2021
Preclinical Models for the Study of Lung Cancer Pathogenesis and Therapy Development
Arnal-Estapé A, Foggetti G, Starrett JH, Nguyen DX, Politi K. Preclinical Models for the Study of Lung Cancer Pathogenesis and Therapy Development. Cold Spring Harbor Perspectives In Medicine 2021, 11: a037820. PMID: 34518338, PMCID: PMC8634791, DOI: 10.1101/cshperspect.a037820.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsPatient-derived xenograftsPreclinical modelsLung cancer translational researchExperimental preclinical modelsLung cancer pathogenesisLung cancer cell linesNumerous preclinical modelsLung cancer subtypesLung cancer researchCancer translational researchCancer cell linesMouse modelNew therapeutic vulnerabilitiesCancer subtypesTumor progressionCancer pathogenesisTherapeutic vulnerabilitiesTranslational researchTherapy developmentCell linesCancer researchThree-dimensional culture systemCulture systemPathogenesisXenografts
2020
Tumor progression and chromatin landscape of lung cancer are regulated by the lineage factor GATA6
Arnal-Estapé A, Cai WL, Albert AE, Zhao M, Stevens LE, López-Giráldez F, Patel KD, Tyagi S, Schmitt EM, Westbrook TF, Nguyen DX. Tumor progression and chromatin landscape of lung cancer are regulated by the lineage factor GATA6. Oncogene 2020, 39: 3726-3737. PMID: 32157212, PMCID: PMC7190573, DOI: 10.1038/s41388-020-1246-z.Peer-Reviewed Original ResearchConceptsChromatin landscapeTranscription factorsBone morphogenetic protein (BMP) signalingDiverse transcriptional programsAlters chromatin accessibilityMultiple genomic lociMorphogenetic protein signalingDistal enhancer elementsSelective transcription factorsEpithelial cell typesSurfactant protein CChromatin accessibilityGenomic lociTranscriptional programsLung adenocarcinoma progressionTumor progressionEpigenetic mechanismsProtein signalingBiological functionsLUAD progressionLUAD cellsEnhancer elementsLineage dependencyTumor suppressionLung cancer cells
2019
Nestin+NG2+ Cells Form a Reserve Stem Cell Population in the Mouse Prostate
Hanoun M, Arnal-Estapé A, Maryanovich M, Zahalka AH, Bergren SK, Chua CW, Leftin A, Brodin PN, Shen MM, Guha C, Frenette PS. Nestin+NG2+ Cells Form a Reserve Stem Cell Population in the Mouse Prostate. Stem Cell Reports 2019, 12: 1201-1211. PMID: 31130357, PMCID: PMC6565923, DOI: 10.1016/j.stemcr.2019.04.019.Peer-Reviewed Original ResearchConceptsReserve stem cell populationLineage-tracing analysisStem cell populationStem cell activityProstate stem cellsEpithelial cellsBipotential capacityProstate epithelial cellsTissue maintenanceLuminal epithelial cellsMesenchymal cellsStem cellsCell populationsOrgan damageProstate organoidsNG2 expressionRegenerative capacityRare subsetMouse prostateProstate epitheliumTransgenic miceTissue graftCell activityClonal levelCellsTranscriptomic Hallmarks of Tumor Plasticity and Stromal Interactions in Brain Metastasis
Wingrove E, Liu ZZ, Patel KD, Arnal-Estapé A, Cai WL, Melnick MA, Politi K, Monteiro C, Zhu L, Valiente M, Kluger HM, Chiang VL, Nguyen DX. Transcriptomic Hallmarks of Tumor Plasticity and Stromal Interactions in Brain Metastasis. Cell Reports 2019, 27: 1277-1292.e7. PMID: 31018140, PMCID: PMC6592283, DOI: 10.1016/j.celrep.2019.03.085.Peer-Reviewed Original ResearchConceptsBrain metastasesBrain tumor microenvironmentLineage programTumor microenvironmentTumor plasticityStromal gene expressionTranscriptomic hallmarksGene expressionTranscriptional hallmarksMultiple tumor typesMolecular landscapeStromal interactionsMajor siteIntact tissueNeuroinflammatory responseSyngeneic modelPatient biopsiesTumor typesMetastasisMalignant cellsDifferent subtypesTumor cellsHallmarkTranscriptomeCells
2018
Pre-Conditioning the Airways of Mice with Bleomycin Increases the Efficiency of Orthotopic Lung Cancer Cell Engraftment.
