2024
MIF contribution to progressive brain diseases
Matejuk A, Benedek G, Bucala R, Matejuk S, Offner H, Vandenbark A. MIF contribution to progressive brain diseases. Journal Of Neuroinflammation 2024, 21: 8. PMID: 38178143, PMCID: PMC10765708, DOI: 10.1186/s12974-023-02993-6.Peer-Reviewed Original ResearchConceptsBrain diseasesMultiple sclerosisAlzheimer's diseaseMacrophage migration inhibitory factorModulation of neuroinflammationNumerous neurologic diseasesMigration inhibitory factorProgressive brain diseaseNew therapeutic strategiesInflammatory mediatorsChronic inflammationAutoimmune diseasesVascular diseaseNervous system developmentNeurologic diseaseNeuroendocrine functionPsychiatric disordersTherapeutic strategiesEconomic burdenNeurological diseasesNew biomarkersInhibitory factorNeurodegenerative pathologiesDiseaseNovel therapeutics
2023
Potential of Dietary HDAC2i in Breast Cancer Patients Receiving PD-1/PD-L1 Inhibitors
Wang Y, Lu L, Ling C, Zhang P, Han R. Potential of Dietary HDAC2i in Breast Cancer Patients Receiving PD-1/PD-L1 Inhibitors. Nutrients 2023, 15: 3984. PMID: 37764768, PMCID: PMC10537481, DOI: 10.3390/nu15183984.Peer-Reviewed Original ResearchConceptsImmune checkpoint inhibitorsPD-1/PD-L1 inhibitorsPD-L1 inhibitorsICI therapyDietary interventionBC patientsBreast cancerTherapeutic strategiesNovel immune checkpoint inhibitorsHDAC2 inhibitorsIntegrated therapeutic strategiesOptimal clinical benefitKaplan-Meier plotter platformNew therapeutic strategiesAnti-cancer effectsCheckpoint inhibitorsSupportive therapyClinical benefitHigh morbidityCombination therapyTreatment outcomesLethal malignancyTherapeutic effectEffective treatmentPrognostic analysisNovel epigenetic molecular therapies for imprinting disorders
Wang S, Jiang Y. Novel epigenetic molecular therapies for imprinting disorders. Molecular Psychiatry 2023, 28: 3182-3193. PMID: 37626134, PMCID: PMC10618104, DOI: 10.1038/s41380-023-02208-7.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsActive alleleImprinting disordersMolecular mechanismsGenome editing approachesEpigenetic-based therapiesUnique molecular mechanismGenomic imprinting disordersImprinted genesGenome editingMolecular approachesEditing approachesInactive allelesNew therapeutic strategiesAllelesSmall moleculesMolecular therapyTherapeutic strategiesLeptomeningeal disease in melanoma: An update on the developments in pathophysiology and clinical care
Smalley I, Boire A, Brastianos P, Kluger H, Hernando‐Monge E, Forsyth P, Ahmed K, Smalley K, Ferguson S, Davies M, Oliva I. Leptomeningeal disease in melanoma: An update on the developments in pathophysiology and clinical care. Pigment Cell & Melanoma Research 2023, 37: 51-67. PMID: 37622466, DOI: 10.1111/pcmr.13116.Peer-Reviewed Original ResearchLeveraging immune resistance archetypes in solid cancer to inform next-generation anticancer therapies
Anderson K, Braun D, Buqué A, Gitto S, Guerriero J, Horton B, Keenan B, Kim T, Overacre-Delgoffe A, Ruella M, Triplett T, Veeranki O, Verma V, Zhang F. Leveraging immune resistance archetypes in solid cancer to inform next-generation anticancer therapies. Journal For ImmunoTherapy Of Cancer 2023, 11: e006533. PMID: 37399356, PMCID: PMC10314654, DOI: 10.1136/jitc-2022-006533.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsImmune resistance mechanismsImmune resistanceChimeric antigen receptor T cellsAntigen receptor T cellsImmune checkpoint inhibitorsReceptor T cellsVariety of malignanciesNew therapeutic strategiesResistance mechanismsCheckpoint inhibitorsDurable responsesMost patientsAnticancer immunotherapyTherapy combinationsCurrent therapiesT cellsIndividual patientsSolid cancersTherapeutic strategiesTumor profilingPatientsOverall efficacySuppressive mechanismsBispecific antibodiesTumor microenvironment
