2024
Pharmacological management of pediatric metabolic dysfunction‐associated steatotic liver disease
Jaoudeh R, Hartmann P, Olson O, Gupta O, Kumar S, Ibrahim S, Fawaz R, Aqul A, Hassan S. Pharmacological management of pediatric metabolic dysfunction‐associated steatotic liver disease. Journal Of Pediatric Gastroenterology And Nutrition 2024, 80: 14-24. PMID: 39526564, DOI: 10.1002/jpn3.12402.Peer-Reviewed Original ResearchGLP-1RABody mass indexLiver diseasePediatric patientsPediatric obesityEfficacy of GLP-1RADisease progressionGlucagon-like peptide-1 receptor agonistsSteatotic liver diseaseManagement of pediatric patientsPeptide-1 receptor agonistsClinical management of pediatric patientsAdverse liver outcomesInduce weight lossLong-term efficacyHepatic manifestation of obesityLiver enzyme levelsAlternative therapeutic strategiesHalting disease progressionManifestation of obesityNonalcoholic fatty liver diseaseChildhood obesity ratesFatty liver diseaseReceptor agonistsLiver transplantation
2022
AML-055 Outcomes Based on Sequential Use of Venetoclax Based Therapy and Targeted Therapy in Acute Myeloid Leukemia (AML)
Stahl M, Shallis R, Derkach A, Goldberg A, Stein A, Stein E, Marcucci G, Zeidan A, Shimony S, DeAngelo D, Stone R, Aldoss I, Ball B, Bewersdorf J. AML-055 Outcomes Based on Sequential Use of Venetoclax Based Therapy and Targeted Therapy in Acute Myeloid Leukemia (AML). Clinical Lymphoma Myeloma & Leukemia 2022, 22: s209-s210. DOI: 10.1016/s2152-2650(22)01214-9.Peer-Reviewed Original ResearchOverall response rateAcute myeloid leukemiaMorphologic leukemia-free stateOverall survivalComplete responseIDH2 inhibitorsMedian OSPartial remissionTargeted therapyEffective salvage therapyIncomplete count recoveryMedian overall survivalShorter median OSRetrospective cohort studyShorter overall survivalAcademic cancer centerFLT3-ITD mutationAlternative therapeutic strategiesSalvage therapyCohort studyCount recoveryInhibitor therapyTargeted agentsClinical efficacyCancer Center
2021
Weakly Acidic Bile Is a Risk Factor for Hypopharyngeal Carcinogenesis Evidenced by DNA Damage, Antiapoptotic Function, and Premalignant Dysplastic Lesions In Vivo
Sasaki CT, Doukas SG, Doukas PG, Vageli DP. Weakly Acidic Bile Is a Risk Factor for Hypopharyngeal Carcinogenesis Evidenced by DNA Damage, Antiapoptotic Function, and Premalignant Dysplastic Lesions In Vivo. Cancers 2021, 13: 852. PMID: 33670587, PMCID: PMC7923205, DOI: 10.3390/cancers13040852.Peer-Reviewed Original ResearchAcidic bileBile acidsDeoxycholic acidUnconjugated secondary bile acidsDNA/RNA oxidative damageConjugated primary bile acidsUpper aerodigestive tractSecondary bile acidsPrimary bile acidsAlternative therapeutic strategiesPremalignant dysplastic lesionsHypopharyngeal carcinogenesisAntacid therapyRelevant molecular pathwaysRNA oxidative damageSimilar oncogenic effectsEsophageal refluxRefractory GERDAerodigestive tractDysplastic lesionsRisk factorsPremalignant lesionsBile contentTherapeutic strategiesP53 expression
2020
Scaffold association factor B (SAFB) is required for expression of prenyltransferases and RAS membrane association
Zhou M, Kuruvilla L, Shi X, Viviano S, Ahearn IM, Amendola CR, Su W, Badri S, Mahaffey J, Fehrenbacher N, Skok J, Schlessinger J, Turk BE, Calderwood DA, Philips MR. Scaffold association factor B (SAFB) is required for expression of prenyltransferases and RAS membrane association. Proceedings Of The National Academy Of Sciences Of The United States Of America 2020, 117: 31914-31922. PMID: 33257571, PMCID: PMC7749360, DOI: 10.1073/pnas.2005712117.Peer-Reviewed Original ResearchMeSH KeywordsAlkyl and Aryl TransferasesCell MembraneComputational BiologyCRISPR-Cas SystemsDatasets as TopicDimethylallyltranstransferaseGene Knockdown TechniquesHumansMatrix Attachment Region Binding ProteinsNeoplasmsNuclear Matrix-Associated ProteinsProtein PrenylationProtein SubunitsProto-Oncogene Proteins p21(ras)Receptors, EstrogenConceptsMembrane associationRAS membrane associationFarnesyltransferase inhibitorsPrenylation pathwayGenome-wide CRISPRGTP loadingAlternative prenylationMutant cellsNuclear proteinsKRAS membrane associationsRAS isoformsΑ-subunitGrowth inhibitionExpressionFactor BPathwayAnticancer therapyAlternative therapeutic strategiesPrenyltransferasesRasTherapeutic strategiesCRISPRFarnesyltransferaseMislocalizationPrenylation
2017
Successful treatment of arthritis induced by checkpoint inhibitors with tocilizumab: a case series
Kim S, Tayar J, Trinh V, Suarez-Almazor M, Garcia S, Hwu P, Johnson D, Uemura M, Diab A. Successful treatment of arthritis induced by checkpoint inhibitors with tocilizumab: a case series. Annals Of The Rheumatic Diseases 2017, 76: 2061-2064. PMID: 28830882, DOI: 10.1136/annrheumdis-2017-211560.Peer-Reviewed Original ResearchConceptsImmune-related adverse eventsImmune checkpoint inhibitorsCheckpoint inhibitorsReceptor antibodiesAssociated with immune-related adverse eventsMild immune-related adverse eventsEffective alternative to corticosteroidsEfficacy of ICI therapyICI-induced inflammatory arthritisImmune checkpoint inhibitor therapyAnti-IL-6 receptor antibodyAlternative to corticosteroidsTreated with corticosteroidsTreated with tocilizumabTumor necrosis factor-aImmune dampening effectsInflammatory side effectsAlternative therapeutic strategiesFood and Drug AdministrationTreatment of rheumatoid arthritisJuvenile idiopathic arthritisAntitumour responseICI therapyTNFa inhibitorsCheckpoint inhibitionA Tick Antivirulence Protein Potentiates Antibiotics against Staphylococcus aureus
Abraham NM, Liu L, Jutras BL, Murfin K, Acar A, Yarovinsky TO, Sutton E, Heisig M, Jacobs-Wagner C, Fikrig E. A Tick Antivirulence Protein Potentiates Antibiotics against Staphylococcus aureus. Antimicrobial Agents And Chemotherapy 2017, 61: 10.1128/aac.00113-17. PMID: 28438938, PMCID: PMC5487661, DOI: 10.1128/aac.00113-17.Peer-Reviewed Original ResearchConceptsNovel alternative therapeutic strategyAlternative therapeutic strategiesEfficacy of antibioticsTherapeutic strategiesTransgenic miceBacterial infectionsInfection modelDifferent antibioticsAntibioticsAntibiotic resistanceStaphylococcus aureusPotency of antibioticsClinical pathogensPeptides representativeImproved permeationPathogensPotent antibiofilm propertiesIAFGP
2015
VEGFR inhibitors upregulate CXCR4 in VEGF receptor-expressing glioblastoma in a TGFβR signaling-dependent manner
Pham K, Luo D, Siemann DW, Law BK, Reynolds BA, Hothi P, Foltz G, Harrison JK. VEGFR inhibitors upregulate CXCR4 in VEGF receptor-expressing glioblastoma in a TGFβR signaling-dependent manner. Cancer Letters 2015, 360: 60-67. PMID: 25676691, PMCID: PMC7294457, DOI: 10.1016/j.canlet.2015.02.005.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAngiogenesis InhibitorsAnimalsBenzylaminesBrain NeoplasmsCell Line, TumorCell MovementCyclamsFemaleGlioblastomaHeterocyclic CompoundsHumansInterleukin-2 Receptor alpha SubunitMaleMice, Inbred NODMice, KnockoutMice, SCIDMiddle AgedNeoplasm InvasivenessPiperidinesProtein Kinase InhibitorsQuinazolinesReceptor Cross-TalkReceptors, CXCR4Receptors, Transforming Growth Factor betaReceptors, Vascular Endothelial Growth FactorSignal TransductionTime FactorsUp-RegulationXenograft Model Antitumor AssaysConceptsTGFβ/TGFβRAnti-VEGF/VEGFR therapiesSignaling-dependent mannerMechanisms of crosstalkEnhanced invasive phenotypeVEGFR inhibitorsSurvival benefitHGF/METGBM cell linesInvasive phenotypeCXCL12/CXCR4 pathwayGreater survival benefitExpression of CXCR4VEGF/VEGFRMalignant phenotypeTumor-bearing animalsUpregulation of CXCR4Alternative therapeutic strategiesGBM progressionCell linesTGFβRRecurrent tumorsCXCR4 pathwayStandard treatmentCXCR4 antagonist
2014
AI-24VEGFR INHIBITORS ENHANCE PROGRESSION OF GLIOBLASTOMA BY UPREGULATING CXCR4 IN A TGFβR SIGNALING-DEPENDENT MANNER
Pham K, Luo D, Siemann D, Law B, Reynolds B, Hothi P, Foltz G, Harrison J. AI-24VEGFR INHIBITORS ENHANCE PROGRESSION OF GLIOBLASTOMA BY UPREGULATING CXCR4 IN A TGFβR SIGNALING-DEPENDENT MANNER. Neuro-Oncology 2014, 16: v6-v6. PMCID: PMC4217863, DOI: 10.1093/neuonc/nou238.24.Peer-Reviewed Original ResearchAnti-VEGF/VEGFR therapiesVascular endothelial growth factorVEGF/VEGFRSurvival benefitGBM patientsOverall survival benefitPhase III trialsGreater survival benefitExpression of CXCR4Early clinical studiesPatient-derived GBM cell linesCXCL12/CXCR4Tumor-bearing animalsAnti-angiogenic therapyUpregulation of CXCR4Chemokine receptor CXCR4Combination of cediranibAlternative therapeutic strategiesHGF/METFailure of standardEndothelial growth factorGrowth factor beta receptorTGFβ/TGFβRProgression of tumorsEnhanced invasive phenotype
2009
The HDAC Inhibitor TSA Inhibits Cell Proliferation, Induces Apoptosis and Down-Regulates HER2 Protein and Gene Expression as a Single Agent and in Combination with Trastuzumab in Trastuzumab-Sensitive and -Resistant Breast Cancer Cell Lines.
Radke S, Perincheri S, Schulz V, Lerner B, Kumar A, Chandrasekan L, Tuck D, Harris L. The HDAC Inhibitor TSA Inhibits Cell Proliferation, Induces Apoptosis and Down-Regulates HER2 Protein and Gene Expression as a Single Agent and in Combination with Trastuzumab in Trastuzumab-Sensitive and -Resistant Breast Cancer Cell Lines. Cancer Research 2009, 69: 3133-3133. DOI: 10.1158/0008-5472.sabcs-09-3133.Peer-Reviewed Original ResearchRole of HDACiHistone deacetylase inhibitorsTrastuzumab-resistant breast cancerBreast cancerBreast cancer cell linesHER2 proteinCancer cell linesSingle agentResistant breast cancer cell linesCell linesHER2-positive breast cancerFirst biological therapyHER2 antibody trastuzumabValue of HER2Positive breast cancerTSA treatmentNormal breast epitheliumNormal breast cell lineAlternative therapeutic strategiesBreast cancer cellsGrowth inhibitory effectsInhibited cell survivalHDAC inhibitor trichostatinResistant cell linesMechanism of actionNovel therapeutic strategies in prostate cancer: establishing a stratification system for patient selection in targeted trials.
Priolo C, Oh W, Loda M. Novel therapeutic strategies in prostate cancer: establishing a stratification system for patient selection in targeted trials. IDrugs 2009, 12: 165-8. PMID: 19333896.Peer-Reviewed Original ResearchConceptsProstate cancerClinical trialsProstate tumorsMetastatic hormone-refractory prostate cancerHormone-refractory prostate cancerTherapeutic strategiesResponse to specific drugsPhase I/II clinical trialsHuman prostate tumorsMetastatic prostate cancerStratification of patientsAlternative therapeutic strategiesStandard of treatmentRecombinant human mAbsNovel therapeutic strategiesTargeted clinical trialsPredictive markerHuman mAbsImproved survivalPatient selectionStandard treatmentPreclinical settingSmall molecule inhibitorsMolecular classificationSpecific drugs
1999
Use of rituximab and irradiated donor-derived lymphocytes to control Epstein–Barr virus-associated lymphoproliferation in patients undergoing related haplo-identical stem cell transplantation
McGuirk J, Seropian S, Howe G, Smith B, Stoddart L, Cooper D. Use of rituximab and irradiated donor-derived lymphocytes to control Epstein–Barr virus-associated lymphoproliferation in patients undergoing related haplo-identical stem cell transplantation. Bone Marrow Transplantation 1999, 24: 1253-1258. PMID: 10642818, DOI: 10.1038/sj.bmt.1702052.Peer-Reviewed Original ResearchMeSH KeywordsAdultAntibodies, MonoclonalAntibodies, Monoclonal, Murine-DerivedAntigens, ViralAntineoplastic AgentsBlood Component TransfusionBlood DonorsDNA, ViralGraft vs Host DiseaseHematologic NeoplasmsHematopoietic Stem Cell TransplantationHerpesvirus 4, HumanHumansImmunosuppression TherapyLymphocytesLymphoproliferative DisordersMalePolymerase Chain ReactionRituximabConceptsEpstein-Barr virus-associated lymphoproliferative disorderStem cell transplantationEBV DNA titersB cell populationsCell transplantationTherapeutic strategiesEpstein-Barr virus-associated lymphoproliferationHaplo-identical stem cell transplantationEffective alternative therapeutic strategyAllogeneic stem cell transplantationCourses of rituximabDonor-derived lymphocytesPost-transplant immunosuppressionMonoclonal B-cell populationCD20 monoclonal antibodyCell populationsAlternative therapeutic strategiesImmunosuppressive medicationsSevere GVHDHost diseaseLymphocyte infusionPost transplantFatal complicationCurative therapyLymphoproliferative disorders
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