Stevens LE, Arnal-Estapé A, Nguyen DX. Pre-Conditioning the Airways of Mice with Bleomycin Increases the Efficiency of Orthotopic Lung Cancer Cell Engraftment. Journal Of Visualized Experiments 2018 PMID: 30010648, PMCID: PMC6102009, DOI: 10.3791/56650.Peer-Reviewed Original ResearchConceptsCancer cell engraftmentAirways of miceLung cancer cellsCell engraftmentLung cancerTumor cellsTumorigenic capacityNew orthotopic modelNon-physiological sitesTumor cell injectionCancer cellsLung tumor incidenceTreatment-refractory diseaseFull clinical spectrumLung cancer subtypesLung adenocarcinoma subtypesAdditional animal modelsStrains of miceFlanks of miceRefractory diseaseThoracic malignanciesAdenocarcinoma subtypeClinical spectrumOrthotopic transplantationTumor incidenceMSK1 regulates luminal cell differentiation and metastatic dormancy in ER+ breast cancer
Gawrzak S, Rinaldi L, Gregorio S, Arenas E, Salvador F, Urosevic J, Figueras-Puig C, Rojo F, del Barco Barrantes I, Cejalvo J, Palafox M, Guiu M, Berenguer-Llergo A, Symeonidi A, Bellmunt A, Kalafatovic D, Arnal-Estapé A, Fernández E, Müllauer B, Groeneveld R, Slobodnyuk K, Stephan-Otto Attolini C, Saura C, Arribas J, Cortes J, Rovira A, Muñoz M, Lluch A, Serra V, Albanell J, Prat A, Nebreda A, Benitah S, Gomis R. MSK1 regulates luminal cell differentiation and metastatic dormancy in ER+ breast cancer. Nature Cell Biology 2018, 20: 211-221. PMID: 29358704, DOI: 10.1038/s41556-017-0021-z.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAnimalsBiomarkers, TumorBone NeoplasmsBreast NeoplasmsCell DifferentiationChromatinFemaleGATA3 Transcription FactorGene Expression Regulation, NeoplasticGenome, HumanHepatocyte Nuclear Factor 3-alphaHumansMiceMiddle AgedNeoplasm MetastasisPrognosisReceptors, EstrogenRibosomal Protein S6 Kinases, 90-kDaRNA, Small InterferingXenograft Model Antitumor AssaysConceptsER+ breast cancerLuminal cell differentiationBreast cancerMetastatic dormancyProgression of ER+ breast cancerDifferentiation of breast cancer cellsGenome-wide short hairpin RNA screenSymptomatic bone metastasesEstrogen receptor-positiveShort hairpin RNA screenMSK1 expressionBreast cancer cellsCell differentiationFOXA1 transcription factorMetastatic latencyReceptor-positiveEarly relapseBone metastasesYears of latencyBone homingStratify patientsExpression of genesMicrometastatic lesionsImprove prognosisMetastatic progression
2017
Adrenergic nerves activate an angio-metabolic switch in prostate cancer
Zahalka AH, Arnal-Estapé A, Maryanovich M, Nakahara F, Cruz CD, Finley LWS, Frenette PS. Adrenergic nerves activate an angio-metabolic switch in prostate cancer. Science 2017, 358: 321-326. PMID: 29051371, PMCID: PMC5783182, DOI: 10.1126/science.aah5072.Peer-Reviewed Original ResearchMeSH KeywordsAlkyl and Aryl TransferasesAnimalsCarrier ProteinsElectron Transport Complex IVEndothelium, VascularGene DeletionHumansMaleMembrane ProteinsMiceMitochondrial ProteinsNeovascularization, PathologicNerve FibersNorepinephrineOxidative PhosphorylationProstateProstatic NeoplasmsReceptors, Adrenergic, beta-2Signal TransductionTumor MicroenvironmentExtracellular Matrix Receptor Expression in Subtypes of Lung Adenocarcinoma Potentiates Outgrowth of Micrometastases
