2025
Contemporary understanding of myeloid-derived suppressor cells in the acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) tumor microenvironment
Alhajahjeh A, Stahl M, Kim T, Kewan T, Stempel J, Zeidan A, Bewersdorf J. Contemporary understanding of myeloid-derived suppressor cells in the acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) tumor microenvironment. Expert Review Of Anticancer Therapy 2025, ahead-of-print: 1-22. PMID: 40122075, DOI: 10.1080/14737140.2025.2483855.Peer-Reviewed Original ResearchMyeloid-derived suppressor cellsAcute myeloid leukemiaMyelodysplastic syndromeSuppressor cellsTumor microenvironmentMyeloid leukemiaEffects of myeloid-derived suppressor cellsTargets myeloid-derived suppressor cellsLeukemic stem cell survivalRisk of leukemia relapseMDSC-targeted therapiesMDSC-mediated immunosuppressionBone marrow nicheStem cell survivalCytokine-mediated pathwaysLeukemia relapseMyeloid diseasesImprove patient outcomesMarrow nichePost-transplantationPreclinical modelsImmunosuppressive propertiesImmunosuppressive componentsFunctional reprogrammingImmune evasionRecommendations for Design, Execution, and Reporting of Studies on Experimental Thoracic Aortopathy in Preclinical Models.
Daugherty A, Milewicz D, Dichek D, Ghaghada K, Humphrey J, LeMaire S, Li Y, Mallat Z, Saeys Y, Sawada H, Shen Y, Suzuki T, Zhou Z. Recommendations for Design, Execution, and Reporting of Studies on Experimental Thoracic Aortopathy in Preclinical Models. Arteriosclerosis Thrombosis And Vascular Biology 2025 PMID: 40079138, DOI: 10.1161/atvbaha.124.320259.Peer-Reviewed Original ResearchProceedings of the National Cancer Institute Workshop on combining immunotherapy with radiotherapy: challenges and opportunities for clinical translation
Morris Z, Demaria S, Monjazeb A, Formenti S, Weichselbaum R, Welsh J, Enderling H, Schoenfeld J, Brody J, McGee H, Mondini M, Kent M, Young K, Galluzzi L, Karam S, Theelen W, Chang J, Huynh M, Daib A, Pitroda S, Chung C, Serre R, Grassberger C, Deng J, Sodji Q, Nguyen A, Patel R, Krebs S, Kalbasi A, Kerr C, Vanpouille-Box C, Vick L, Aguilera T, Ong I, Herrera F, Menon H, Smart D, Ahmed J, Gartrell R, Roland C, Fekrmandi F, Chakraborty B, Bent E, Berg T, Hutson A, Khleif S, Sikora A, Fong L. Proceedings of the National Cancer Institute Workshop on combining immunotherapy with radiotherapy: challenges and opportunities for clinical translation. The Lancet Oncology 2025, 26: e152-e170. PMID: 40049206, DOI: 10.1016/s1470-2045(24)00656-9.Peer-Reviewed Original ResearchConceptsAnti-tumor immune responseDelivery of radiotherapyTumor immune recognitionSelection of immunotherapyBiomarker-guided approachesNational Cancer Institute workshopClinical trial dataImmunotherapy combinationsClinical responseImprove patient outcomesPreclinical modelsPatient selectionRadiotherapyImmunotherapyClinical endpointsClinical dataClinical studiesImmune recognitionImmune responseImmune effectsAnimal studiesClinical translationPatient outcomesTrial dataNegative trialsExploring Calcium Channels as Potential Therapeutic Targets in Blast Traumatic Brain Injury
