2025
PTEN mutations impair CSF dynamics and cortical networks by dysregulating periventricular neural progenitors
DeSpenza T, Kiziltug E, Allington G, Barson D, McGee S, O’Connor D, Robert S, Mekbib K, Nanda P, Greenberg A, Singh A, Duy P, Mandino F, Zhao S, Lynn A, Reeves B, Marlier A, Getz S, Nelson-Williams C, Shimelis H, Walsh L, Zhang J, Wang W, Prina M, OuYang A, Abdulkareem A, Smith H, Shohfi J, Mehta N, Dennis E, Reduron L, Hong J, Butler W, Carter B, Deniz E, Lake E, Constable R, Sahin M, Srivastava S, Winden K, Hoffman E, Carlson M, Gunel M, Lifton R, Alper S, Jin S, Crair M, Moreno-De-Luca A, Luikart B, Kahle K. PTEN mutations impair CSF dynamics and cortical networks by dysregulating periventricular neural progenitors. Nature Neuroscience 2025, 28: 536-557. PMID: 39994410, DOI: 10.1038/s41593-024-01865-3.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCerebral CortexCerebral VentriclesCerebrospinal FluidFemaleHumansHydrocephalusMaleMiceMutationNeural Stem CellsPTEN PhosphohydrolaseThyroid Nuclear Factor 1ConceptsNeural progenitor cellsCongenital hydrocephalusCSF dynamicsIncreased CSF productionDe novo mutationsFrequent monogenic causeEverolimus treatmentCSF shuntingNonsurgical treatmentPTEN mutationsAqueductal stenosisInhibitory interneuronsVentriculomegalyProgenitor cellsChoroid plexusMonogenic causeCortical networksIncreased survivalBrain ventriclesCortical deficitsNeural progenitorsGene PTENCSF productionNkx2.1PTEN
2017
Reaching the limits of prognostication in non-small cell lung cancer: an optimized biomarker panel fails to outperform clinical parameters
Grinberg M, Djureinovic D, Brunnström H, Mattsson J, Edlund K, Hengstler J, La Fleur L, Ekman S, Koyi H, Branden E, Ståhle E, Jirström K, Tracy D, Pontén F, Botling J, Rahnenführer J, Micke P. Reaching the limits of prognostication in non-small cell lung cancer: an optimized biomarker panel fails to outperform clinical parameters. Modern Pathology 2017, 30: 964-977. PMID: 28281552, DOI: 10.1038/modpathol.2017.14.Peer-Reviewed Original ResearchMeSH KeywordsBiomarkers, TumorCarcinoma, Non-Small-Cell LungCell Adhesion Molecule-1Enhancer of Zeste Homolog 2 ProteinGlucose Transporter Type 1HumansImmunohistochemistryIntracellular Signaling Peptides and ProteinsLung NeoplasmsNuclear ProteinsPrognosisThyroid Nuclear Factor 1Tissue Array AnalysisConceptsNon-small cell lung cancerCell lung cancerNon-small cell lung cancer patientsCell lung cancer patientsLung cancer patientsLung cancerBiomarker panelClinical parametersCancer patientsPrognostic associationClinicopathological parametersClinical practicePrognostic modelSurvival predictionProtein expressionBest prognostic modelPrognostic biomarker panelBetter prognostic performanceImmunohistochemistry-based assessmentCorresponding concordance indexProtein biomarkersClinicopathological dataConcordance indexPrognostic performanceTissue microarray
2012
Loss of Shp2 in alveoli epithelia induces deregulated surfactant homeostasis, resulting in spontaneous pulmonary fibrosis
Zhang X, Zhang Y, Tao B, Teng L, Li Y, Cao R, Gui Q, Ye M, Mou X, Cheng H, Hu H, Zhou R, Wu X, Xie Q, Ning W, Lai M, Shen H, Feng G, Ke Y. Loss of Shp2 in alveoli epithelia induces deregulated surfactant homeostasis, resulting in spontaneous pulmonary fibrosis. The FASEB Journal 2012, 26: 2338-2350. PMID: 22362894, DOI: 10.1096/fj.11-200139.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsATP-Binding Cassette TransportersFibroblast Growth FactorsHomeostasisMiceMice, KnockoutNuclear ProteinsProtein Tyrosine Phosphatase, Non-Receptor Type 11Pulmonary AlveoliPulmonary FibrosisPulmonary Surfactant-Associated ProteinsPulmonary SurfactantsThyroid Nuclear Factor 1Transcription FactorsConceptsATP-binding cassette subfamily A member 3Thyroid transcription factor-1Spontaneous pulmonary fibrosisPulmonary fibrosisSurfactant homeostasisTyrosine phosphatase SHP2Expression of thyroid transcription factor-1Surfactant proteinsAlveolar epithelial apoptosisInterstitial pulmonary fibrosisPhosphatase SHP2Investigate in vivo functionsTranscription factor 1Lung branching morphogenesisEpithelial apoptosisPulmonary surfactant proteinsAlveolar epitheliaLung injuryIneffective repairLoss of Shp2Minimal inflammationAT-IIEpithelial budsAlveolar functionFibrosis
2008
Thyroid Transcription Factor 1 Is an Independent Prognostic Factor for Patients With Stage I Lung Adenocarcinoma
Anagnostou VK, Syrigos KN, Bepler G, Homer RJ, Rimm DL. Thyroid Transcription Factor 1 Is an Independent Prognostic Factor for Patients With Stage I Lung Adenocarcinoma. Journal Of Clinical Oncology 2008, 27: 271-278. PMID: 19064983, DOI: 10.1200/jco.2008.17.0043.Peer-Reviewed Original ResearchConceptsThyroid transcription factor-1Stage I lung adenocarcinomaTTF1 expressionTranscription factor 1Lung adenocarcinomaStage IIndependent lower riskMedian overall survivalProtein expressionIndependent prognostic factorPotential prognostic parametersSubgroup of patientsFactor 1Overall survivalPrognostic factorsPatient survivalPrognostic parametersPrognostic stratificationLung cancerFavorable outcomeSitu protein expressionIndependent cohortLower riskPatientsAdenocarcinoma
2001
Expression of thyroid transcription factor-1 and other markers in sclerosing hemangioma of the lung.