Stevens LE, Cheung WKC, Adua SJ, Arnal-Estapé A, Zhao M, Liu Z, Brewer K, Herbst RS, Nguyen DX. Extracellular Matrix Receptor Expression in Subtypes of Lung Adenocarcinoma Potentiates Outgrowth of Micrometastases. Cancer Research 2017, 77: 1905-1917. PMID: 28196904, PMCID: PMC5468792, DOI: 10.1158/0008-5472.can-16-1978.Peer-Reviewed Original ResearchConceptsBrain metastatic nicheRisk of relapseDistant metastasisPoor prognosisLUAD subtypesLung tumorsLung adenocarcinomaLUAD cellsMetastatic outgrowthMetastatic nicheCancer ResCancer cellsECM-mediated signalingExtracellular matrix moleculesCell survivalMolecular signaturesDifferential expressionHMMRMatrix moleculesImportant mechanismCellsRelapseAdenocarcinomaPrognosisMetastasis
2015
Fetal liver hematopoietic stem cell niches associate with portal vessels
Khan J, Mendelson A, Kunisaki Y, Birbrair A, Kou Y, Arnal-Estapé A, Pinho S, Ciero P, Nakahara F, Ma'ayan A, Bergman A, Merad M, Frenette P. Fetal liver hematopoietic stem cell niches associate with portal vessels. Science 2015, 351: 176-180. PMID: 26634440, PMCID: PMC4706788, DOI: 10.1126/science.aad0084.Peer-Reviewed Original ResearchEnhanced MAF Oncogene Expression and Breast Cancer Bone Metastasis
Pavlovic M, Arnal-Estapé A, Rojo F, Bellmunt A, Tarragona M, Guiu M, Planet E, Garcia-Albéniz X, Morales M, Urosevic J, Gawrzak S, Rovira A, Prat A, Nonell L, Lluch A, Jean-Mairet J, Coleman R, Albanell J, Gomis R. Enhanced MAF Oncogene Expression and Breast Cancer Bone Metastasis. Journal Of The National Cancer Institute 2015, 107: djv256. PMID: 26376684, PMCID: PMC4681582, DOI: 10.1093/jnci/djv256.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiomarkers, TumorBone NeoplasmsBreast NeoplasmsCell Line, TumorDNA Copy Number VariationsFemaleGene Expression Regulation, NeoplasticHeterograftsHumansImmunohistochemistryIn Situ Hybridization, FluorescenceIncidenceMiceMice, Inbred BALB COdds RatioPredictive Value of TestsPrognosisProportional Hazards ModelsProto-Oncogene Proteins c-mafUp-RegulationConceptsBreast cancer bone metastasisCopy number aberrationsCancer bone metastasisBone metastasesRisk of bone metastasisAssociated with bone metastasisBreast cancer cells in vivoPrimary breast tumorsBreast cancer patient populationCancer cells in vivoMetastasis to boneClinical follow-upBreast cancer cellsAssociated with riskCells in vivoCancer patient populationBone relapseCause-specific hazard modelBreast tumorsFollow-upMAF overexpressionMetastasisPatient populationProtein overexpressionCancer cells
2012
Epithelial-mesenchymal transition can suppress major attributes of human epithelial tumor-initiating cells