Wachtler N, O’Brien R, Ehrlich B, McGuone D. Exploring Calcium Channels as Potential Therapeutic Targets in Blast Traumatic Brain Injury. Pharmaceuticals 2025, 18: 223. PMID: 40006037, PMCID: PMC11859800, DOI: 10.3390/ph18020223.Peer-Reviewed Original ResearchCalcium signalingCalcium channelsTherapeutic strategiesCalcium homeostasisFunction of calcium channelsDysregulated calcium signalingModulation of injuryTraumatic brain injuryBrain injuryLoss of calcium homeostasisBlast-related traumatic brain injuryDevelopment of neuroprotective interventionsIntracellular calcium dynamicsPlasma membrane stabilityExtracellular calciumBlast traumatic brain injuryPreclinical modelsTherapeutic outcomesNeuroprotective interventionsMembrane abnormalitiesPharmacological inhibitorsNeuronal somataExclusion criteriaCalcium dynamicsSecondary injuryGenetic deficiency or pharmacological inhibition of cGAS–STING signalling suppresses kidney inflammation and fibrosis
Jiao B, An C, Du H, Tran M, Yang D, Zhao Y, Wang P, Hu Z, Zhou D, Wang Y. Genetic deficiency or pharmacological inhibition of cGAS–STING signalling suppresses kidney inflammation and fibrosis. British Journal Of Pharmacology 2025, 182: 1741-1762. PMID: 39833988, DOI: 10.1111/bph.17412.Peer-Reviewed Original ResearchChronic kidney diseaseMacrophage proinflammatory activationDevelopment of renal fibrosisObstructive injuryCGAS-STING signalingProinflammatory activityCGAS-STINGRenal inflammationRenal fibrosisPharmacological inhibitionMyofibroblast formationDamaged tubular epithelial cellsCyclic GMP-AMP synthase (cGAS)-stimulatorBone marrow-derived macrophagesAttenuated kidney fibrosisMarrow-derived macrophagesCGAS-STING signaling pathwayTubular epithelial cellsSignaling in vitroCell-derived DNAPreclinical modelsTubular atrophySTING deficiencyInhibition of cGASKidney inflammationN-acetylcysteine modulates markers of oxidation, inflammation and infection in tuberculosis
Mapamba D, Sabi I, Lalashowi J, Sauli E, Buza J, Olomi W, Mtafya B, Kibona M, Bakuli A, Rachow A, Velen K, Hoelscher M, Ntinginya N, Charalambous S, Churchyard G, Wallis R, consortium T. N-acetylcysteine modulates markers of oxidation, inflammation and infection in tuberculosis. Journal Of Infection 2025, 90: 106379. PMID: 39756697, DOI: 10.1016/j.jinf.2024.106379.Peer-Reviewed Original ResearchAdjunctive N-acetylcysteineN-acetylcysteinePulmonary tuberculosisEx vivo whole blood cultureAffecting IL-10Effect of N-acetylcysteineFar-advanced pulmonary tuberculosisRecovery of lung functionN-acetylcysteine treatmentWhole blood culturesHost-directed therapiesPost-tuberculosis lung diseaseReduction of oxidative stressClearance of MtbAnti-inflammatory effectsBiomarkers of oxidationBlood culturesSecondary endpointsTotal glutathionePreclinical modelsClinical outcomesMtb burdenMonth 1Healthy volunteersIL-10
2024
Neuroinflammatory history results in overlapping transcriptional signatures with heroin exposure in the nucleus accumbens and alters responsiveness to heroin in male rats
Floris G, Zanda M, Dabrowski K, Daws S. Neuroinflammatory history results in overlapping transcriptional signatures with heroin exposure in the nucleus accumbens and alters responsiveness to heroin in male rats. Translational Psychiatry 2024, 14: 500. PMID: 39702361, PMCID: PMC11659471, DOI: 10.1038/s41398-024-03203-4.Peer-Reviewed Original ResearchConceptsResponse to heroinNucleus accumbensHeroin exposureOpioid use disorderSelf-administrationHeroin self-administrationMesolimbic dopamine systemOpioid-induced behaviorsMolecular neuroadaptationsDopamine systemOpioid rewardHeroin intakeBehavioral effectsUse disorderPsychiatric researchLipopolysaccharide (LPS)-induced neuroinflammationPreclinical modelsBehavioral ramificationsSensitivity to opioidsOpioid heroinHeroinMale ratsAccumbensHeightened immune responseNeuroinflammationDecoy-resistant IL-18 reshapes the tumor microenvironment and enhances rejection by anti-CTLA-4 in renal cell carcinoma
