2025
An integrative analysis of circulating and tumor microenvironment (TME) determinants of patient response in the Checkmate 9ER (CM 9ER) trial of nivolumab and cabozantinib (NIVO+CABO) in advanced renal cell carcinoma (aRCC).
Braun D, Vemula S, Cook D, Verma A, Carrigan P, Kelly K, Choueiri T, Gupta S. An integrative analysis of circulating and tumor microenvironment (TME) determinants of patient response in the Checkmate 9ER (CM 9ER) trial of nivolumab and cabozantinib (NIVO+CABO) in advanced renal cell carcinoma (aRCC). Journal Of Clinical Oncology 2025, 43: 4511-4511. DOI: 10.1200/jco.2025.43.16_suppl.4511.Peer-Reviewed Original ResearchAdvanced renal cell carcinomaPD-L1 stainingObjective response rateTumor microenvironmentLogistic regression modelsPD-L1Patient responseIncreased objective response rateTumoral PD-L1 stainingCirculating factorsDeterminants of therapeutic responseTumor response to therapyCirculating immune cell populationsTrials of nivolumabResponse to therapyImmune cell populationsRenal cell carcinomaCancer cell numberPlasma cell numbersCell numberActivation of stromal cellsAssociated with responseExtracellular matrixProgression-freeRegression modelsDissecting the physics of bacterial biofilms with agent-based simulations
Nam K, Li C, Cockx B, Nguyen D, Li Y, Kreft J, Yan J. Dissecting the physics of bacterial biofilms with agent-based simulations. Current Opinion In Solid State And Materials Science 2025, 37: 101228. PMID: 40538632, PMCID: PMC12176386, DOI: 10.1016/j.cossms.2025.101228.Peer-Reviewed Original ResearchVibrio cholerae</i> biofilmsBiofilm developmentExtracellular matrixDevelopment of bacterial coloniesSingle-cell resolutionBacterial communitiesCellular organizationBacterial coloniesBacterial biofilmsBiofilmBiological entitiesDevelopment of modeling approachesOrientational orderPhysical mechanismsExternal perturbationsComplex networksVibrioMechanistic originMacromolecular crowding-based biofabrication utilizing unmodified extracellular matrix bioinks
Jordan S, Li X, Rossello-Martinez A, Liang Z, Gong X, Xiao H, Mak M. Macromolecular crowding-based biofabrication utilizing unmodified extracellular matrix bioinks. Acta Biomaterialia 2025, 198: 37-48. PMID: 40268621, DOI: 10.1016/j.actbio.2025.02.052.Peer-Reviewed Original ResearchConceptsDecellularized extracellular matrixExtrusion bioprintingComplex 3D structuresLayer-by-layer buildingCell scaffold materialsNatural extracellular matrixBiofabrication applicationsSolubilized extracellular matrixRobust hydrogelsLow printabilityTissue engineeringBioinkFabrication methodPromote biocompatibilityGelation timeBioactive scaffoldsPrintabilityBiofabricationNative tissueOrgan-specific extracellular matrixCrosslinkingExtracellular matrixBiocompatibilityExtrusionRegenerative medicineExome sequencing reveals low-frequency and rare variant contributions to multiple sclerosis susceptibility in Turkish families
Büyükgöl F, Gürdamar B, Aluçlu M, Beckmann Y, Bilguvar K, Boz C, Bülbül A, Bünül S, Çetin Ö, Demir C, Demir S, Duman T, Efendi H, Ekmekçi Ö, Ertetik U, Ethemoğlu Ö, Everest E, Gümüş H, Gündüz T, Karabudak R, Karaman B, Kürtüncü M, Mutluer M, Reda M, Saip S, Seferoğlu M, Sever E, Sezerman O, Şen S, Taşdelen B, Tecellioğlu M, Terzi M, Tuncer A, Turan Ö, Tütüncü M, Uncu G, Uygunoğlu U, Uzunköprü C, Voyvoda U, Yetkin M, Yüceyar N, Siva A, Turanlı E. Exome sequencing reveals low-frequency and rare variant contributions to multiple sclerosis susceptibility in Turkish families. Scientific Reports 2025, 15: 11682. PMID: 40188234, PMCID: PMC11972333, DOI: 10.1038/s41598-025-94691-x.Peer-Reviewed Original ResearchConceptsSegregation analysisExome sequencingGene-based burden testsGene-based burden analysisRare coding variantsVariants associated with MSWhole-exome sequencingPathway enrichment analysisMultiplex MS familiesHuman leukocyte antigen lociContribution of low-frequencyAdmixed populationsBurden testsHemidesmosome assemblyMultiple sclerosis susceptibilityAllele frequenciesAntigen lociEnrichment analysisBurden analysisMS familiesGenesTurkish familyExtracellular matrixProgressive neurodegenerationITPR1 geneMatrix-producing neutrophils populate and shield the skin
