2018
Amplification of Wild-type KRAS Imparts Resistance to Crizotinib in MET Exon 14 Mutant Non–Small Cell Lung Cancer
Bahcall M, Awad MM, Sholl LM, Wilson FH, Xu M, Wang S, Palakurthi S, Choi J, Ivanova E, Leonardi GC, Ulrich BC, Paweletz CP, Kirschmeier PT, Watanabe M, Baba H, Nishino M, Nagy RJ, Lanman RB, Capelletti M, Chambers ES, Redig AJ, VanderLaan PA, Costa DB, Imamura Y, Jänne P. Amplification of Wild-type KRAS Imparts Resistance to Crizotinib in MET Exon 14 Mutant Non–Small Cell Lung Cancer. Clinical Cancer Research 2018, 24: 5963-5976. PMID: 30072474, PMCID: PMC6279568, DOI: 10.1158/1078-0432.ccr-18-0876.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsCarcinoma, Non-Small-Cell LungCell Line, TumorCrizotinibDisease Models, AnimalDNA Copy Number VariationsDrug Resistance, NeoplasmExonsGene AmplificationGene Expression Regulation, NeoplasticHumansIn Situ Hybridization, FluorescenceLung NeoplasmsMiceModels, BiologicalMutationPhosphatidylinositol 3-KinasesPositron Emission Tomography Computed TomographyProtein Kinase InhibitorsProto-Oncogene Proteins c-metProto-Oncogene Proteins p21(ras)Signal TransductionXenograft Model Antitumor AssaysConceptsNon-small cell lung cancerMutant non-small cell lung cancerCell lung cancerPatient-derived cell linesCrizotinib resistanceLung cancerCell linesLong-term efficacyPI3KEGFR ligandsPI3K inhibitionCombination therapyEffective therapyMET inhibitorsSuperior efficacyPatient tumorsDrug combinationsMET inhibitionTherapeutic strategiesParental cell lineMEK inhibitionDrug resistanceRecurrent genetic eventsK inhibitionCompensatory inductionERBB Signaling Interrupted: Targeting Ligand-Induced Pathway Activation
Wilson FH, Politi K. ERBB Signaling Interrupted: Targeting Ligand-Induced Pathway Activation. Cancer Discovery 2018, 8: 676-678. PMID: 29858224, PMCID: PMC6330656, DOI: 10.1158/2159-8290.cd-18-0368.Commentaries, Editorials and LettersMeSH KeywordsAdenocarcinoma of LungCell Line, TumorHumansLigandsNeuregulin-1Receptor, ErbB-2Receptor, ErbB-3Signal Transduction
2015
A Functional Landscape of Resistance to ALK Inhibition in Lung Cancer
Wilson FH, Johannessen CM, Piccioni F, Tamayo P, Kim JW, Van Allen EM, Corsello SM, Capelletti M, Calles A, Butaney M, Sharifnia T, Gabriel SB, Mesirov JP, Hahn WC, Engelman JA, Meyerson M, Root DE, Jänne PA, Garraway LA. A Functional Landscape of Resistance to ALK Inhibition in Lung Cancer. Cancer Cell 2015, 27: 397-408. PMID: 25759024, PMCID: PMC4398996, DOI: 10.1016/j.ccell.2015.02.005.Peer-Reviewed Original ResearchConceptsFunctional genetic studiesG protein-coupled receptorsResistance driversALK inhibitionFunctional landscapeGenetic studiesLung cancer cellsALK inhibitor resistanceResistance pathwaysMechanisms of resistanceReceptor familyPKC activationPurinergic receptor familyPKC inhibitionCrizotinib-resistant ALKCancer cellsInhibitor resistanceGene signatureDependent mechanismLung cancerLung tumorsALK inhibitorsInhibitionALKMechanism
2007
An SGK1 site in WNK4 regulates Na+ channel and K+ channel activity and has implications for aldosterone signaling and K+ homeostasis
Ring AM, Leng Q, Rinehart J, Wilson FH, Kahle KT, Hebert SC, Lifton RP. An SGK1 site in WNK4 regulates Na+ channel and K+ channel activity and has implications for aldosterone signaling and K+ homeostasis. Proceedings Of The National Academy Of Sciences Of The United States Of America 2007, 104: 4025-4029. PMID: 17360471, PMCID: PMC1803763, DOI: 10.1073/pnas.0611728104.Peer-Reviewed Original ResearchConceptsIntravascular volume depletionNa-Cl cotransporterAldosterone signalingPseudohypoaldosteronism type IIVolume depletionPhysiologic responsesNaCl reabsorptionPHAII-mutant WNK4Steroid hormone aldosteroneRenal outer medullaryRenal NaCl reabsorptionFunctional stateWNK4 mutationsROMK activityHormone aldosteroneOuter medullaryHyperkalemiaSecretionKidneyWild-type WNK4ReabsorptionAldosteroneChannel activityChannel ENaCWNK4
2004
WNK kinases: molecular regulators of integrated epithelial ion transport
Kahle KT, Wilson FH, Lalioti M, Toka H, Qin H, Lifton RP. WNK kinases: molecular regulators of integrated epithelial ion transport. Current Opinion In Nephrology & Hypertension 2004, 13: 557-562. PMID: 15300163, DOI: 10.1097/00041552-200409000-00012.Peer-Reviewed Original ResearchMeSH KeywordsEpitheliumHumansIon TransportKidneyPoint MutationProtein Serine-Threonine KinasesPseudohypoaldosteronismSignal TransductionConceptsPseudohypoaldosteronism type IIWNK kinasesPotassium ion channelsChloride ion fluxIon channelsSerine-threonine kinaseCoordinated regulationDiverse epitheliaMolecular regulatorsMolecular switchKinasePotassium ion secretionDynamic regulatorGeneral roleDisease physiologyIon fluxIntegrated regulationElectrolyte homeostasisEpithelial ion transportEpithelial transportersEssential roleWNK4HomeostasisFlux pathwaysMutations
2001
Human Hypertension Caused by Mutations in WNK Kinases
Wilson F, Disse-Nicodème S, Choate K, Ishikawa K, Nelson-Williams C, Desitter I, Gunel M, Milford D, Lipkin G, Achard J, Feely M, Dussol B, Berland Y, Unwin R, Mayan H, Simon D, Farfel Z, Jeunemaitre X, Lifton R. Human Hypertension Caused by Mutations in WNK Kinases. Science 2001, 293: 1107-1112. PMID: 11498583, DOI: 10.1126/science.1062844.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceBase SequenceChromosome MappingChromosomes, Human, Pair 12Chromosomes, Human, Pair 17CytoplasmFemaleGene Expression Regulation, EnzymologicGenetic LinkageHumansHypertensionIntercellular JunctionsIntracellular Signaling Peptides and ProteinsIntronsKidney Tubules, CollectingKidney Tubules, DistalMaleMembrane ProteinsMicroscopy, FluorescenceMinor Histocompatibility AntigensMolecular Sequence DataMutationMutation, MissensePedigreePhosphoproteinsProtein Serine-Threonine KinasesPseudohypoaldosteronismSequence DeletionSignal TransductionWNK Lysine-Deficient Protein Kinase 1Zonula Occludens-1 ProteinConceptsMajor public health problemPublic health problemRenal salt reabsorptionAntihypertensive drugsHuman hypertensionUnknown causeDistal nephronKidney segmentsPseudohypoaldosteronism type IIHealth problemsSalt reabsorptionHypertensionWNK1 expressionNew targetsWNK kinasesTight junctionsType IISerine-threonine kinaseIntronic deletionWNK4WNK familyMutationsWNK1KinaseExcretion