Schoenfeld D, Djureinovic D, Su D, Zhang L, Lu B, Kamga L, Mann J, Huck J, Hurwitz M, Braun D, Jilaveanu L, Ring A, Kluger H. Decoy-resistant IL-18 reshapes the tumor microenvironment and enhances rejection by anti-CTLA-4 in renal cell carcinoma. JCI Insight 2024, 10: e184545. PMID: 39561007, PMCID: PMC11721305, DOI: 10.1172/jci.insight.184545.Peer-Reviewed Original ResearchAnti-CTLA-4Renal cell carcinomaIL-18IL-18BPCell carcinomaTumor microenvironmentTumor typesPatients treated with immune checkpoint inhibitorsRegulatory T cell levelsAnti-PD-1 treatmentCD8+ T cellsAnti-PD-1Immune checkpoint inhibitorsCell renal cell carcinomaNon-responder patientsMyeloid cell populationsT cell levelsCytokine interleukin-18Anti-cancer efficacySecreted binding proteinCheckpoint inhibitorsResponding patientsPreclinical modelsT cellsMurine modelNew Horizons in Nuclear Cardiology: Imaging of Peripheral Arterial Disease
Callegari S, Mena-Hurtado C, Smolderen K, Thorn S, Sinusas A. New Horizons in Nuclear Cardiology: Imaging of Peripheral Arterial Disease. Journal Of Nuclear Cardiology 2024, 102079. PMID: 39549830, DOI: 10.1016/j.nuclcard.2024.102079.Peer-Reviewed Original ResearchPeripheral arterial diseaseDiagnostic modalitiesRisk stratificationArtery diseaseEarly diagnosisImprove risk stratificationAssociated with higher ratesLower extremity peripheral arterial diseaseEvaluation of therapyClinically relevant areasPreclinical modelsObstructive atherosclerotic diseaseClinical studiesArtery stenosisMicrovascular diseasePreprocedural assessmentPeripheral vasculaturePET imagingAtherosclerotic diseaseNuclear cardiologyTherapeutic interventionsClinical diseaseDiseaseComplex physiologyPerfusionThe Teplizumab Saga: The Challenge of Not Getting Lost in Clinical Translation.
Chatenoud L, Herold K, Bach J, Bluestone J. The Teplizumab Saga: The Challenge of Not Getting Lost in Clinical Translation. Cold Spring Harbor Perspectives In Medicine 2024, a041600. PMID: 39284671, DOI: 10.1101/cshperspect.a041600.Peer-Reviewed Original ResearchMetFinder: A Tool for Automated Quantitation of Metastatic Burden in Histological Sections From Preclinical Models
Karz A, Coudray N, Bayraktar E, Galbraith K, Jour G, Shadaloey A, Eskow N, Rubanov A, Navarro M, Moubarak R, Baptiste G, Levinson G, Mezzano V, Alu M, Loomis C, Lima D, Rubens A, Jilaveanu L, Tsirigos A, Hernando E. MetFinder: A Tool for Automated Quantitation of Metastatic Burden in Histological Sections From Preclinical Models. Pigment Cell & Melanoma Research 2024, 38: e13195. PMID: 39254030, DOI: 10.1111/pcmr.13195.Peer-Reviewed Original ResearchTumor contentMetastasis burdenMetastatic burdenTumor burdenMelanoma metastasesPreclinical modelsMurine modelPreclinical studiesMeasurable metastasesMelanoma researchTherapeutic approachesDeep neural networksHistopathological sectionsMechanisms of melanoma metastasisMetastasisHistological sectionsAI-based algorithmsAutomated quantificationWhole slide imagesAutomated quantitationNeural networkToll-like Receptor 9 Inhibition Mitigates Fibroproliferative Responses in Translational Models of Pulmonary Fibrosis.
