2025
A neoantigen vaccine generates antitumour immunity in renal cell carcinoma
Braun D, Moranzoni G, Chea V, McGregor B, Blass E, Tu C, Vanasse A, Forman C, Forman J, Afeyan A, Schindler N, Liu Y, Li S, Southard J, Chang S, Hirsch M, LeBoeuf N, Olive O, Mehndiratta A, Greenslade H, Shetty K, Klaeger S, Sarkizova S, Pedersen C, Mossanen M, Carulli I, Tarren A, Duke-Cohan J, Howard A, Iorgulescu J, Shim B, Simon J, Signoretti S, Aster J, Elagina L, Carr S, Leshchiner I, Getz G, Gabriel S, Hacohen N, Olsen L, Oliveira G, Neuberg D, Livak K, Shukla S, Fritsch E, Wu C, Keskin D, Ott P, Choueiri T. A neoantigen vaccine generates antitumour immunity in renal cell carcinoma. Nature 2025, 639: 474-482. PMID: 39910301, PMCID: PMC11903305, DOI: 10.1038/s41586-024-08507-5.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAntigens, NeoplasmCancer VaccinesCarcinoma, Renal CellClass I Phosphatidylinositol 3-KinasesDNA-Binding ProteinsFemaleHumansIpilimumabKidney NeoplasmsMaleMiddle AgedMutationPrecision MedicineT-LymphocytesTranscription FactorsTumor Suppressor ProteinsUbiquitin ThiolesteraseVon Hippel-Lindau Tumor Suppressor ProteinConceptsPersonalized cancer vaccinesRenal cell carcinomaDriver mutationsAntitumour immunityCell carcinomaI trialResected clear cell renal cell carcinomaImmune responseT cell immune responsesClear cell renal cell carcinomaHigh-risk RCCDose-limiting toxicityLow mutational burdenCell renal cell carcinomaEffective adjuvant therapyPhase I trialT cell reactivityAbsence of recurrenceCirculating immune responsesCell immune responseAutologous tumorNeoantigen vaccinesCancer vaccinesAdjuvant therapyMutational burdenMultiomics dissection of human RAG deficiency reveals distinctive patterns of immune dysregulation but a common inflammatory signature
Bosticardo M, Dobbs K, Delmonte O, Martins A, Pala F, Kawai T, Kenney H, Magro G, Rosen L, Yamazaki Y, Yu H, Calzoni E, Lee Y, Liu C, Stoddard J, Niemela J, Fink D, Castagnoli R, Ramba M, Cheng A, Riley D, Oikonomou V, Shaw E, Belaid B, Keles S, Al-Herz W, Cancrini C, Cifaldi C, Baris S, Sharapova S, Schuetz C, Gennery A, Freeman A, Somech R, Choo S, Giliani S, Güngör T, Drozdov D, Meyts I, Moshous D, Neven B, Abraham R, El-Marsafy A, Kanariou M, King A, Licciardi F, Cruz-Muñoz M, Palma P, Poli C, Adeli M, Algeri M, Alroqi F, Bastard P, Bergerson J, Booth C, Brett A, Burns S, Butte M, Padem N, de la Morena M, Dbaibo G, de Ravin S, Dimitrova D, Djidjik R, Dorna M, Dutmer C, Elfeky R, Facchetti F, Fuleihan R, Geha R, Gonzalez-Granado L, Haljasmägi L, Ale H, Hayward A, Hifanova A, Ip W, Kaplan B, Kapoor N, Karakoc-Aydiner E, Kärner J, Keller M, Dávila Saldaña B, Kiykim A, Kuijpers T, Kuznetsova E, Latysheva E, Leiding J, Locatelli F, Alva-Lozada G, McCusker C, Celmeli F, Morsheimer M, Ozen A, Parvaneh N, Pasic S, Plebani A, Preece K, Prockop S, Sakovich I, Starkova E, Torgerson T, Verbsky J, Walter J, Ward B, Wisner E, Draper D, Myint-Hpu K, Truong P, Lionakis M, Similuk M, Walkiewicz M, Klion A, Holland S, Oguz C, Bogunovic D, Kisand K, Su H, Tsang J, Kuhns D, Villa A, Rosenzweig S, Pittaluga S, Notarangelo L, Ghosh R, Siefert B, Tokita M, Yan J, Jodarski C, Kamen M, Gore R, Reynolds-Lallement N, Lewis K, Bannon S, Borges