2022
Cell death in development, maintenance, and diseases of the nervous system
Mercau ME, Patwa S, Bhat KPL, Ghosh S, Rothlin CV. Cell death in development, maintenance, and diseases of the nervous system. Seminars In Immunopathology 2022, 44: 725-738. PMID: 35508671, DOI: 10.1007/s00281-022-00938-4.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsCell deathTissue-level responsesNervous system homeostasisNervous systemCentral nervous system tumorsMolecular modalitiesAcute brain injuryNervous system tumorsChronic neurodegenerative diseasesSystem homeostasisDead cellsNew therapeutic strategiesNeurodegenerative diseasesMechanisms of disposalGlial cellsNovel understandingAdult neurogenesisSystem tumorsBrain injuryPathological responseDisease statesTherapeutic strategiesCellsRecent studiesDeathMutant IDH Inhibits IFNγ–TET2 Signaling to Promote Immunoevasion and Tumor Maintenance in CholangiocarcinomaMutant-IDH1 Promotes Immunoevasion in Cholangiocarcinoma
Wu M, Shi L, Dubrot J, Merritt J, Vijay V, Wei T, Kessler E, Olander K, Adil R, Pankaj A, Tummala K, Weeresekara V, Zhen Y, Wu Q, Luo M, Shen W, García-Beccaria M, Fernández-Vaquero M, Hudson C, Ronseaux S, Sun Y, Saad-Berreta R, Jenkins R, Wang T, Heikenwälder M, Ferrone C, Goyal L, Nicolay B, Deshpande V, Kohli R, Zheng H, Manguso R, Bardeesy N. Mutant IDH Inhibits IFNγ–TET2 Signaling to Promote Immunoevasion and Tumor Maintenance in CholangiocarcinomaMutant-IDH1 Promotes Immunoevasion in Cholangiocarcinoma. Cancer Discovery 2022, 12: 812-835. PMID: 34848557, PMCID: PMC8904298, DOI: 10.1158/2159-8290.cd-21-1077.Peer-Reviewed Original ResearchConceptsTumor maintenanceKetoglutarate-dependent enzymesDiscovery of mechanismsDNA demethylaseResponse genesCell-specific ablationCTLA4 blockadeMouse modelEnzyme inhibitsImmune checkpoint activationCytotoxic T-cell functionTumor cellsSuppression of CD8T-cell depletionIssue featureT cell activityT cell recruitmentT cell functionNew therapeutic strategiesInterferon γ expressionIsocitrate dehydrogenase 1 (IDH1) mutationTET2Receptor 1Γ expressionInhibitor efficacyClinicopathological Review of Micropapillary Urothelial Carcinoma
Kumar D, Adeniran AJ. Clinicopathological Review of Micropapillary Urothelial Carcinoma. Current Oncology Reports 2022, 24: 603-610. PMID: 35199295, DOI: 10.1007/s11912-022-01219-x.Peer-Reviewed Original ResearchConceptsMicropapillary urothelial carcinomaUrothelial carcinomaNew therapeutic strategiesModerate interobserver reproducibilityClinicopathological reviewUrothelial componentAggressive variantHistopathologic characteristicsClinical managementWorse outcomesERBB2 amplificationTherapeutic strategiesDiagnostic criteriaReviewThis reviewCarcinomaOptimal managementReproducible criteriaInterobserver reproducibilityGenetic findingsIntratumoral heterogeneityHigh rateMolecular featuresRecent reportsLacunar spacesReview
2021
A Benzenesulfonamide-based Mitochondrial Uncoupler Induces Endoplasmic Reticulum Stress and Immunogenic Cell Death in Epithelial Ovarian Cancer