Vicanolo T, Özcan A, Li J, Huerta-López C, Ballesteros I, Rubio-Ponce A, Dumitru A, Nicolás-Ávila J, Molina-Moreno M, Reyes-Gutierrez P, Johnston A, Martone C, Greto E, Quílez-Alvarez A, Calvo E, Bonzon-Kulichenko E, Álvarez-Velez R, Chooi M, Kwok I, González-Bermúdez B, Malleret B, Espinosa F, Zhang M, Wang Y, Sun D, Zhen Chong S, El-Armouche A, Kim K, Udalova I, Greco V, Garcia R, Vázquez J, Dopazo A, Plaza G, Alegre-Cebollada J, Uderhardt S, Ng L, Hidalgo A. Matrix-producing neutrophils populate and shield the skin. Nature 2025, 641: 740-748. PMID: 40108463, PMCID: PMC12074881, DOI: 10.1038/s41586-025-08741-5.Peer-Reviewed Original ResearchRepertoire of proteinsExtracellular matrixInnate immune systemPopulation of neutrophilsImmune diversityPromote barrier functionBacterial invasionInnate immune cellsTGFB signalingForeign moleculesPhysical barrierRing formationBarrier functionImmune systemEnvironmental threatsDefenceDiverse strategiesToxic chemicalsNaive skinTGFBImmune cellsBacteriaNeutrophilsEnzymeProteinFibronectin matrix assembly at a glance.
Sun Y, Hamlin A, Schwarzbauer J. Fibronectin matrix assembly at a glance. Journal Of Cell Science 2025, 138 PMID: 40130407, PMCID: PMC12050093, DOI: 10.1242/jcs.263834.Peer-Reviewed Original ResearchConceptsAbundant ECM proteinFibronectin matrix assemblyOrganization of FNExtracellular matrixMechanisms of extracellular matrixSecrete ECM componentsFN assemblyDomain organizationFN fibrilsFN matrixGlance articleECM proteinsMatrix assemblyECM componentsIntracellular pathwaysFibrillar matrixReceptor-mediated processFibronectinCell scienceProteinAssemblyCellsCell-mediated processPathwayMechanismA Matrigel-Free 3D Chondrocytic Spheroid Model for Rheumatoid Arthritis-Associated Synoviocytes Invasion Studies
Zhao Y, Yang X, Yao F, Ouyang Z, Hu W, Li L, Cheng J, Wang K, Ding J, Zheng L, Qu B, Sun C, Li S, Jiang C, Chen Y, Zhou R, Hu W. A Matrigel-Free 3D Chondrocytic Spheroid Model for Rheumatoid Arthritis-Associated Synoviocytes Invasion Studies. Journal Of Inflammation Research 2025, 18: 4319-4334. PMID: 40162078, PMCID: PMC11952051, DOI: 10.2147/jir.s504701.Peer-Reviewed Original ResearchChondrocyte spheroidsCartilage extracellular matrixArticular cartilageExtracellular matrixSensitive to genesDepth ratioCatabolism-related genesThree-dimensionalTranscriptome sequencingInvasion ratioFibroblast-like synoviocytesCartilageGene overexpressionGenesDrug screeningInvasion of cartilageInvasive capacityEfficient in vitro modelMorphogenesis of confined biofilms: how mechanical interactions determine cellular patterning and global geometry
Nam K, Yan J. Morphogenesis of confined biofilms: how mechanical interactions determine cellular patterning and global geometry. Soft Matter 2025, 21: 1436-1450. PMID: 39901805, PMCID: PMC11791476, DOI: 10.1039/d4sm01180e.Peer-Reviewed Original ResearchConceptsVibrio cholerae</i> biofilmsBiofilm developmentTransmission of mechanical stressExtracellular matrixSingle-cell levelBacterial communitiesDevelopmental biologyBacterial coloniesBiofilmSingle-cellReview recent studiesMechanical interplayFluorescence microscopyMorphogenesisActive nematicsGlobal geometryCellular patternOrientational orderContinuum levelVibrioConfining mediumRecent studiesMechanical interactionTracing the origins of fibrotic fibroblasts: does the name matter? Look at the genes!