Trujillo G, Regueiro-Ren A, Liu C, Hu B, Sun Y, Ahangari F, Fiorini V, Ishikawa G, Al Jumaily K, Khoury J, McGovern J, Lee C, Peng X, Pivarnik T, Sun H, Walia A, Woo S, Yu S, Antin-Ozerkis D, Sauler M, Kaminski N, Herzog E, Ryu C. Toll-like Receptor 9 Inhibition Mitigates Fibroproliferative Responses in Translational Models of Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2024, 211: 91-102. PMID: 39189851, PMCID: PMC11755360, DOI: 10.1164/rccm.202401-0065oc.Peer-Reviewed Original ResearchToll-like receptor 9Model of pulmonary fibrosisIdiopathic pulmonary fibrosisPulmonary fibrosisFibroproliferative responseLung diseaseIdiopathic pulmonary fibrosis cohortsExpression of toll-like receptor 9Toll-like receptor 9 activationTransplant-free survivalExpression of MCP-1Cohort of patientsSlow clinical progressionFibrotic lung diseaseAccelerated disease courseFatal lung diseaseIP-10Pharmacodynamic endpointsPreclinical modelsDisease courseClinical progressionPlasma mtDNAMCP-1Receptor 9Mouse modelRenalase peptides reduce pancreatitis severity in mice
Kolodecik T, Guo X, Shugrue C, Guo X, Desir G, Wen L, Gorelick F. Renalase peptides reduce pancreatitis severity in mice. AJP Gastrointestinal And Liver Physiology 2024, 327: g466-g480. PMID: 39010833, PMCID: PMC11427088, DOI: 10.1152/ajpgi.00143.2024.Peer-Reviewed Original ResearchAcute pancreatitisRecombinant renalaseProsurvival propertiesSeverity of acute pancreatitisModel of acute pancreatitisAcute inflammatory injuryClinically relevant modelAnti-inflammatoryHistological tissue injuryPost-ERCPCerulein modelCerulein-inducedInitial dosePancreatitis severityPreclinical modelsImmunohistochemical markersQuantify inflammationInflammatory changesMale micePancreatitisMacrophage populationsTissue injuryCerulein pancreatitisTherapeutic effectRenalaseA multicenter, randomized, double-blind, placebo-controlled ascending dose study to evaluate the safety, tolerability, pharmacokinetics (PK) and pharmacodynamic (PD) effects of Posiphen in subjects with early Alzheimer’s Disease
Galasko D, Farlow M, Lucey B, Honig L, Elbert D, Bateman R, Momper J, Thomas R, Rissman R, Pa J, Aslanyan V, Balasubramanian A, West T, Maccecchini M, Feldman H. A multicenter, randomized, double-blind, placebo-controlled ascending dose study to evaluate the safety, tolerability, pharmacokinetics (PK) and pharmacodynamic (PD) effects of Posiphen in subjects with early Alzheimer’s Disease. Alzheimer's Research & Therapy 2024, 16: 151. PMID: 38970127, PMCID: PMC11225352, DOI: 10.1186/s13195-024-01490-z.Peer-Reviewed Original ResearchConceptsOrally administered small moleculeFractional synthesis rateAscending dose studyDose-dependent loweringIRB-approved protocolEarly ADMini-Mental State ExamDose-dependent effectAlzheimer's diseaseBlood patchDouble-blindWell-toleratedCatheter placementPreclinical modelsLumbar punctureDose studyIntravenous infusionMild cognitive impairmentEvaluate safetyPlacebo participantsCognitive measuresStable isotope labeling kineticsActive drugClinical trialsADAS-Cog12Inhibition of lysine acetyltransferase KAT6 in ER+HER2− metastatic breast cancer: a phase 1 trial
Mukohara T, Park Y, Sommerhalder D, Yonemori K, Hamilton E, Kim S, Kim J, Iwata H, Yamashita T, Layman R, Mita M, Clay T, Chae Y, Oakman C, Yan F, Kim G, Im S, Lindeman G, Rugo H, Liyanage M, Saul M, Le Corre C, Skoura A, Liu L, Li M, LoRusso P. Inhibition of lysine acetyltransferase KAT6 in ER+HER2− metastatic breast cancer: a phase 1 trial. Nature Medicine 2024, 30: 2242-2250. PMID: 38824244, PMCID: PMC11333285, DOI: 10.1038/s41591-024-03060-0.Peer-Reviewed Original ResearchConceptsProgression-free survivalAntitumor activityEpidermal growth factor receptor-negativeBreast cancer preclinical modelsMedian progression-free survivalPhase 1 dose-escalationTreatment-related adverse eventsDose-expansion studyEstrogen receptor-positiveMetastatic breast cancerPhase 1 trialFirst-in-humanFulvestrant combinationReceptor-negativeReceptor-positiveEvaluation of antitumor activitySecondary endpointsPreclinical modelsSafety profileAdverse eventsBreast cancerApproximately doseClinical proofMonotherapyResponse rateEvolution of biotechnological advances and regenerative therapies for endometrial disorders: a systematic review
