Peer-Reviewed Original ResearchConceptsTrophoblast cell surface antigen 2Uterine serous carcinomaAntibody-dependent cell-mediated cytotoxicityAntibody-drug conjugatesCell-mediated cytotoxicitySerous carcinomaPreclinical activityCell linesTargets trophoblast cell-surface antigen-2Presence of peripheral blood lymphocytesTreatment of uterine serous carcinomaInduce antibody-dependent cell-mediated cytotoxicityPrimary USC cell linesRecurrent uterine serous carcinomaUSC xenograftsUterine serous carcinoma cell linesAntigen 2In vivoPrimary tumor cell linesTROP2 overexpressionBiomarker-targeted therapiesControl ADCChromium release assayHigher recurrence rateTumor growth suppressionGeneration of stable brain cell cultures from embryonic zebrafish to interrogate phenotypes in zebrafish mutants of neurodevelopmental disorders
Odierna G, Stednitz S, Pruitt A, Arnold J, Hoffman E, Scott E. Generation of stable brain cell cultures from embryonic zebrafish to interrogate phenotypes in zebrafish mutants of neurodevelopmental disorders. Journal Of Neuroscience Methods 2025, 418: 110426. PMID: 40086601, DOI: 10.1016/j.jneumeth.2025.110426.Peer-Reviewed Original ResearchBrain cell culturesCell culturesCell typesNeuronal culture protocolCultured primary neuronsEmbryonic zebrafishPrimary brain cell culturesZebrafish mutantsCellular consequencesStructural hallmarksMature synaptic connectionsPrimary neuronsCell survivalMammalian tissuesTranscriptional signatureCell linesEmbryonic tissuesZebrafish neuronsZebrafishNeuron purityNeuronal culturesNetwork of neuronsMixed cell typeDays in vitroModel systemQuantitative Protein Expression of Antibody-Drug Conjugate Targets in EGFR Mutated and Wild-Type Non-Small Cell Lung Cancer.
Trontzas I, He M, Wurtz A, Robbins C, Robinson N, Bates K, Liu M, Aung T, Scott L, Chan N, Burela S, Schillo J, Liebler D, Hill S, Morrison R, Vathiotis I, Syrigos K, Goldberg S, Politi K, Rimm D. Quantitative Protein Expression of Antibody-Drug Conjugate Targets in EGFR Mutated and Wild-Type Non-Small Cell Lung Cancer. Clinical Cancer Research 2025 PMID: 40047548, DOI: 10.1158/1078-0432.ccr-24-3347.Peer-Reviewed Original ResearchNon-small cell lung cancerAntibody-drug conjugatesAntibody-drug conjugate targetsEGFR mutationsCell lung cancerEGFR expressionQuantitative immunofluorescenceWild-type non-small cell lung cancerLung cancerAssociated with EGFR mutationsAssociated with EGFR expressionTissue microarray cohortAssociation of HER2Management of patientsAssay limitProportion of casesMutation statusTROP2 expressionMicroarray cohortEGFRQuantitative protein expressionTreatment sequencePatientsCell linesWild-typeExploring Glypican-3 targeted CAR-NK treatment and potential therapy resistance in hepatocellular carcinoma
Yang L, Pham K, Xi Y, Wu Q, Liu D, Robertson K, Liu C. Exploring Glypican-3 targeted CAR-NK treatment and potential therapy resistance in hepatocellular carcinoma. PLOS ONE 2025, 20: e0317401. PMID: 39841705, PMCID: PMC11753693, DOI: 10.1371/journal.pone.0317401.Peer-Reviewed Original ResearchConceptsGlypican-3Hepatocellular carcinomaCAR-NKNatural killerCell linesCAR-NK therapyCAR-NK cellsTreatment of hepatocellular carcinomaNK cell lineAnti-tumor effectsCancer-related mortalitySuppressed tumor growthPrimary liver cancerInfluence therapeutic outcomesCells in vitroHepatocellular carcinoma treatmentHepG2 cells in vitroNK92MI cellsImmunotherapy strategiesNSG miceImmunotherapy targetOncofetal glycoproteinTherapy resistanceImprove patient outcomesPoor prognosisGPR55 in the tumor microenvironment of pancreatic cancer controls tumorigenesis