Mailleux A, Justet A. Tracing the origins of fibrotic fibroblasts: does the name matter? Look at the genes! European Respiratory Journal 2025, 65: 2402170. PMID: 39915043, DOI: 10.1183/13993003.02170-2024.Peer-Reviewed Original ResearchAtgl-dependent adipocyte lipolysis promotes lipodystrophy and restrains fibrogenic responses during skin fibrosis
Caves E, Jussila A, Forni M, Benvie A, Lei V, King D, Edelman H, Hamdan M, Odell I, Hinchcliff M, Atit R, Horsley V. Atgl-dependent adipocyte lipolysis promotes lipodystrophy and restrains fibrogenic responses during skin fibrosis. Journal Of Investigative Dermatology 2025 PMID: 39884454, DOI: 10.1016/j.jid.2024.12.022.Peer-Reviewed Original ResearchLipid storageAdipocyte lipolysisExtracellular matrix proteinsFatty acidsTranscriptional analysisSkin fibrosisAdipocyte lipid storageTranscriptional changesSkin fibrosis developmentExtracellular matrix remodelingFibrosis developmentLipid-filled adipocytesDermal extracellular matrixHuman diseasesTreating fibrotic diseasesMouse modelMatrix proteinsDermal adipocytesFibrogenic responseGenetic modelsExtracellular matrixAdipocytesLoss of adipose tissueBleomycin-treated miceFibrotic mouse modelSurface remodeling and inversion of cell-matrix interactions underlie community recognition and dispersal in Vibrio cholerae biofilms
Moreau A, Nguyen D, Hinbest A, Zamora A, Weerasekera R, Matej K, Zhou X, Sanchez S, Rodriguez Brenes I, Tai J, Nadell C, Ng W, Gordon V, Komarova N, Olson R, Li Y, Yan J. Surface remodeling and inversion of cell-matrix interactions underlie community recognition and dispersal in Vibrio cholerae biofilms. Nature Communications 2025, 16: 327. PMID: 39747177, PMCID: PMC11695861, DOI: 10.1038/s41467-024-55602-2.Peer-Reviewed Original ResearchConceptsCell-matrix interactionsCausative agent of choleraSurface-associated bacterial communitiesAgent of choleraV. cholerae cellsVibrio cholerae biofilmsSurface remodelingInvestigate cell-matrix interactionsBiofilm cellsBacterial communitiesVibrio choleraeBiofilm developmentBiofilmCausative agentBiofilm growthBiochemical analysisExtracellular matrixVibrioBiofilm ageCell dispersionMatrix componentsCholeraCellsRbmBShed light
2024
A Multi‐Omic Analysis of Molecular Risk and Resilience Factors in Late‐Onset Alzheimer’s Disease in APOEe4 Carriers
Markov Y, Priyanka A, Higgins‐Chen A. A Multi‐Omic Analysis of Molecular Risk and Resilience Factors in Late‐Onset Alzheimer’s Disease in APOEe4 Carriers. Alzheimer's & Dementia 2024, 20: e092941. PMCID: PMC11709863, DOI: 10.1002/alz.092941.Peer-Reviewed Original ResearchLate-onset Alzheimer's diseaseMulti-omics analysisApolipoprotein ESusceptible to AD pathologyDisease resilienceDeep whole-exome sequencingMulti-omics datasetsDNA methylation profilesAlzheimer's diseaseWhole-exome sequencingMolecular signaturesLabel-free mass spectrometryIllumina EPIC arrayDNA methylationExome sequencingMethylation profilesEPIC arrayOmics levelsReligious Orders StudyAD pathologyMulti-tissueMutated genesGenesE4 alleleExtracellular matrixEzrin drives adaptation of monocytes to the inflamed lung microenvironment
