2019
Beyond Ruxolitinib: Fedratinib and Other Emergent Treatment Options for Myelofibrosis
Bewersdorf JP, Jaszczur SM, Afifi S, Zhao JC, Zeidan AM. Beyond Ruxolitinib: Fedratinib and Other Emergent Treatment Options for Myelofibrosis. Cancer Management And Research 2019, 11: 10777-10790. PMID: 31920387, PMCID: PMC6935287, DOI: 10.2147/cmar.s212559.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsTreatment optionsFavorable risk/benefit ratioRisk/benefit ratioEmergent treatment optionsHigh-risk patientsPhase II trialMain side effectsFuture treatment optionsBone marrow fibrosisGastrointestinal symptomsII trialLiver transaminasesAdverse eventsSymptom burdenOngoing trialsJAK1/2 inhibitorMF patientsMarrow fibrosisClinical trialsSecondary myelofibrosisBox warningSelective JAK2 inhibitorExtramedullary hematopoiesisSecond drugThiamine levelsRuxolitinib, a selective JAK1/2 inhibitor, for the treatment of serious diseases caused by Staphylococcus aureus superantigens
Carnes H, Mehrkens B, Stegman M, Rajagopalan G. Ruxolitinib, a selective JAK1/2 inhibitor, for the treatment of serious diseases caused by Staphylococcus aureus superantigens. The Journal Of Immunology 2019, 202: 190.34-190.34. DOI: 10.4049/jimmunol.202.supp.190.34.Peer-Reviewed Original ResearchSystemic inflammatory response syndromeMulti-organ failureT cellsHLA-DR3 transgenic miceHLA class II moleculesVehicle-treated miceVivo studiesInflammatory response syndromeT cell subsetsToxic shock syndromeJAK 1/2 inhibitorSelective JAK1/2 inhibitorClass II moleculesStaphylococcus aureusDose-dependent mannerSerious diseaseJanus kinaseIL-17Response syndromeOrgan failureJAK1/2 inhibitorActivation markersCell subsetsShock syndromeIL-2
2018
Phase II study of ruxolitinib, a selective JAK1/2 inhibitor, in patients with metastatic triple-negative breast cancer
Stover DG, Gil Del Alcazar CR, Brock J, Guo H, Overmoyer B, Balko J, Xu Q, Bardia A, Tolaney SM, Gelman R, Lloyd M, Wang Y, Xu Y, Michor F, Wang V, Winer EP, Polyak K, Lin NU. Phase II study of ruxolitinib, a selective JAK1/2 inhibitor, in patients with metastatic triple-negative breast cancer. Npj Breast Cancer 2018, 4: 10. PMID: 29761158, PMCID: PMC5935675, DOI: 10.1038/s41523-018-0060-z.Peer-Reviewed Original ResearchMetastatic triple-negative breast cancerTriple-negative breast cancerPhase II studyBreast cancerII studyObjective responseNon-randomized phase II studyIL-6/JAK2/STAT3Efficacy of ruxolitinibInfrequent grade 3Refractory patient populationPrimary efficacy endpointMetastatic breast cancerInflammatory breast cancerSelective JAK1/2 inhibitorArchival tumor tissueJAK2/STAT3Central immunohistochemistryCommon toxicitiesRECIST 1.1Efficacy endpointPrimary endpointProtocol therapyJAK1/2 inhibitorPatient populationSurfactant protein C dampens inflammation by decreasing JAK/STAT activation during lung repair
Jin H, Ciechanowicz AK, Kaplan AR, Wang L, Zhang P, Lu YC, Tobin RE, Tobin BA, Cohn L, Zeiss CJ, Lee PJ, Bruscia EM, Krause DS. Surfactant protein C dampens inflammation by decreasing JAK/STAT activation during lung repair. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2018, 314: l882-l892. PMID: 29345196, PMCID: PMC6008135, DOI: 10.1152/ajplung.00418.2017.Peer-Reviewed Original ResearchConceptsAcute respiratory distress syndromeKO miceSurfactant protein CClinical acute respiratory distress syndromeProtein CAlveolar type 2 cellsAnti-inflammatory mediatorsRespiratory distress syndromeBronchoalveolar lavage fluidAnti-inflammatory moleculesPhosphorylated signal transductionType 2 cellsSPC expressionInducible suicide geneJanus kinaseLevels of suppressorDistress syndromeBAL fluidGranulocyte infiltrationJAK1/2 inhibitorLavage fluidProinflammatory phenotypeInflammatory cytokinesSevere inflammationInjury model
2017
Management of myelofibrosis: JAK inhibition and beyond
Stahl M, Zeidan AM. Management of myelofibrosis: JAK inhibition and beyond. Expert Review Of Hematology 2017, 10: 459-477. PMID: 28395559, DOI: 10.1080/17474086.2017.1317590.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsBone marrow fibrosisMarrow fibrosisAbnormal cytokine expressionClinical trial evidenceJAK2 V617F allele burdenErythropoiesis stimulating agentsNovel therapeutic optionsAnti-fibrosis agentsV617F allele burdenJAK2 inhibitor ruxolitinibNovel therapeutic agentsJAK2 V617F mutationConstitutional symptomsCytoreductive drugsSymptom burdenImmunomodulatory drugsSurvival improvementJAK1/2 inhibitorMF patientsTherapeutic optionsTrial evidenceCytokine expressionExtramedullary hematopoiesisPrognostic assessmentRuxolitinib monotherapy
2016
Triple-negative breast cancers with amplification of JAK2 at the 9p24 locus demonstrate JAK2-specific dependence
Balko JM, Schwarz LJ, Luo N, Estrada MV, Giltnane JM, Dávila-González D, Wang K, Sánchez V, Dean PT, Combs SE, Hicks D, Pinto JA, Landis MD, Doimi FD, Yelensky R, Miller VA, Stephens PJ, Rimm DL, Gómez H, Chang JC, Sanders ME, Cook RS, Arteaga CL. Triple-negative breast cancers with amplification of JAK2 at the 9p24 locus demonstrate JAK2-specific dependence. Science Translational Medicine 2016, 8: 334ra53. PMID: 27075627, PMCID: PMC5256931, DOI: 10.1126/scitranslmed.aad3001.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic AgentsCell Line, TumorCell ProliferationChromosomes, Human, Pair 9Cohort StudiesFemaleGene AmplificationGene Knockdown TechniquesGenetic LociHumansJanus Kinase 2Middle AgedSignal TransductionSpheroids, CellularSTAT3 Transcription FactorSTAT6 Transcription FactorTriple Negative Breast NeoplasmsConceptsTriple-negative breast cancerJAK2 amplificationBreast cancerUntreated triple-negative breast cancerEventual metastatic spreadBasal-like cancersBreast cancer subtypesTNBC cell linesAmplification of JAK2Janus kinase 2 (JAK2) geneNeoadjuvant chemotherapyOverall survivalTNBC xenograftsJAK1/2 inhibitorClinical trialsMetastatic spreadKinase 2 geneJAK2-specific inhibitorTumor growthCancer subtypesMammosphere formationPatientsPotential biomarkersTumor progressionJAK2 inhibitors
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