A, Gentile N. Multiomics dissection of human RAG deficiency reveals distinctive patterns of immune dysregulation but a common inflammatory signature. Science Immunology 2025, 10: eadq1697. PMID: 39792639, DOI: 10.1126/sciimmunol.adq1697.Peer-Reviewed Original ResearchMeSH KeywordsB-LymphocytesChild, PreschoolDNA-Binding ProteinsFemaleHomeodomain ProteinsHumansInflammationMaleMultiomicsMutationNuclear ProteinsPhenotypeConceptsRAG deficiencyRecombination-activating geneImmune dysregulationInflammatory signaturePattern of immune dysregulationT helper 2B cell developmentType I interferonOmenn syndromeImmunological phenotypeImmune profileSelf-antigensB cellsClinical managementDefective TI interferonCellular indicesImmunopathologyPatientsMultiomics approachPhenotypeHypomorphic formDysregulationLineage-specific contributionsDeficiency
2024
Human HDAC6 senses valine abundancy to regulate DNA damage
Jin J, Meng T, Yu Y, Wu S, Jiao C, Song S, Li Y, Zhang Y, Zhao Y, Li X, Wang Z, Liu Y, Huang R, Qin J, Chen Y, Cao H, Tan X, Ge X, Jiang C, Xue J, Yuan J, Wu D, Wu W, Jiang C, Wang P. Human HDAC6 senses valine abundancy to regulate DNA damage. Nature 2024, 637: 215-223. PMID: 39567688, DOI: 10.1038/s41586-024-08248-5.Peer-Reviewed Original ResearchConceptsHuman histone deacetylase 6Active DNA demethylationDNA demethylationValine deprivationDNA damageTen-eleven translocationRegulating DNA damageHistone deacetylase 6Repeat domainTherapeutic efficacy of PARP inhibitorsBind valineEfficacy of PARP inhibitorsCellular functionsPatient-derived xenograft modelsCytoplasmic shuttlingInduce DNA damageBranched amino acidsProtein synthesisAmino acidsIntracellular levelsPARP inhibitorsDNALevels of valineTumor growthTherapeutic efficacySubunit-specific analysis of cohesin-mutant myeloid malignancies reveals distinct ontogeny and outcomes
Jann J, Hergott C, Winkler M, Liu Y, Braun B, Charles A, Copson K, Barua S, Meggendorfer M, Nadarajah N, Shimony S, Winer E, Wadleigh M, Stone R, DeAngelo D, Garcia J, Haferlach T, Lindsley R, Luskin M, Stahl M, Tothova Z. Subunit-specific analysis of cohesin-mutant myeloid malignancies reveals distinct ontogeny and outcomes. Leukemia 2024, 38: 1992-2002. PMID: 39033241, PMCID: PMC11347381, DOI: 10.1038/s41375-024-02347-y.Peer-Reviewed Original ResearchConceptsAcute myeloid leukemiaDana-Farber Cancer InstituteMyelodysplastic neoplasmsCohesin complex componentSubunit specificityAssociated with secondary AMLCohesin complexDe novo acute myeloid leukemiaSecondary acute myeloid leukemiaComplex mutationsCohesinGenetic driversGenetic characteristicsSTAG2 mutationsCo-occurrenceSubunit mutationsMutationsMyeloid malignanciesPrognostic significanceAdverse prognosisPrognostic classificationMyeloid leukemiaClinical characteristicsDana-FarberOntogenyZNF397 Deficiency Triggers TET2-driven Lineage Plasticity and AR-Targeted Therapy Resistance in Prostate Cancer