Gudneppanavar R, Di Pietro C, H Öz H, Zhang P, Cheng E, Huang P, Tebaldi T, Biancon G, Halene S, Hoppe A, Kim C, Gonzalez A, Krause D, Egan M, Gupta N, Murray T, Bruscia E. Ezrin drives adaptation of monocytes to the inflamed lung microenvironment. Cell Death & Disease 2024, 15: 864. PMID: 39613751, PMCID: PMC11607083, DOI: 10.1038/s41419-024-07255-8.Peer-Reviewed Original ResearchConceptsActivation of focal adhesion kinaseExtracellular matrixActin-binding proteinsFocal adhesion kinaseLung extracellular matrixKnock-out mouse modelProtein kinase signalingCortical cytoskeletonLoss of ezrinKinase signalingPlasma membraneCell migrationSignaling pathwayEzrinResponse to lipopolysaccharideTissue-resident macrophagesMouse modelLipopolysaccharideCytoskeletonEzrin expressionLung microenvironmentKinaseMonocyte recruitmentProteinAktViscosity regulates cell spreading and cell‐extracellular matrix interactions
Xiao H, Gong X, Jordan S, Liang Z, Mak M. Viscosity regulates cell spreading and cell‐extracellular matrix interactions. The FEBS Journal 2024, 292: 740-758. PMID: 39529371, PMCID: PMC12002552, DOI: 10.1111/febs.17306.Peer-Reviewed Original ResearchCell spreadingRho-associated protein kinase 1Actin-related protein 2/3Regulation of cell locomotionRegulation of ECM remodelingCollagen substrateRas-related C3 botulinum toxin substrate 1Cell-extracellular matrix interactionsECM remodelingCellular remodelingExtracellular matrixEnhanced cell spreadingProtein kinase 1Membrane rufflingCell locomotionRemodeling of extracellular matrixCellular forcesSubstrate 1Cell migrationCellular spreadingKinase 1Matrix interactionsRac1MicrotubulesRegulationComparative single-cell multiome identifies evolutionary changes in neural progenitor cells during primate brain development
Liu Y, Luo X, Sun Y, Chen K, Hu T, You B, Xu J, Zhang F, Cheng Q, Meng X, Yan T, Li X, Qi X, He X, Guo X, Li C, Su B. Comparative single-cell multiome identifies evolutionary changes in neural progenitor cells during primate brain development. Developmental Cell 2024, 60: 414-428.e8. PMID: 39481377, DOI: 10.1016/j.devcel.2024.10.005.Peer-Reviewed Original ResearchEvolutionary changesDistal regulatory elementsGene regulatory mechanismsExtracellular matrixSingle-cell multiomicsProgenitor cellsTranscriptional divergenceEvolutionary divergenceChromatin regionsChromatin accessibilityNeural progenitorsRegulatory elementsSequence changesTranscriptional rewiringGenetic mechanismsMouse prefrontal cortexRegulatory mechanismsPrefrontal cortexHuman neural progenitorsHuman-specific featuresUpper-layer neuronsNeural progenitor cellsChromatinCellular propertiesProgenitor proliferationProteomic basis for pancreatic acinar cell carcinoma and pancreatoblastoma as similar yet distinct entities
Tanaka A, Ogawa M, Zhou Y, Hendrickson R, Miele M, Li Z, Klimstra D, Wang J, Roehrl M. Proteomic basis for pancreatic acinar cell carcinoma and pancreatoblastoma as similar yet distinct entities. Npj Precision Oncology 2024, 8: 221. PMID: 39363045, PMCID: PMC11449907, DOI: 10.1038/s41698-024-00708-5.Peer-Reviewed Original ResearchAcinar cell carcinomaPancreatic ductal adenocarcinomaActin-based processesPathway activity differencesCell carcinomaChromosome organizationChromosomal proteinsProteomic basisRNA processingIGF2 pathwayProtein expression patternsEpithelial-to-mesenchymal transitionProteogenomic profilingPancreatic acinar cell carcinomaProteomic landscapeDNA repairCell cycleRare pancreatic malignancyExpression patternsMitochondrial dysfunctionStem cell phenotypeMetabolic adaptationProteinExtracellular matrixPancreatic malignancyTwo Decades of Advances and Limitations in Organ Recellularization