Illei P, Rosai J, Klimstra D. Expression of thyroid transcription factor-1 and other markers in sclerosing hemangioma of the lung. Archives Of Pathology & Laboratory Medicine 2001, 125: 1335-9. PMID: 11570910, DOI: 10.5858/2001-125-1335-eottfa.Peer-Reviewed Original ResearchConceptsThyroid transcription factor-1Sclerosing hemangiomaTranscription factor 1Tumor cellsPulmonary epitheliumThyroid transcription factor-1 positivityFactor 1Expression of thyroid transcription factor-1Pale cellsLining cellsSolid areasPulmonary sclerosing hemangiomaCell typesPan-epithelialEpithelial tumorsFocal stainingEMA stainingVascular neoplasmPapillary structuresEpithelial markersAlveolar epitheliumHemangiomaNeoplastic cellsStaining intensityTumorExpression of Thyroid Transcription Factor-1, Surfactant Proteins, Type I Cell–associated Antigen, and Clara Cell Secretory Protein in Pulmonary Hypoplasia
Zhou H, Morotti R, Profitt S, Langston C, Wert S, Whitsett J, Greco M. Expression of Thyroid Transcription Factor-1, Surfactant Proteins, Type I Cell–associated Antigen, and Clara Cell Secretory Protein in Pulmonary Hypoplasia. Pediatric And Developmental Pathology 2001, 4: 364-371. PMID: 11441338, DOI: 10.1007/s10024001-0002-9.Peer-Reviewed Original ResearchConceptsClara cell secretory proteinPulmonary hypoplasiaWeeks gestational ageTranscription factor 1Thyroid transcription factor-1Cell-associated antigensSecretory proteinsTTF-1Surfactant proteinsHomeodomain transcription factorGestational ageFactor 1Distal lung developmentProximal-distal axisEpithelial gene expressionDistal lung parenchymaNormal fetal lungTranscription factorsFinal common pathwayLung organogenesisExpression patternsGene expressionImmunolocalization patternsProteinLung parenchyma
2000
Expression of Thyroid Transcription Factor-1 in Congenital Cystic Adenomatoid Malformation of the Lung
Morotti R, Gutierrez M, Askin F, Profitt S, Wert S, Whitsett J, Greco M. Expression of Thyroid Transcription Factor-1 in Congenital Cystic Adenomatoid Malformation of the Lung. Pediatric And Developmental Pathology 2000, 3: 455-461. PMID: 10890930, DOI: 10.1007/s100240010092.Peer-Reviewed Original ResearchConceptsCongenital cystic adenomatoid malformationCCAM type 1TTF-1 expressionCystic adenomatoid malformationThyroid transcription factor-1Gestational ageTTF-1Type 1Adenomatoid malformationTranscription factor 1Fetal lungAlveolar cell markersBasal cellsEpithelial cellsWeeks gestational ageTTF-1 stainingType 4Factor 1Bronchiolar basal cellsDistal air spacesAlveolar type II cellsType I cellsEarly lung developmentType II cellsCCAM casesActivation of surfactant protein‐B transcription: Signaling through the SP‐A receptor utilizing the PI3 kinase pathway
Strayer D, Korutla L. Activation of surfactant protein‐B transcription: Signaling through the SP‐A receptor utilizing the PI3 kinase pathway. Journal Of Cellular Physiology 2000, 184: 229-238. PMID: 10867648, DOI: 10.1002/1097-4652(200008)184:2<229::aid-jcp11>3.0.co;2-x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCells, CulturedDNA-Binding ProteinsFemaleGlycoproteinsHepatocyte Nuclear Factor 3-alphaLungNuclear ProteinsPhosphatidylinositol 3-KinasesPromoter Regions, GeneticProtein IsoformsProteolipidsPulmonary Surfactant-Associated Protein APulmonary Surfactant-Associated ProteinsPulmonary SurfactantsRatsReceptors, Cell SurfaceThyroid Nuclear Factor 1Transcription FactorsTranscription, GeneticConceptsSP-B promoterSP-B transcriptionPI3-kinaseHNF-3Consensus recognition elementSurfactant proteinsPI3-kinase pathwaySP-A receptorGel shift analysisCell transcriptional activityKinase localizationCellular functionsInteraction of SPTranscription factorsCell biologyNuclear localizationPlasma membraneKinase pathwayTranscriptional activityTranscriptionProteinSpCognate receptorsPromoterType II cells
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