Xu Y, Yang Y, Wang Z, Sjostrom M, Jiang Y, Tang Y, Cheng S, Deng S, Wang C, Gonzalez J, Johnson N, Li X, Li X, Metang L, Mukherji A, Xu Q, Tirado C, Wainwright G, Yu X, Barnes S, Hofstad M, Chen Y, Zhu H, Hanker A, Raj G, Zhu G, He H, Wang Z, Arteaga C, Liang H, Feng F, Wang Y, Wang T, Mu P. ZNF397 Deficiency Triggers TET2-driven Lineage Plasticity and AR-Targeted Therapy Resistance in Prostate Cancer. Cancer Discovery 2024, 14: 1496-1521. PMID: 38591846, PMCID: PMC11285331, DOI: 10.1158/2159-8290.cd-23-0539.Peer-Reviewed Original ResearchConceptsLineage plasticityTherapy resistanceProstate cancerCancer cellsAndrogen receptorResistance to AR-targeted therapiesLuminal lineageAR-targeted therapiesOvercome therapy resistanceTransition of cancer cellsEpigenetic regulatory machineryBona fide coactivatorTherapy responseAR signalingEpigenetic rewiringDrug resistanceTherapeutic strategiesEpigenetic reprogrammingProstateTherapyCancerPhenotypic plasticityRegulatory machineryAndrogenTranscriptional programsRational Design of TDP-43 Derived α‑Helical Peptide Inhibitors: An In Silico Strategy to Prevent TDP-43 Aggregation in Neurodegenerative Disorders
Salaikumaran M, Gopal P. Rational Design of TDP-43 Derived α‑Helical Peptide Inhibitors: An In Silico Strategy to Prevent TDP-43 Aggregation in Neurodegenerative Disorders. ACS Chemical Neuroscience 2024, 15: 1096-1109. PMID: 38466778, PMCID: PMC10959110, DOI: 10.1021/acschemneuro.3c00659.Peer-Reviewed Original ResearchMeSH KeywordsAmyotrophic Lateral SclerosisDNA-Binding ProteinsHumansMolecular Docking SimulationPeptidesProtein Conformation, alpha-HelicalConceptsMolecular dynamics simulationsTDP-43 aggregationTDP-43Disordered C-terminal regionDynamics simulationsIntramolecular hydrogen bondsAmyloid-like filamentsPeptide inhibitorRNA/DNA-binding proteinC-terminal regionPathology of neurodegenerative diseasesNeurodegenerative diseasesAggregation of TDP-43Binding affinityStructure-based computational approachDesign of peptide inhibitorsRNA/DNA-bindingLow root-mean-square deviationRNA splicingMRNA transportPeptide-based therapeuticsRoot-mean-square deviationDevelopment of novel therapeuticsFree energy landscapeStructure predictionARID1A orchestrates SWI/SNF-mediated sequential binding of transcription factors with ARID1A loss driving pre-memory B cell fate and lymphomagenesis
Barisic D, Chin C, Meydan C, Teater M, Tsialta I, Mlynarczyk C, Chadburn A, Wang X, Sarkozy M, Xia M, Carson S, Raggiri S, Debek S, Pelzer B, Durmaz C, Deng Q, Lakra P, Rivas M, Steidl C, Scott D, Weng A, Mason C, Green M, Melnick A. ARID1A orchestrates SWI/SNF-mediated sequential binding of transcription factors with ARID1A loss driving pre-memory B cell fate and lymphomagenesis. Cancer Cell 2024, 42: 583-604.e11. PMID: 38458187, PMCID: PMC11407687, DOI: 10.1016/j.ccell.2024.02.010.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDNA-Binding ProteinsHumansLymphomaMemory B CellsMiceMutationNuclear ProteinsTranscription FactorsConceptsFollicular lymphomaGerminal centersB cell fateAggressive follicular lymphomasMemory B cellsHigh-risk patientsSequential bindingNucleosome remodeling complexAggressive diseaseARID1A mutationsBinding of PUClonal precursorsBCL2 oncogeneB cellsPrecision therapyARID1ACD40 signalingLymphomaARID1A inactivationNF-kBRemodeling complexCell fateTranscription factorsPatientsMutationsHead-to-head comparison of [18F]-Flortaucipir, [18F]-MK-6240 and [18F]-PI-2620 postmortem binding across the spectrum of neurodegenerative diseases