Stoian A, Adil A, Biniazan F, Haykal S. Two Decades of Advances and Limitations in Organ Recellularization. Current Issues In Molecular Biology 2024, 46: 9179-9214. PMID: 39194760, PMCID: PMC11352560, DOI: 10.3390/cimb46080543.Peer-Reviewed Original ResearchCellular stiffness sensing through talin 1 in tissue mechanical homeostasis
Chanduri M, Kumar A, Weiss D, Emuna N, Barsukov I, Shi M, Tanaka K, Wang X, Datye A, Kanyo J, Collin F, Lam T, Schwarz U, Bai S, Nottoli T, Goult B, Humphrey J, Schwartz M. Cellular stiffness sensing through talin 1 in tissue mechanical homeostasis. Science Advances 2024, 10: eadi6286. PMID: 39167642, PMCID: PMC11338229, DOI: 10.1126/sciadv.adi6286.Peer-Reviewed Original ResearchConceptsTissue mechanical homeostasisStiffness sensingExtracellular matrixTalin-1Mechanical homeostasisExtracellular matrix mechanicsIncreased cell spreadingCell spreadingTalinMutationsCellular sensingFibrillar collagenReduced axial stiffnessTissue mechanical propertiesMechanical propertiesAxial stiffnessCompliant substratesHomeostasisRupture pressureArp2/3ARPC5LStiffnessHomeostasis hypothesisResident cellsTissue stiffnessBone-derived extracellular matrix hydrogel from thrombospondin-2 knock-out mice for bone repair
Chen Z, Zhang J, Lee F, Kyriakides T. Bone-derived extracellular matrix hydrogel from thrombospondin-2 knock-out mice for bone repair. Acta Biomaterialia 2024, 186: 85-94. PMID: 39134130, PMCID: PMC11500023, DOI: 10.1016/j.actbio.2024.08.011.Peer-Reviewed Original ResearchECM hydrogelsWild typeBone repairLack of mechanical integrityExtracellular matrixRepair of bone defectsExtracellular matrix hydrogelDecellularized extracellular matrixMurine calvarial defect modelCalvarial defect modelPromote bone repairHuman umbilical vein endothelial cellsMesenchymal stem cellsThrombospondin-2Fabricated hydrogelsBone extracellular matrixNovel hydrogelsMechanical propertiesCollagen fibril assemblyMatrix hydrogelRepair damaged boneDecellularized ECMMechanical integrityHydrogelsInvasion in vitroThe amalgam of naive CD4+ T cell transcriptional states is reconfigured by helminth infection to dampen the amplitude of the immune response
Even Z, Meli A, Tyagi A, Vidyarthi A, Briggs N, de Kouchkovsky D, Kong Y, Wang Y, Waizman D, Rice T, De Kumar B, Wang X, Palm N, Craft J, Basu M, Ghosh S, Rothlin C. The amalgam of naive CD4+ T cell transcriptional states is reconfigured by helminth infection to dampen the amplitude of the immune response. Immunity 2024, 57: 1893-1907.e6. PMID: 39096910, PMCID: PMC11421571, DOI: 10.1016/j.immuni.2024.07.006.Peer-Reviewed Original ResearchT cell receptorImmune responseNaive CD4<sup>+</sup> T cellsCD4<sup>+</sup> T cellsIFN-IHelminth infectionsNippostrongylus brasiliensis infectionDecreased immune responseType I interferonNaive TT cellsMemory-likeUnrelated antigensTranscriptional changesExtracellular matrixSPF miceCell receptorsI interferonGerm-freeResponse to certain environmental cuesInfectionMiceFunctional changesCell transcriptional statesTranscriptional heterogeneity
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