Ristić D, Bärnthaler T, Gruden E, Kienzl M, Danner L, Herceg K, Sarsembayeva A, Kargl J, Schicho R. GPR55 in the tumor microenvironment of pancreatic cancer controls tumorigenesis. Frontiers In Immunology 2025, 15: 1513547. PMID: 39885986, PMCID: PMC11779727, DOI: 10.3389/fimmu.2024.1513547.Peer-Reviewed Original ResearchConceptsPancreatic ductal adenocarcinomaModel of pancreatic ductal adenocarcinomaImmune tumor microenvironmentTumor microenvironmentT cellsKO miceEndocannabinoid systemWT miceTumor growthCD8<sup>+</sup> T cellsG protein-coupled receptor 55Suppress T cell functionCancer cellsMurine pancreatic ductal adenocarcinomaCD3<sup>+</sup> T cellsExpression of PDL1T cell influxImmune cell compositionT cell functionTumor microenvironment cellsMigration of T cellsReduced tumor weightImmune cell populationsT cell activationCell linesCyclin E1/CDK2 activation defines a key vulnerability to WEE1 kinase inhibition in gynecological cancers
Kim D, Chung H, Liu W, Jeong K, Ozmen T, Ozmen F, Rames M, Kim S, Guo X, Jameson N, de Jong P, Yea S, Harford L, Li J, Mathews C, Doroshow D, Charles V, Kim D, Fischer K, Samatar A, Jubb A, Bunker K, Blackwell K, Simpkins F, Meric-Bernstam F, Mills G, Harismendy O, Ma J, Lackner M. Cyclin E1/CDK2 activation defines a key vulnerability to WEE1 kinase inhibition in gynecological cancers. Npj Precision Oncology 2025, 9: 3. PMID: 39755818, PMCID: PMC11700143, DOI: 10.1038/s41698-024-00787-4.Peer-Reviewed Original ResearchUterine serous carcinomaSerous carcinomaCyclin E1 expressionOvarian cancer cell linesWEE1 kinase inhibitionE1 expressionPhase I studyClasses of chemotherapyUpregulation of cyclin E1Levels of replication stressIn vivo modelsCancer cell linesGynecologic malignanciesGynecologic cancerOncogenic driversCell cycle checkpointsClinical activityG1 to S phaseBaseline levelsMultiple cell cycle checkpointsActivity of CDK2Cell cycle progressionKinase inhibitionCell linesCyclin E1
2024
Vesicle docking and fusion pore modulation by the neuronal calcium sensor Synaptotagmin-1
Tsemperouli M, Cheppali S, Rivera-Molina F, Chetrit D, Landajuela A, Toomre D, Karatekin E. Vesicle docking and fusion pore modulation by the neuronal calcium sensor Synaptotagmin-1. Biophysical Journal 2024 PMID: 39719826, DOI: 10.1016/j.bpj.2024.12.023.Peer-Reviewed Original ResearchVesicle dockingSynaptotagmin-1C2 domainFusion triggeringCalcium sensor synaptotagmin 1Neuronal SNARE complexFusion pore dynamicsSensor synaptotagmin-1Domains of Syt1Neuroendocrine cell linePolybasic patchSNARE complexTriggers exocytosisFusion poreFusion eventsDense-core vesiclesSyt1Synaptic vesiclesPlasma membranePore regulationCalcium sensorNegatively charged phospholipidsBind calciumPore dynamicsCell linesA novel sensitizer reduces EGFR-TKI resistance by regulating the PI3K/Akt/mTOR pathway and autophagy
Zhang J, Qu Z, Xiao X, Adelson D, Wang F, Wei A, Harata-Lee Y, Cui J, He D, Xie L, Sun L, Li J, Huang Z, Aung T, Yao H, Lin L. A novel sensitizer reduces EGFR-TKI resistance by regulating the PI3K/Akt/mTOR pathway and autophagy. Heliyon 2024, 11: e41104. PMID: 39844968, PMCID: PMC11750466, DOI: 10.1016/j.heliyon.2024.e41104.Peer-Reviewed Original ResearchEpidermal growth factor receptor tyrosine kinase inhibitorsEGFR-TKI-resistant cell linesNon-small cell lung cancerInhibition of drug resistanceLung cancerEpidermal growth factor receptor tyrosine kinase inhibitor resistanceDrug resistanceGrowth factor receptor tyrosine kinase inhibitorsCell linesReceptor tyrosine kinase inhibitorsEGFR-TKI resistanceResistance to gefitinibCell lung cancerFirst-line treatmentPI3K/AKT/mTOR pathwayMortality of lung cancerEGFR mutationsTreatment failureMolecular mechanismsDose-dependentlyKinase inhibitorsFlow cytometryAnticancer effectsGefitinibH1650 cellsAn integrative TAD catalog in lymphoblastoid cell lines discloses the functional impact of deletions and insertions in human genomes.