Aguero C, Dhaynaut M, Amaral A, Moon S, Neelamegam R, Scapellato M, Carazo-Casas C, Kumar S, El Fakhri G, Johnson K, Frosch M, Normandin M, Gómez-Isla T. Head-to-head comparison of [18F]-Flortaucipir, [18F]-MK-6240 and [18F]-PI-2620 postmortem binding across the spectrum of neurodegenerative diseases. Acta Neuropathologica 2024, 147: 25. PMID: 38280071, PMCID: PMC10822013, DOI: 10.1007/s00401-023-02672-z.Peer-Reviewed Original ResearchConceptsNon-AD tauopathiesTau aggregationTau PET tracersDNA-binding proteinsBinds to neurofibrillary tanglesSecond-generation tau tracersTransactive response DNA-binding proteinSpectrum of neurodegenerative diseasesNeurofibrillary tanglesTau lesionsMelanin-containing cellsTDP-43Binding signalTauopathiesBinding targetsCerebral amyloid angiopathyOff-target bindingB-amyloidBinding patternsNeurodegenerative diseasesTau tracersTauBinding to areasBinding profilesBinding“Deficiency in ELF4, X-Linked”: a Monogenic Disease Entity Resembling Behçet’s Syndrome and Inflammatory Bowel Disease
Olyha S, O’Connor S, Kribis M, Bucklin M, Uthaya Kumar D, Tyler P, Alam F, Jones K, Sheikha H, Konnikova L, Lakhani S, Montgomery R, Catanzaro J, Du H, DiGiacomo D, Rothermel H, Moran C, Fiedler K, Warner N, Hoppenreijs E, van der Made C, Hoischen A, Olbrich P, Neth O, Rodríguez-Martínez A, Lucena Soto J, van Rossum A, Dalm V, Muise A, Lucas C. “Deficiency in ELF4, X-Linked”: a Monogenic Disease Entity Resembling Behçet’s Syndrome and Inflammatory Bowel Disease. Journal Of Clinical Immunology 2024, 44: 44. PMID: 38231408, PMCID: PMC10929603, DOI: 10.1007/s10875-023-01610-8.Peer-Reviewed Original ResearchMeSH KeywordsArthralgiaArthritisBehcet SyndromeBiological ProductsDNA-Binding ProteinsHumansInflammatory Bowel DiseasesMaleTranscription FactorsConceptsDEX patientsClass-switched memory B cellsInborn errors of immunityTreated with anti-inflammatory agentsLow natural killerX-linkedMemory B cellsErrors of immunityCohort of patientsIncreased inflammatory cytokinesLoss-of-function variantsHeterogeneous clinical phenotypesInflammatory bowel diseaseTargeted therapeutic interventionsNatural killerAnti-inflammatory agentsAphthous ulcersTherapeutic responseAutoinflammatory syndromeInflammatory markersClinical manifestationsB cellsBehcet's syndromeGastrointestinal symptomsMechanisms of disease
2023
Ten-Eleven-Translocation Genes in Cancer
Wang Y, Wang X, Lu J. Ten-Eleven-Translocation Genes in Cancer. Cancer Treatment And Research 2023, 190: 363-373. PMID: 38113007, DOI: 10.1007/978-3-031-45654-1_11.Peer-Reviewed Original ResearchMeSH Keywords5-MethylcytosineDNA MethylationDNA-Binding ProteinsHematologic NeoplasmsHumansMixed Function OxygenasesMutationProto-Oncogene ProteinsConceptsTET mutationsTen-ElevenBiochemical functionsTranslocation (TET) familyTranslocation geneHematopoietic malignanciesHematopoietic expansionGenesHuman cancersMutationsCritical roleImmune responseTET2Clonal hematopoiesisSolid cancersEpigenomeTET1TET3RNABiologyUnanswered questionsDNAHematopoiesisCooperateTETsTranscriptional responses of cancer cells to heat shock-inducing stimuli involve amplification of robust HSF1 binding