Bi F, Jiang Z, Park W, Hartwich TMP, Ge Z, Chong KY, Yang K, Morrison MJ, Kim D, Kim J, Zhang W, Kril LM, Watt DS, Liu C, Yang-Hartwich Y. A Benzenesulfonamide-based Mitochondrial Uncoupler Induces Endoplasmic Reticulum Stress and Immunogenic Cell Death in Epithelial Ovarian Cancer. Molecular Cancer Therapeutics 2021, 20: molcanther.mct-21-0396-a.2021. PMID: 34625503, PMCID: PMC8643344, DOI: 10.1158/1535-7163.mct-21-0396.Peer-Reviewed Original ResearchConceptsEpithelial ovarian cancerImmunogenic cell deathOvarian cancerTumor progressionAntitumor adaptive immune responsesDamage-associated molecular patternsCancer cellsMitochondrial uncouplerAdaptive immune responsesOvarian cancer modelCause of deathCurrent chemotherapeutic agentsNew therapeutic strategiesOvarian cancer cellsCancer cell proliferationCell deathEndoplasmic reticulum stressGynecologic malignanciesClinical outcomesEndoplasmic reticulum stress sensorNew anticancer therapiesPeritoneal fluidInduces Endoplasmic Reticulum StressImmune responseAbdominal cavityTreatment of Human Babesiosis: Then and Now
Renard I, Ben Mamoun C. Treatment of Human Babesiosis: Then and Now. Pathogens 2021, 10: 1120. PMID: 34578153, PMCID: PMC8469882, DOI: 10.3390/pathogens10091120.Peer-Reviewed Original ResearchHuman babesiosisSevere adverse eventsNew therapeutic strategiesPublic health concernTick-borne diseaseAdverse eventsBlood transfusionCombination therapySafe therapyRisk of humanTherapeutic strategiesHuman transmissionApicomplexan parasitesDrug resistanceHealth concernBabesiosisTherapyTreatmentDiseaseCurrent arsenalParasitesRapid emergenceTransfusionClindamycinAzithromycinDual therapeutic targeting of intra-articular inflammation and intracellular bacteria enhances chondroprotection in septic arthritis
Kwon HK, Lee I, Yu KE, Cahill SV, Alder KD, Lee S, Dussik CM, Back J, Choi J, Song L, Kyriakides TR, Lee FY. Dual therapeutic targeting of intra-articular inflammation and intracellular bacteria enhances chondroprotection in septic arthritis. Science Advances 2021, 7: eabf2665. PMID: 34172438, PMCID: PMC8232912, DOI: 10.1126/sciadv.abf2665.Peer-Reviewed Original ResearchConceptsIntra-articular inflammationSeptic arthritisBacterial infectionsDual therapeutic targetingKnee septic arthritisPromising new therapeutic strategyArticular cartilageChallenging clinical problemNovel treatment modalitiesIntracellular bacteriaNew therapeutic strategiesAdjuvant targetingTreatment modalitiesBacterial eradicationSuccessful treatmentHost inflammationCausative bacteriaMurine modelTherapeutic strategiesArthritisTherapeutic goalsClinical problemTherapeutic targetingInflammationVital organsAlcohol-induced Hsp90 acetylation is a novel driver of liver sinusoidal endothelial dysfunction and alcohol-related liver disease
Yang Y, Sangwung P, Kondo R, Jung Y, McConnell MJ, Jeong J, Utsumi T, Sessa WC, Iwakiri Y. Alcohol-induced Hsp90 acetylation is a novel driver of liver sinusoidal endothelial dysfunction and alcohol-related liver disease. Journal Of Hepatology 2021, 75: 377-386. PMID: 33675874, PMCID: PMC8292196, DOI: 10.1016/j.jhep.2021.02.028.Peer-Reviewed Original ResearchConceptsEndothelial nitric oxide synthaseAlcohol-induced liver injuryLiver sinusoidal endothelial cellsAlcohol-related liver diseaseLiver injuryLSEC dysfunctionHsp90 acetylationNO productionHistone deacetylase 6Liver diseaseTherapeutic strategiesHeat shock protein 90 (Hsp90) acetylationLiver sinusoidal endothelial dysfunctionSinusoidal endothelial cell dysfunctionMouse liver sinusoidal endothelial cellsEndothelial cell dysfunctionNitric oxide synthaseEthanol-fed miceSinusoidal endothelial dysfunctionPotential therapeutic approachPotential therapeutic strategyNitric oxide productionNew therapeutic strategiesSinusoidal endothelial cellsAcetylation of Hsp90