Li C, Bonder M, Syed S, Jensen M, Gerstein M, Zody M, Chaisson M, Talkowski M, Marschall T, Korbel J, Eichler E, Lee C, Shi X. An integrative TAD catalog in lymphoblastoid cell lines discloses the functional impact of deletions and insertions in human genomes. Genome Research 2024, 34: 2304-2318. PMID: 39638559, PMCID: PMC11694747, DOI: 10.1101/gr.279419.124.Peer-Reviewed Original ResearchConceptsTopologically associating domainsTopologically associating domains boundariesImpact of structural variantsLymphoblastoid cell linesStructural variantsHuman genomeGene regulationAdjacent TADsHuman lymphoblastoid cell linesCell linesSub-TADGenomic structureInsulate genesChromatin architectureImpact of deletionChromatin structureGenomeAberrant regulationAnalysis pipelineMammalian speciesGenesCCREsFunctional impactChromatinRegulationDevelopment of a small molecule-based two-photon photosensitizer for targeting cancer cells
Lee D, Cao Y, Juvekar V, Sauraj, Noh C, Shin S, Liu Z, Kim H. Development of a small molecule-based two-photon photosensitizer for targeting cancer cells. Journal Of Materials Chemistry B 2024, 12: 12232-12238. PMID: 39469993, DOI: 10.1039/d4tb01706d.Peer-Reviewed Original ResearchConceptsTarget cancer cellsReactive oxygen speciesPhotodynamic therapyCancer cellsDiverse cell linesInduced ROS productionColon cancer tissuesTwo-photon (TPCell deathLow dark toxicityCancer modelsTwo-photon photosensitizerROS productionCancer selectivityInduce cell damageThree-dimensional spheroidsCell linesTP excitationImaging-guided photodynamic therapyCancer tissuesOxygen speciesTP-PDTExpression of Random Sequences and de novo Evolved Genes From the Mouse in Human Cells Reveals Functional Diversity and Specificity
Aldrovandi S, Castro J, Ullrich K, Karger A, Luria V, Tautz D. Expression of Random Sequences and de novo Evolved Genes From the Mouse in Human Cells Reveals Functional Diversity and Specificity. Genome Biology And Evolution 2024, 16: evae175. PMID: 39663928, PMCID: PMC11635099, DOI: 10.1093/gbe/evae175.Peer-Reviewed Original ResearchConceptsOpen reading frameGene open reading frameCellular regulatory pathwaysNoncoding DNAReading frameHuman cell linesHuman genomeAlpha-helicesGrowth experimentsCellular physiologyFunctional diversityPositive selectionBeta-sheetTranscriptomic responseRegulatory pathwaysAdaptive advantageHuman cellsGenesCell clonesCell linesSequenceClonesRandom sequencePathwayCellsColibactin Exerts Androgen-dependent and -independent Effects on Prostate Cancer
Agrawal R, Al-Hiyari S, Hugh-White R, Hromas R, Patel Y, Williamson E, Mootor M, Gonzalez A, Fu J, Haas R, Jordan M, Wickes B, Mohammed G, Tian M, Doris M, Jobin C, Wernke K, Pan Y, Yamaguchi T, Herzon S, Boutros P, Liss M. Colibactin Exerts Androgen-dependent and -independent Effects on Prostate Cancer. European Urology Oncology 2024 PMID: 39547899, DOI: 10.1016/j.euo.2024.10.015.Peer-Reviewed Original ResearchProstate cancerInduction of genomic instabilityPC diagnosisPC etiologyColibactin-producing Escherichia coliEtiology of prostate cancerProstate cancer cellsProstate cancer diagnosisSomatic point mutationsCombination in vitroGenomic instabilityAndrogen-dependentColon cancerPatient populationProstateClinical cohortInitial cancerSomatic mutationsCancer cellsDihydrotestosteroneGenetic dysfunctionSingle cell lineCancerCell linesDiagnosisEfficient and selective kidney targeting by chemically modified carbohydrate conjugates
