2024
Neuroendocrine Differentiation in Prostate Cancer Requires ASCL1.
Rodarte K, Nir Heyman S, Guo L, Flores L, Savage T, Villarreal J, Deng S, Xu L, Shah R, Oliver T, Johnson J. Neuroendocrine Differentiation in Prostate Cancer Requires ASCL1. Cancer Research 2024, 84: 3522-3537. PMID: 39264686, PMCID: PMC11534540, DOI: 10.1158/0008-5472.can-24-1388.Peer-Reviewed Original ResearchConceptsLoss of RB1Prostate cancerAndrogen receptorEmergence of treatment resistanceGenetically engineered mouse modelsLoss of ASCL1Luminal-like tumorsNeuroendocrine prostate cancerDecreased tumor incidencePoor survival outcomesTranscription factor Ascl1In vivo modelsNE differentiationProstatic adenocarcinomaNeuroendocrine differentiationAllograft tumorsProstate organoidsSurvival outcomesLineage plasticityTreatment resistanceNE featuresTumor incidenceNE lineageProgressive cancerAggressive formASCL1 Drives Tolerance to Osimertinib in EGFR Mutant Lung Cancer in Permissive Cellular Contexts.
Hu B, Wiesehöfer M, de Miguel F, Liu Z, Chan L, Choi J, Melnick M, Arnal Estape A, Walther Z, Zhao D, Lopez-Giraldez F, Wurtz A, Cai G, Fan R, Gettinger S, Xiao A, Yan Q, Homer R, Nguyen D, Politi K. ASCL1 Drives Tolerance to Osimertinib in EGFR Mutant Lung Cancer in Permissive Cellular Contexts. Cancer Research 2024, 84: 1303-1319. PMID: 38359163, DOI: 10.1158/0008-5472.can-23-0438.Peer-Reviewed Original ResearchTyrosine kinase inhibitorsPatient-derived xenograftsEGFR mutant lung cancerMutant lung cancerPre-treatment tumorsResidual diseaseDrug toleranceLung cancerResidual tumor cells in vivoEGFR mutant lung adenocarcinomaTyrosine kinase inhibitor osimertinibEGFR tyrosine kinase inhibitorsTyrosine kinase inhibitor treatmentTumor cells in vivoMutant lung adenocarcinomaMaximal tumor regressionTranscription factor Ascl1Drug-tolerant cellsTime of maximal responseEvidence of cellsCells in vivoOsimertinib treatmentTumor regressionSingle cell transcriptional profilingTumor cells
2023
Abstract PR004: Exploring the role of ASCL1 in neuroendocrine prostate cancer
Rodarte K, Flores L, Kandagatla V, Villarreal J, Savage T, Deng S, Mu P, Shah R, Oliver T, Johnson J. Abstract PR004: Exploring the role of ASCL1 in neuroendocrine prostate cancer. Cancer Research 2023, 83: pr004-pr004. DOI: 10.1158/1538-7445.prca2023-pr004.Peer-Reviewed Original ResearchSmall cell lung carcinomaGenetically engineered mouse modelsNeuroendocrine prostate cancerSmall cell histologyCell histologyLoss of RB1Prostatic adenocarcinomaProstate cancerNeuroendocrine markersAndrogen receptorMost patientsNeuroendocrine prostate cancer tumorsNeuroendocrine lineageAdenovirus expressing Cre recombinaseLoss of ASCL1Tumor cell growth in vitroProstate tumor formationCell lung carcinomaExpressing Cre recombinaseLineage programsCell growth in vitroPoor survival outcomesProstate cancer researchSmall cell featuresTranscription factor Ascl1
2019
Targeting NOTCH activation in small cell lung cancer through LSD1 inhibition
Augert A, Eastwood E, Ibrahim A, Wu N, Grunblatt E, Basom R, Liggitt D, Eaton K, Martins R, Poirier J, Rudin C, Milletti F, Cheng W, Mack F, MacPherson D. Targeting NOTCH activation in small cell lung cancer through LSD1 inhibition. Science Signaling 2019, 12 PMID: 30723171, PMCID: PMC6530478, DOI: 10.1126/scisignal.aau2922.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBasic Helix-Loop-Helix Transcription FactorsCell Line, TumorEnzyme InhibitorsGene Expression Regulation, NeoplasticHistone DemethylasesHumansKaplan-Meier EstimateLung NeoplasmsMice, Inbred NODMice, KnockoutMice, SCIDReceptors, NotchSignal TransductionSmall Cell Lung CarcinomaTumor BurdenXenograft Model Antitumor AssaysConceptsSmall cell lung cancerCell lung cancerNonsmall cell lung cancerLung cancerNotch activationLSD1 inhibitionPatient-derived xenograft modelsLSD1 inhibitorsReactivation of NotchFirst-line standardExpression of Ascl1Durable tumor regressionTranscription factor Ascl1Notch pathway activationLineage genesKnockdown studiesNotch pathwayDownstream signalingCare treatmentPDX modelsTumor regressionTargeted therapySCLC tumorigenesisActionable mutationsXenograft model
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