2020
Enhanced Meningeal Lymphatic Drainage Ameliorates Neuroinflammation and Hepatic Encephalopathy in Cirrhotic Rats
Hsu SJ, Zhang C, Jeong J, Lee SI, McConnell M, Utsumi T, Iwakiri Y. Enhanced Meningeal Lymphatic Drainage Ameliorates Neuroinflammation and Hepatic Encephalopathy in Cirrhotic Rats. Gastroenterology 2020, 160: 1315-1329.e13. PMID: 33227282, PMCID: PMC7956141, DOI: 10.1053/j.gastro.2020.11.036.Peer-Reviewed Original ResearchConceptsMeningeal lymphatic drainageLymphatic drainageMicroglia activationMotor functionBile duct ligation modelTumor necrosis factor αSerious neurologic complicationsMeningeal lymphatic systemNecrosis factor αDuct ligation modelNew therapeutic strategiesBrain inflammationNeurologic complicationsHepatic encephalopathyLiver cirrhosisLymph nodesRotarod testMotor dysfunctionCirrhotic ratsInterleukin-1βLigation modelInterferon γProinflammatory genesCisterna magnaTherapeutic strategiesPonatinib is a potential therapeutic approach for malignant pleural mesothelioma
Yang YW, Marrufo A, Chase J, Woodard GA, Jablons DM, Lemjabbar-Alaoui H. Ponatinib is a potential therapeutic approach for malignant pleural mesothelioma. Experimental Lung Research 2020, 47: 9-25. PMID: 33107354, DOI: 10.1080/01902148.2020.1836691.Peer-Reviewed Original ResearchConceptsMalignant pleural mesotheliomaPonatinib treatmentPleural mesotheliomaMPM linesTherapeutic approachesPotential therapeutic approachExpression levelsNew therapeutic strategiesHuman MPM cellsMPM therapyPSTAT5 levelsWestern blot analysisMPM patientsMPM treatmentDeadly malignancyLevels of γH2AXPotential utilityTherapeutic strategiesTumor growthMPM cellsPathway inhibitionTumor modelPonatinibActivation of AblTumor samplesMulti-Omics Investigation of Innate Navitoclax Resistance in Triple-Negative Breast Cancer Cells
Marczyk M, Patwardhan GA, Zhao J, Qu R, Li X, Wali VB, Gupta AK, Pillai MM, Kluger Y, Yan Q, Hatzis C, Pusztai L, Gunasekharan V. Multi-Omics Investigation of Innate Navitoclax Resistance in Triple-Negative Breast Cancer Cells. Cancers 2020, 12: 2551. PMID: 32911681, PMCID: PMC7563413, DOI: 10.3390/cancers12092551.Peer-Reviewed Original ResearchTriple-negative breast cancer cellsCancer cellsBreast cancer cellsStress response genesMulti-omics landscapeCell population compositionDrug-induced cell deathMulti-omics investigationsCell linesBCL2 family inhibitorsSingle-cell analysisChromatin accessibilityGenome structureMDA-MB-231 triple-negative breast cancer cellsChromatin structureMethylation stateResponse genesFamily inhibitorsCell deathTNBC cell linesNumber variationsDefense mechanismsResistance mechanismsNew therapeutic strategiesGenesThe Role of Tricellular Junctions in the Transport of Macromolecules Across Endothelium
Ghim M, Mohamied Y, Weinberg P. The Role of Tricellular Junctions in the Transport of Macromolecules Across Endothelium. Cardiovascular Engineering And Technology 2020, 12: 101-113. PMID: 32820467, PMCID: PMC7904563, DOI: 10.1007/s13239-020-00483-x.Peer-Reviewed Original ResearchConceptsDensity lipoproteinHigh-density lipoproteinLow-density lipoproteinNew therapeutic strategiesEffects of agonistsEndothelial barrier functionConclusionThese dataInfluence of agonistsTherapeutic strategiesVascular endotheliumEndotheliumBarrier functionEndothelial monolayersNormal physiologyTransendothelial transportAgonistsLipoproteinDiseaseFurther investigationCOVID-19, Renin-Angiotensin System and Endothelial Dysfunction