Kumar V, Wahane A, Tham M, Somlo S, Gupta A, Bahal R. Efficient and selective kidney targeting by chemically modified carbohydrate conjugates. Molecular Therapy 2024, 32: 4383-4400. PMID: 39532098, PMCID: PMC11638880, DOI: 10.1016/j.ymthe.2024.10.020.Peer-Reviewed Original ResearchProximal convoluted tubulesPeptide nucleic acidConvoluted tubulesNucleic acid analogsDecreased collagen depositionAntisense peptide nucleic acidFibrosis mouse modelCarbohydrate conjugatesKidney disease modelsSystemic deliveryFibrosis progressionSmall moleculesKidney cell lineAdverse reactionsMiR-33Mouse modelBiodistribution studiesImmunofluorescence stainingCollagen depositionKidney targetingTargeted deliveryLigandCell linesEndocytic uptakeAcid analogsEXTH-23. NEW DNA-CROSSLINKING CHEMOTHERAPY IS EFFECTIVE AGAINST POST-TEMOZOLOMIDE MISMATCH REPAIR-DEFICIENT PATIENT-DERIVED HYPERMUTANT GLIOMAS
McCord M, Wang W, An S, Sears T, Sarkaria J, James C, Ruggieri B, Bindra R, Horbinski C. EXTH-23. NEW DNA-CROSSLINKING CHEMOTHERAPY IS EFFECTIVE AGAINST POST-TEMOZOLOMIDE MISMATCH REPAIR-DEFICIENT PATIENT-DERIVED HYPERMUTANT GLIOMAS. Neuro-Oncology 2024, 26: viii241-viii241. PMCID: PMC11553709, DOI: 10.1093/neuonc/noae165.0954.Peer-Reviewed Original ResearchPatient-derived xenograftsDNA inter-strand cross-linksMismatch repairDNA mismatch repairGlioblastoma cell linesBase mismatchesShRNA knockdownGlioblastoma patient-derived xenograftsMGMT deficiencyMGMT-deficient cellsDNA damageInter-strand cross-linksDNAMMR-deficient tumor cellsCell linesPatient-derived xenograft modelsComplementary in vitro studiesAlkylating agent temozolomideMMR genesVehicle control miceDays post-engraftmentApoptosisMismatch repair mutationsDNA basesResistance to temozolomideInducible cell lines producing replication-defective human immunodeficiency virus particles containing envelope glycoproteins stabilized in a pretriggered conformation
Ding H, Nguyen H, Li W, Deshpande A, Zhang S, Jiang F, Zhang Z, Anang S, Mothes W, Sodroski J, Kappes J. Inducible cell lines producing replication-defective human immunodeficiency virus particles containing envelope glycoproteins stabilized in a pretriggered conformation. Journal Of Virology 2024, 98: e01720-24. PMID: 39508605, PMCID: PMC11650979, DOI: 10.1128/jvi.01720-24.Peer-Reviewed Original ResearchHuman immunodeficiency virusEnv trimersNeutralizing antibodiesHIV-1Virus-like particlesEnvelope glycoproteinEnv conformationImmunodeficiency virusInducible cell linesCell linesImmune systemEffective HIV/AIDS vaccineHIV-1 persistenceHuman immunodeficiency virus particlesEnvelope glycoprotein spikeHIV-1 EnvPoorly neutralizing antibodiesHIV-like particlesHIV-1 particlesDefective virus-like particlesHost immune systemEnv immunogensHIV/AIDS vaccineCreation of stable cell linesHost cell receptorsThe Role of NOXA in Venetoclax Treatment Response in Multiple Myeloma