Celià-Terrassa T, Meca-Cortés Ó, Mateo F, de Paz A, Rubio N, Arnal-Estapé A, Ell B, Bermudo R, Díaz A, Guerra-Rebollo M, Lozano J, Estarás C, Ulloa C, ρlvarez-Simón D, Milà J, Vilella R, Paciucci R, Martínez-Balbás M, de Herreros A, Gomis R, Kang Y, Blanco J, Fernández P, Thomson T. Epithelial-mesenchymal transition can suppress major attributes of human epithelial tumor-initiating cells. Journal Of Clinical Investigation 2012, 122: 1849-1868. PMID: 22505459, PMCID: PMC3366719, DOI: 10.1172/jci59218.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, DifferentiationCadherinsCell Line, TumorCell MovementCell ShapeCoculture TechniquesEpithelial CellsEpithelial-Mesenchymal TransitionGene Expression ProfilingGene Regulatory NetworksHomeodomain ProteinsHumansMaleMiceMice, Inbred NODMice, SCIDNeoplasm InvasivenessNeoplasm MetastasisNeoplasm StagingNeoplasm TransplantationProstatic NeoplasmsRepressor ProteinsSnail Family Transcription FactorsSpheroids, CellularTranscription FactorsTwist-Related Protein 1Urinary Bladder NeoplasmsZinc Finger E-box-Binding Homeobox 1ConceptsEpithelial-mesenchymal transitionDistant metastasisSelf-renewalGene programTumor-initiating cellsEpithelial-mesenchymal transition programProstate cancer cellsIn vitro invasionPrimary implantation sitesHuman cellular modelsMetastatic populationBladder cancerTumor subpopulationsLocal invasionMesenchymal-likeEpithelial featuresMetastatic phenotypeNeoplastic cellsMalignant progressionImplantation sitesMesenchymal traitsEMT factorsCancer cellsMesenchymal genesIn vivo
2010
HER2 Silences Tumor Suppression in Breast Cancer Cells by Switching Expression of C/EBPβ Isoforms
Arnal-Estapé A, Tarragona M, Morales M, Guiu M, Nadal C, Massagué J, Gomis R. HER2 Silences Tumor Suppression in Breast Cancer Cells by Switching Expression of C/EBPβ Isoforms. Cancer Research 2010, 70: 9927-9936. PMID: 21098707, DOI: 10.1158/0008-5472.can-10-0869.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntineoplastic AgentsBlotting, WesternBreast NeoplasmsCCAAT-Enhancer-Binding Protein-betaCell LineCell Line, TumorCellular SenescenceGene Expression Regulation, NeoplasticHumansIn Situ Hybridization, FluorescenceMiceMice, NudePhosphorylationPromoter Regions, GeneticProtein BindingProtein BiosynthesisProtein IsoformsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mycReceptor, ErbB-2Reverse Transcriptase Polymerase Chain ReactionRNA InterferenceTransforming Growth Factor betaTrastuzumabConceptsBreast cancer cellsTumor suppressionBreast cancerOncogene-induced senescenceCancer cellsHER2-overexpressing breast cancer cellsSubtypes of breast cancerHER2 antibody trastuzumabTransforming growth factor-bBreast cancer developmentGrowth factor BTranscriptional repressor complexHER2 signalingSuppressor responseTumor progressionMammary epithelial cellsAntibody trastuzumabHER2Cancer developmentEpithelial cellsSuppressor functionSwitching expressionInterfere with activitiesMYC promoterBreast
2006
Monoclonal anti-mouse laminin antibodies: AL-1 reacts with laminin α1 chain, AL-2 with laminin β1 chain, and AL-4 with the coiled-coil domain of laminin β1 chain
Schéele S, Sasaki T, Arnal-Estapé A, Durbeej M, Ekblom P. Monoclonal anti-mouse laminin antibodies: AL-1 reacts with laminin α1 chain, AL-2 with laminin β1 chain, and AL-4 with the coiled-coil domain of laminin β1 chain. Matrix Biology 2006, 25: 301-305. PMID: 16631359, DOI: 10.1016/j.matbio.2006.03.004.Peer-Reviewed Original Research