Dastidar S, De Kumar B, Lauckner B, Parrello D, Perley D, Vlasenok M, Tyagi A, Koney N, Abbas A, Nechaev S. Transcriptional responses of cancer cells to heat shock-inducing stimuli involve amplification of robust HSF1 binding. Nature Communications 2023, 14: 7420. PMID: 37973875, PMCID: PMC10654513, DOI: 10.1038/s41467-023-43157-7.Peer-Reviewed Original ResearchReduction of Nemo-like kinase increases lysosome biogenesis and ameliorates TDP-43-related neurodegeneration
Tejwani L, Jung Y, Kokubu H, Sowmithra S, Ni L, Lee C, Sanders B, Lee P, Xiang Y, Luttik K, Soriano A, Yoon J, Park J, Ro H, Ju H, Liao C, Tieze S, Rigo F, Jafar-Nejad P, Lim J. Reduction of Nemo-like kinase increases lysosome biogenesis and ameliorates TDP-43-related neurodegeneration. Journal Of Clinical Investigation 2023, 133: e138207. PMID: 37384409, PMCID: PMC10425213, DOI: 10.1172/jci138207.Peer-Reviewed Original ResearchMeSH KeywordsAmyotrophic Lateral SclerosisAnimalsDNA-Binding ProteinsHumansLysosomesMiceNeurodegenerative DiseasesConceptsAmyotrophic lateral sclerosisTDP-43-related neurodegenerationNeurodegenerative disordersTransactive response DNA-binding protein 43Sporadic amyotrophic lateral sclerosisDNA-binding protein 43Subset of patientsTDP-43 speciesTDP-43 inclusionsDistinct mouse modelsTDP-43 proteinopathyFamilial amyotrophic lateral sclerosisNemo-like kinaseMultiple neurodegenerative disordersAutophagy/lysosome pathwayTDP-43-positive aggregatesALS patientsALS casesSporadic ALSPharmacological reductionProtein 43Lateral sclerosisMouse modelParkinson's diseaseTDP-43Pot1b −/− tumors activate G-quadruplex-induced DNA damage to promote telomere hyper-elongation
Takasugi T, Gu P, Liang F, Staco I, Chang S. Pot1b −/− tumors activate G-quadruplex-induced DNA damage to promote telomere hyper-elongation. Nucleic Acids Research 2023, 51: 9227-9247. PMID: 37560909, PMCID: PMC10516629, DOI: 10.1093/nar/gkad648.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDNA DamageDNA-Binding ProteinsHumansMiceReplication Protein ASarcomaShelterin ComplexTelomereTelomere-Binding ProteinsConceptsDNA damage responseDamage responseReplication protein A (RPA) complexDependent DNA damage responseTelomere length homeostasisTelomere maintenance mechanismLength homeostasisTelomerase recruitmentPOT1 proteinsHuman POT1Mouse genomeLength maintenanceFunction disruptsReplicative immortalityTelomeresPOT1 mutationsDNA damageHuman cancersLonger telomeresPOT1bMaintenance mechanismsSerial transplantationA complexesSimilar mechanismMutationsAdvancing evolution: Bacteria break down gene silencer to express horizontally acquired genes
Groisman E, Choi J. Advancing evolution: Bacteria break down gene silencer to express horizontally acquired genes. BioEssays 2023, 45: e2300062. PMID: 37533411, PMCID: PMC10530229, DOI: 10.1002/bies.202300062.Peer-Reviewed Original ResearchMeSH KeywordsBacteriaBacterial ProteinsDNA-Binding ProteinsDNA-Directed RNA PolymerasesGene Expression Regulation, BacterialSalmonella typhimuriumConceptsH-NSAT-rich DNAHeat-stable nucleoid-structuring (H-NS) proteinConserved amino acid sequencesNucleoid structuring proteinHorizontal gene transferAmino acid sequenceSalmonella enterica serovar TyphimuriumBacterial evolutionLon proteaseProtease LonDiverse bacteriaEnterica serovar TyphimuriumRNA polymeraseAlternative promotersAcid sequenceStructuring proteinGene silencersGenesCleavage siteEnteric bacteriaEscherichia coliGene transferCommensal Escherichia coliSerovar TyphimuriumLoss of ZNF148 enhances insulin secretion in human pancreatic β cells