Rodríguez-Eguren A, Bueno-Fernandez C, Gómez-Álvarez M, Francés-Herrero E, Pellicer A, Bellver J, Seli E, Cervelló I. Evolution of biotechnological advances and regenerative therapies for endometrial disorders: a systematic review. Human Reproduction Update 2024, 30: 584-613. PMID: 38796750, PMCID: PMC11369227, DOI: 10.1093/humupd/dmae013.Peer-Reviewed Original ResearchPlatelet-rich plasmaAsherman's syndromeEndometrial atrophyIntrauterine adhesionsThin endometriumRegenerative therapyMesenchymal stem cellsEndometrial pathologyStem cellsPreclinical modelsEndometrial disordersClinical studiesRisk of poor pregnancy outcomesGrowth factorTreated with surgeryStem cell-based treatmentsPoor pregnancy outcomesTissue repairMaintenance of pregnancyPersonalized treatment regimensImprove reproductive outcomesCell-based treatmentsSystematic reviewHuman bone marrowEndometrial proliferationAn overview of preclinical models of traumatic brain injury (TBI): relevance to pathophysiological mechanisms
Fesharaki-Zadeh A, Datta D. An overview of preclinical models of traumatic brain injury (TBI): relevance to pathophysiological mechanisms. Frontiers In Cellular Neuroscience 2024, 18: 1371213. PMID: 38682091, PMCID: PMC11045909, DOI: 10.3389/fncel.2024.1371213.Peer-Reviewed Original ResearchClosed-Head Impact Model of Engineered Rotational AccelerationModel of traumatic brain injuryPreclinical modelsPreclinical models of traumatic brain injuryAnimal modelsTraumatic brain injuryControlled cortical impact injuryRodent preclinical modelsDisease modifying effectFluid percussion injuryCortical impact injuryBlast injuryAnimal models of traumatic brain injuryBrain injuryMotor vehicle accidentsTherapeutic regimenPathophysiological mechanismsEtiology of traumatic brain injuryPharmacological agentsSports related injuriesInjury modelCalcium dysregulationPrevalence of traumatic brain injuryClinical treatmentClinical settingDNA damage response in brain tumors: A Society for Neuro-Oncology consensus review on mechanisms and translational efforts in neuro-oncology
Rahman R, Shi D, Reitman Z, Hamerlik P, de Groot J, Haas-Kogan D, D’Andrea A, Sulman E, Tanner K, Agar N, Sarkaria J, Tinkle C, Bindra R, Mehta M, Wen P. DNA damage response in brain tumors: A Society for Neuro-Oncology consensus review on mechanisms and translational efforts in neuro-oncology. Neuro-Oncology 2024, 26: 1367-1387. PMID: 38770568, PMCID: PMC11300028, DOI: 10.1093/neuonc/noae072.Peer-Reviewed Original ResearchConsensus reviewDNA damage responseIDH wild-type glioblastomaIDH-mutant gliomasClinical trial design considerationsMechanisms of resistanceTrial design considerationsCombination therapyDevelopment of DDR inhibitorsDNA damage response pathwayPreclinical modelsDamage responseDDR inhibitorsNeuro-oncologyBrain tumorsBiomarker developmentTherapyResponse to DNA damageDNA damageTranslational effortsTumorDevelopmental changes in lung function of mice are independent of sex as a biological variable
Bärnthaler T, Ramachandra A, Ebanks S, Guerrera N, Sharma L, Dela Cruz C, Humphrey J, Manning E. Developmental changes in lung function of mice are independent of sex as a biological variable. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2024, 326: l627-l637. PMID: 38375577, PMCID: PMC11380952, DOI: 10.1152/ajplung.00120.2023.Peer-Reviewed Original ResearchPulmonary function testsWeeks of ageStatic complianceMale miceInspiratory capacityLung functionBody weight-basedHuman lung pathologiesLung function of miceFemale C57BL/6J miceLung function parametersSex-dependent changesFunction of miceMeasures of lung functionIndependent of sexPreclinical modelsFemale miceC57BL/6J miceLung pathologyFunction testsMiceWeight-basedLungLung disease researchWeeksWnt Signaling in Atherosclerosis: Mechanisms to Therapeutic Implications
Afroz R, Goodwin J. Wnt Signaling in Atherosclerosis: Mechanisms to Therapeutic Implications. Biomedicines 2024, 12: 276. PMID: 38397878, PMCID: PMC10886882, DOI: 10.3390/biomedicines12020276.Peer-Reviewed Original ResearchWnt pathwayWnt signalingAtherosclerosis progressionSmooth muscle cell proliferationMuscle cell proliferationPathophysiology of atherosclerosisBlock Wnt signalingDownstream signaling moleculesStages of atherosclerosis progressionPreclinical modelsMonocyte infiltrationEndothelial dysfunctionSmall molecule inhibitorsTreatment of atherosclerosisVascular inflammationTherapeutic approachesTherapeutic implicationsCo-receptorVascular diseaseAtherosclerosis developmentAtherosclerosisCell proliferationWnt ligandsMolecule inhibitorsWnt
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply