2021
Targeted therapies: Expanding the role of FGFR3 inhibition in urothelial carcinoma
Zengin Z, Chehrazi-Raffle A, Salgia N, Muddasani R, Ali S, Meza L, Pal S. Targeted therapies: Expanding the role of FGFR3 inhibition in urothelial carcinoma. Urologic Oncology Seminars And Original Investigations 2021, 40: 25-36. PMID: 34840077, DOI: 10.1016/j.urolonc.2021.10.003.Peer-Reviewed Original ResearchConceptsImmune checkpoint inhibitorsUrothelial carcinomaCheckpoint inhibitorsTargeted therapyLower tract diseaseMultiple disease stagesMetastatic urothelial carcinomaOverall response rateAntibody-drug conjugatesGrowth factor receptor familyFGFR3 inhibitionUC tumorsChemotherapy regimensUpper tractOngoing trialsDisease stageTract diseaseTreatment paradigmFactor receptor familyHigh incidenceActionable mutationsFGFR1-4FGFR3 inhibitorsSmall molecule inhibitorsFGFR3 mutations
2014
Neuregulin 1–activated ERBB4 interacts with YAP to induce Hippo pathway target genes and promote cell migration
Haskins JW, Nguyen DX, Stern DF. Neuregulin 1–activated ERBB4 interacts with YAP to induce Hippo pathway target genes and promote cell migration. Science Signaling 2014, 7: ra116. PMID: 25492965, PMCID: PMC4648367, DOI: 10.1126/scisignal.2005770.Peer-Reviewed Original ResearchMeSH KeywordsBreast NeoplasmsCell Cycle ProteinsCell Line, TumorCell MovementConnective Tissue Growth FactorErlotinib HydrochlorideFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHippo Signaling PathwayHumansLapatinibMechanotransduction, CellularNeuregulin-1Nuclear ProteinsProtein Kinase InhibitorsProtein Serine-Threonine KinasesQuinazolinesReceptor, ErbB-4Transcription FactorsConceptsIntracellular domainHippo pathway target genesHippo tumor suppressor pathwayCell migrationTranscriptional coactivator YAPCultured mammary epithelial cellsTumor suppressor pathwayPathway target genesSoluble intracellular domainExpression of genesEpidermal growth factor receptor familyMammary epithelial cellsGrowth factor receptor familyNuclear functionsIntramembrane proteolysisCoactivator YAPFactor receptor familyGrowth factor receptorTarget genesYAP activityNeuregulin-1Receptor tyrosine kinase ErbB4Receptor familyMechanosensory pathwayBreast cancer cell lines
2012
EGFR/HER-targeted therapeutics in ovarian cancer
Wilken JA, Badri T, Cross S, Raji R, Santin AD, Schwartz P, Branscum AJ, Baron AT, Sakhitab AI, Maihle NJ. EGFR/HER-targeted therapeutics in ovarian cancer. Future Medicinal Chemistry 2012, 4: 447-469. PMID: 22416774, PMCID: PMC4620931, DOI: 10.4155/fmc.12.11.Peer-Reviewed Original ResearchConceptsEpithelial ovarian cancerOvarian cancerHuman epidermal growth factor receptor (HER) familyEpidermal growth factor receptor familyGrowth factor receptor familyTreatment modalitiesFactor receptor familyClinical developmentDiverse malignanciesEGFR/Clinical settingUS FDACancerNew drugsReceptor familyPatientsMalignancyTherapeuticsTreatmentTyrosine kinaseSurvivalSame periodCarcinomaMajor roleEtiology
2008
ERBB3/HER3 and ERBB2/HER2 Duet in Mammary Development and Breast Cancer
Stern DF. ERBB3/HER3 and ERBB2/HER2 Duet in Mammary Development and Breast Cancer. Journal Of Mammary Gland Biology And Neoplasia 2008, 13: 215. PMID: 18454306, PMCID: PMC6590701, DOI: 10.1007/s10911-008-9083-7.Peer-Reviewed Original ResearchConceptsBreast cancerCancer etiologyErbB3/HER3Breast cancer etiologyAdditional therapeutic opportunitiesEpidermal growth factor receptor familyGrowth factor receptor familyAkt-dependent pathwayFactor receptor familyMouse modelERBB2 amplificationNeuregulin-2Neuregulin-1Therapeutic opportunitiesTherapeutic toolMammary developmentRegulation of metabolismCancerReceptor familyAggressive propertiesTherapeutic compoundsErbB2ErbB3Eventual developmentEtiology
2002
Signal Transduction Abnormalities as Therapeutic Targets
Halaban R, von Willebrand M. Signal Transduction Abnormalities as Therapeutic Targets. Current Clinical Oncology 2002, 287-323. DOI: 10.1007/978-1-59259-159-6_11.Peer-Reviewed Original ResearchGrowth factor-mediated signalingNormal melanocytesChronic myelogenous leukemiaSignal transduction targetsSpecific kinase inhibitorsCell cycle regulatorsCell cycle progressionAutonomous cell proliferationEpidermal growth factor receptor familyEffective tumor suppressorSignal transduction abnormalitiesGrowth factor receptor familyMelanoma cellsTyrosine kinase receptorsFactor receptor familyReceptor kinaseEnvironmental cuesRegulatory proteinsActive Abl kinasesCycle regulatorsCycle progressionTumor suppressorAbl kinaseKinase receptorsOncogenic mutations
2001
Tumor necrosis factor receptor-associated factors (TRAFs)
Bradley J, Pober J. Tumor necrosis factor receptor-associated factors (TRAFs). Oncogene 2001, 20: 6482-6491. PMID: 11607847, DOI: 10.1038/sj.onc.1204788.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsMeSH KeywordsAmino Acid MotifsAnimalsHumansInterleukin-1Protein BindingProtein Structure, TertiaryProteinsReceptors, Tumor Necrosis FactorSignal TransductionTNF Receptor-Associated Factor 1TNF Receptor-Associated Factor 2TNF Receptor-Associated Factor 3TNF Receptor-Associated Factor 4TNF Receptor-Associated Factor 5TNF Receptor-Associated Factor 6Transcription Factor AP-1Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsConceptsTRAF proteinsNecrosis factor receptor-associated factorReceptor-associated factorZinc finger motifsToll/interleukinTumor necrosis factor receptor familyTRAFs 2Finger motifTRAF domainAdaptor proteinCytoplasmic domainFactor receptor familyHomology regionTRAF familyRegulated fashionDownstream eventsSignal transducerCellular responsesCell deathImportant regulatorReceptor familyProteinPathological processesNF-κBDiseased tissues
1999
Erbb4 Signaling in the Mammary Gland Is Required for Lobuloalveolar Development and Stat5 Activation during Lactation
Jones F, Welte T, Fu X, Stern D. Erbb4 Signaling in the Mammary Gland Is Required for Lobuloalveolar Development and Stat5 Activation during Lactation. Journal Of Cell Biology 1999, 147: 77-88. PMID: 10508857, PMCID: PMC2164978, DOI: 10.1083/jcb.147.1.77.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell LineCell NucleusDNA-Binding ProteinsErbB ReceptorsFemaleGene Expression Regulation, DevelopmentalHumansLactationMammary Glands, AnimalMiceMice, TransgenicMilk ProteinsPhosphorylationPrecipitin TestsPregnancyReceptor, ErbB-4RNA, MessengerSequence DeletionSignal Transductionsrc Homology DomainsSTAT5 Transcription FactorTrans-ActivatorsTransgenesConceptsFunction of ErbB4Dominant-negative alleleMammary glandAlpha-lactalbumin mRNAEpidermal growth factor receptor familyBeta-casein mRNAGrowth factor receptor familyNormal mouse mammary glandMouse mammary glandSH2 domainFactor receptor familyTerminal differentiationProtein mRNAReceptor familyLobuloalveolar developmentAcidic protein mRNASitu hybridizationMammary developmentPhosphorylationErbB4MRNALobuloalveoliUnique responseExpressionImportant role
1994
Distinct developmental expression of a new avian fibroblast growth factor receptor
Marcelle C, Eichmann A, Halevy O, Bréant C, Le Douarin N. Distinct developmental expression of a new avian fibroblast growth factor receptor. Development 1994, 120: 683-694. PMID: 8162862, DOI: 10.1242/dev.120.3.683.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsBase SequenceBlotting, NorthernChick EmbryoCloning, MolecularCoturnixFibroblast Growth Factor 2GastrulaGene ExpressionIn Situ HybridizationMolecular Sequence DataMusclesPolymerase Chain ReactionReceptor Protein-Tyrosine KinasesReceptor, Fibroblast Growth Factor, Type 4Receptors, Fibroblast Growth FactorConceptsFibroblast growth factor receptorGrowth factor receptorMesoderm-derived structuresSkeletal muscle lineageFibroblast growth factor receptor (FGFR) familySatellite cellsStage-specific mannerDistinct developmental expressionFactor receptorNew memberIg-like domainsEarly myotomeGrowth factor receptor familyPattern of expressionSkeletal muscleEmbryonic RNAPrimitive streak stageLateral epiblastMuscle lineageDays of developmentFactor receptor familyPrimary transcriptEarly avian developmentAvian developmentFibroblast growth factor
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