Shivaram S, Yan H, Tang H, Anderson H, Kaddoura M, Wiedmeier-Nutor J, Tian S, Howe M, Bolarinwa A, Zepeda Mendoza C, Gupta V, Lehman S, Mitsiades C, Bergsagel P, Braggio E, Boise L, Fonseca R, Maura F, Kumar S, Baughn L. The Role of NOXA in Venetoclax Treatment Response in Multiple Myeloma. Blood 2024, 144: 4635-4635. DOI: 10.1182/blood-2024-205385.Peer-Reviewed Original ResearchMayo Clinic cohortNoxa proteinMultiple myelomaG alleleIncreased expressionGene expressionCyclin D1Clinical cohortExpression of CCND1Cell linesAllele specific effectsBCL-2 inhibitor venetoclaxLevels of NoxaHistone mark H3K27acG risk allelePrimary cytogenetic abnormalityPlasma cell malignancyAssociated with increased expressionRNA sequencing dataHuman myeloma cell linesKO cell linesWestern blottingAnalyzed whole-exomeChIP-seqWhole genomeIdentification of Nuclear NAD+ Salvage As a Therapeutic Vulnerability in B-Lymphoid Malignancies
Robinson M, Li Q, Zhang C, Zhan C, Cheng Z, Kume K, Cosgun K, Kothari S, Agadzhanian N, Nakada D, Müschen M. Identification of Nuclear NAD+ Salvage As a Therapeutic Vulnerability in B-Lymphoid Malignancies. Blood 2024, 144: 4164-4164. DOI: 10.1182/blood-2024-205729.Peer-Reviewed Original ResearchB-ALL cell linesB-ALLB cellsCell linesTherapeutic vulnerabilitiesGene dependenciesNAD+ synthesisMature B-cell lymphomasElimination of B cellsTreatment of B-ALLNAD+ salvageChemotherapy-based regimensEffects of NAMPT inhibitionB-cell depletionB-cell lymphomaB-lymphoid malignanciesB-ALL cellsNAMPT inhibitorsInhibition of NAMPTATP-utilizing enzymesNAD+ salvage pathwayDrug repurposing platformNAD biosynthetic pathwayNear-complete ablationDe novo pathwayIdentification of High-Efficiency β-Catenin Protein Degradation As Critical Vulnerability in B-Cell Malignancies
Cosgun K, Robinson M, Agadzhanian N, Cheng Z, Oulghazi S, Berning P, Fonseca-Arce D, Kume K, Fontaine J, Chan L, Lee J, Yu F, Qian Z, Song J, Chan W, Chen J, Taketo M, Schjerven H, Müschen M. Identification of High-Efficiency β-Catenin Protein Degradation As Critical Vulnerability in B-Cell Malignancies. Blood 2024, 144: 4125-4125. DOI: 10.1182/blood-2024-208125.Peer-Reviewed Original ResearchProtein degradation pathwaysB-ALL cellsProtein degradationRepression of MYCTranscriptional activity of MYCCell deathAcute cell deathLoss of colony formationChIP-seq analysisActive enhancer marksB-cell malignanciesSuper-enhancer regionsActivation of MYCIkaros transcription factorB-lymphoid cellsCell linesB cell identityDefective protein degradationB-cateninNon-lymphoid cell linesDegradation pathwayMantle cell lymphomaProtein levelsB-ALLChIP-seqTargeted Dynamic Phospho-Proteogenomic Analysis of Gastric Cancer Cells Suggests Host Immunity Provides Survival Benefit
Kume K, Iida M, Iwaya T, Yashima-Abo A, Koizumi Y, Endo A, Wade K, Hiraki H, Calvert V, Wulfkuhle J, Espina V, Siwak D, Lu Y, Takemoto K, Suzuki Y, Sasaki Y, Tokino T, Petricoin E, Liotta L, Mills G, Nishizuka S. Targeted Dynamic Phospho-Proteogenomic Analysis of Gastric Cancer Cells Suggests Host Immunity Provides Survival Benefit. Molecular & Cellular Proteomics 2024, 23: 100870. PMID: 39461475, PMCID: PMC11621936, DOI: 10.1016/j.mcpro.2024.100870.Peer-Reviewed Original ResearchDNA-damaging drugsTotal lymphocyte countCell linesResistance to DNA damaging drugsPD-L1Adjuvant chemotherapyProtein dynamicsProtein-level regulationSurvival benefitCopy number lossExpression time courseGastric cancerRelapse-free survival rateGastric cancer cellsHost immunityAssociated with prolonged survivalIncreased STAT1 phosphorylationResistance to other drugsGlobal protein dynamicsImmune checkpoint blockadePD-L1 positivityPD-L1 expressionAdvanced gastric cancerExpression of STAT1Molecular targeted drugs
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