Amraei R, Rahimi N. COVID-19, Renin-Angiotensin System and Endothelial Dysfunction. Cells 2020, 9: 1652. PMID: 32660065, PMCID: PMC7407648, DOI: 10.3390/cells9071652.Peer-Reviewed Original ResearchConceptsRenin-angiotensin systemSARS-CoV-2Acute respiratory distress syndromeSARS-CoV-2 infectionEndothelial dysfunctionVascular damageCell adhesion moleculeSARS-CoV-2-induced acute respiratory distress syndromeCOVID-19Pre-existing endothelial dysfunctionSARS-CoV-2 entryRespiratory distress syndromeEndothelial cell injuryRole of ACE2Coronavirus disease 2019 (COVID-19) outbreakNovel coronavirus disease 2019 (COVID-19) outbreakCD209/DC-SIGNSARS-CoV-2 virusNew therapeutic strategiesDisease 2019 outbreakHuman vascular endotheliumGlobal public healthHost cellsAngiotensin fragmentsDistress syndromeAcquired Resistance to HER2-Targeted Therapies Creates Vulnerability to ATP Synthase Inhibition
Gale M, Li Y, Cao J, Liu ZZ, Holmbeck MA, Zhang M, Lang SM, Wu L, Do Carmo M, Gupta S, Aoshima K, DiGiovanna MP, Stern DF, Rimm DL, Shadel GS, Chen X, Yan Q. Acquired Resistance to HER2-Targeted Therapies Creates Vulnerability to ATP Synthase Inhibition. Cancer Research 2020, 80: 524-535. PMID: 31690671, PMCID: PMC7002225, DOI: 10.1158/0008-5472.can-18-3985.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic Combined Chemotherapy ProtocolsApoptosisBreast NeoplasmsCell ProliferationDrug Resistance, NeoplasmEnzyme InhibitorsFemaleHumansMiceMice, Inbred NODMice, SCIDMitochondrial Proton-Translocating ATPasesOligomycinsReceptor, ErbB-2TrastuzumabTumor Cells, CulturedXenograft Model Antitumor AssaysConceptsResistant cellsHER2-Targeted TherapyTrastuzumab-resistant tumorsNew therapeutic strategiesNovel potential targetDrug-free mediumAntibody therapySynthase inhibitionLow doseTherapeutic strategiesTrastuzumabBreast tumorsHER2TherapyAcquired ResistanceTumorsPotential targetMitochondrial respirationCellsSelective dependencyInhibitionMinimal changesNovel vulnerabilitiesATP synthase inhibitionOligomycin A
2019
O5‐04‐05: A NEW THERAPEUTIC STRATEGY FOR TAUOPATHIES: DISCOVERY OF HIGHLY POTENT BRAIN PENETRANT PROTACTM DEGRADER MOLECULES THAT TARGET PATHOLOGIC TAU PROTEIN SPECIES
Cacace A, Chandler J, Flanagan J, Berlin M, Cadelina G, Pizzano J, Bookbinder M, Crews C, Crew A, Taylor I, Houston J. O5‐04‐05: A NEW THERAPEUTIC STRATEGY FOR TAUOPATHIES: DISCOVERY OF HIGHLY POTENT BRAIN PENETRANT PROTACTM DEGRADER MOLECULES THAT TARGET PATHOLOGIC TAU PROTEIN SPECIES. Alzheimer's & Dementia 2019, 15: p1624-p1624. DOI: 10.1016/j.jalz.2019.06.4856.Peer-Reviewed Original ResearchTissue-Engineered Stem Cell Models of Cardiovascular Diseases
Anderson C, Luo J, Sewanan L, Kural M, Riaz M, Park J, Huang Y, Niklason L, Campbell S, Qyang Y. Tissue-Engineered Stem Cell Models of Cardiovascular Diseases. 2019, 1-18. DOI: 10.1007/978-3-030-20047-3_1.ChaptersMolecular underpinningsStem cell modelTwo-dimensional cell culture methodsComplex 3D microenvironmentThree-dimensional microenvironmentMolecular mechanismsTissue-engineered modelDisease modelingNew therapeutic strategiesCell culturesCell culture methodsCell modelPathological conditionsCulture systemDisease statesCompelling insightsTherapeutic strategiesMicroenvironmentCulture methodVivo
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