de Klerk E, Xiao Y, Emfinger C, Keller M, Berrios D, Loconte V, Ekman A, White K, Cardone R, Kibbey R, Attie A, Hebrok M. Loss of ZNF148 enhances insulin secretion in human pancreatic β cells. JCI Insight 2023, 8: e157572. PMID: 37288664, PMCID: PMC10393241, DOI: 10.1172/jci.insight.157572.Peer-Reviewed Original ResearchMeSH KeywordsDNA-Binding ProteinsExocytosisGlucoseHumansInsulinInsulin SecretionInsulin-Secreting CellsTranscription FactorsConceptsPancreatic β-cellsΒ-cellsSC-β cellsHuman pancreatic β-cellsInsulin secretionHuman β-cellsVesicle traffickingGenetic regulatorsStem cell-derived β cellsDirect repressionS100 genesCells identifiesZNF148Annexin A2Tetrameric complexCell membraneNovel therapeutic targetNovel therapeutic strategiesHuman isletsRegulatorTherapeutic targetCellsS100A16 expressionGlucose homeostasisTherapeutic strategiesCopy number variants and fetal structural abnormalities in stillborn fetuses: A secondary analysis of the Stillbirth Collaborative Research Network study
Workalemahu T, Dalton S, Son S, Allshouse A, Carey A, Page J, Blue N, Thorsten V, Goldenberg R, Pinar H, Reddy U, Silver R. Copy number variants and fetal structural abnormalities in stillborn fetuses: A secondary analysis of the Stillbirth Collaborative Research Network study. BJOG An International Journal Of Obstetrics & Gynaecology 2023, 131: 157-162. PMID: 37264725, PMCID: PMC10689565, DOI: 10.1111/1471-0528.17561.Peer-Reviewed Original ResearchConceptsCopy number variantsFetal structural malformationsAbnormal copy number variantsNumber variantsSingle nucleotide polymorphism arrayResearch Network StudyStillbirth casesDNA copy number variantsSpecific copy number variantsCardiac defectsPolymorphism arrayStructural malformationsSecondary analysisCraniofacial defectsGenesSpecific malformation typesFetal structural abnormalitiesWald chi-square testUnknown clinical significanceChi-square testKbSkeletal defectsBenign copy number variantsPathogenic deletionsClinical significancePhosphorylation stabilized TET1 acts as an oncoprotein and therapeutic target in B cell acute lymphoblastic leukemia
Chen Z, Zhou K, Xue J, Small A, Xiao G, Nguyen L, Zhang Z, Prince E, Weng H, Huang H, Zhao Z, Qing Y, Shen C, Li W, Han L, Tan B, Su R, Qin H, Li Y, Wu D, Gu Z, Ngo V, He X, Chao J, Leung K, Wang K, Dong L, Qin X, Cai Z, Sheng Y, Chen Y, Wu X, Zhang B, Shi Y, Marcucci G, Qian Z, Xu M, Müschen M, Chen J, Deng X. Phosphorylation stabilized TET1 acts as an oncoprotein and therapeutic target in B cell acute lymphoblastic leukemia. Science Translational Medicine 2023, 15: eabq8513. PMID: 36989375, PMCID: PMC11163962, DOI: 10.1126/scitranslmed.abq8513.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDNA-Binding ProteinsMicePhosphorylationPrecursor Cell Lymphoblastic Leukemia-LymphomaProto-Oncogene ProteinsSignal TransductionStaurosporineConceptsB-cell acute lymphoblastic leukemiaCell acute lymphoblastic leukemiaAcute lymphoblastic leukemiaB-ALLRefractory/Oncogenic roleLymphoblastic leukemiaProtein kinase C epsilonOverall survival rateNormal precursor B cellsCrucial oncogenic rolePrecursor B cellsAdult patientsPDX modelsPharmacological targetingTherapeutic targetB cellsImproved therapiesSurvival rateLeukemia progressionTherapeutic potentialOverexpression of TET1TET1 proteinATM serine/threonine kinaseLeukemiaComprehensive molecular phenotyping of ARID1A-deficient gastric cancer reveals pervasive epigenomic reprogramming and therapeutic opportunities
Xu C, Huang K, Law J, Chua J, Sheng T, Flores N, Pizzi M, Okabe A, Tan A, Zhu F, Kumar V, Lu X, Benitez A, Lian B, Ma H, Ho S, Ramnarayanan K, Anene-Nzelu C, Razavi-Mohseni M, Ghani S, Tay S, Ong X, Lee M, Guo Y, Ashktorab H, Smoot D, Li S, Skanderup A, Beer M, Foo R, Wong J, Sanghvi K, Yong W, Sundar R, Kaneda A, Prabhakar S, Mazur P, Ajani J, Yeoh K, So J, Tan P. Comprehensive molecular phenotyping of ARID1A-deficient gastric cancer reveals pervasive epigenomic reprogramming and therapeutic opportunities. Gut 2023, 72: 1651-1663. PMID: 36918265, DOI: 10.1136/gutjnl-2022-328332.Peer-Reviewed Original ResearchMeSH KeywordsCell Cycle ProteinsDNA-Binding ProteinsEpigenomicsHumansMutationNuclear ProteinsStomach NeoplasmsTranscription FactorsTumor MicroenvironmentConceptsGastric cancerMolecular subtypesPromoter activityMutational signaturesProinflammatory tumor microenvironmentTumor microenvironmental changesMutated driver genesSingle-cell transcriptome profilingCTCF occupancyGC molecular subtypesChromatin profilingDistal enhancerRegulatory networksEpigenetic landscapeBRD4 bindingEpigenomic reprogrammingEpigenomic levelsTumor-intrinsicTumor inflammationTumor microenvironmentTherapeutic vulnerabilitiesTranscriptome profilingDriver genesNFkB inhibitorGene expressionDiagnosis of acinic cell carcinoma of the salivary gland on cytology specimens: Role of NOR‐1 (NR4A3) immunohistochemistry
Meiklejohn K, Hrones M, Wang M, Prasad M, Cai G, Adeniran A, Gilani S. Diagnosis of acinic cell carcinoma of the salivary gland on cytology specimens: Role of NOR‐1 (NR4A3) immunohistochemistry. Cytopathology 2023, 34: 219-224. PMID: 36825365, DOI: 10.1111/cyt.13222.Peer-Reviewed Original Research
2022
Deletion of Jazf1 gene causes early growth retardation and insulin resistance in mice
Lee H, Jang H, Li H, Samuel V, Dudek K, Osipovich A, Magnuson M, Sklar J, Shulman G. Deletion of Jazf1 gene causes early growth retardation and insulin resistance in mice. Proceedings Of The National Academy Of Sciences Of The United States Of America 2022, 119: e2213628119. PMID: 36442127, PMCID: PMC9894197, DOI: 10.1073/pnas.2213628119.Peer-Reviewed Original ResearchConceptsKO miceEarly growth retardationInsulin resistanceFat massGrowth retardationAge-matched wild-type miceHepatic nuclear factor 4 alphaGH-IGF-1 axisHigh-fat diet feedingKO liversHyperinsulinemic-euglycemic clamp techniquePlasma growth hormone concentrationInsulin-like growth factor-1Type 2 diabetesGrowth hormone concentrationsIGF-1 expressionWild-type miceLean body massMuscle insulin resistanceGrowth factor-1Nuclear factor 4 alphaInsulin sensitivityDiet feedingPlasma concentrationsHormone concentrations
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