2019
Somatic PRKAR1A mutation in sporadic atrial myxoma with cerebral parenchymal metastases: a case report
Roque A, Kimbrough T, Traner C, Baehring JM, Huttner A, Adams J, Canosa S, Sklar J, Madri JA. Somatic PRKAR1A mutation in sporadic atrial myxoma with cerebral parenchymal metastases: a case report. Journal Of Medical Case Reports 2019, 13: 389. PMID: 31874650, PMCID: PMC6930684, DOI: 10.1186/s13256-019-2317-z.Peer-Reviewed Original ResearchMeSH KeywordsBrain NeoplasmsCarney ComplexChemoradiotherapyCyclic AMP-Dependent Protein Kinase RIalpha SubunitDopamine AgentsExome SequencingFemaleGene Expression Regulation, NeoplasticGenes, Tumor SuppressorGerm-Line MutationHeart NeoplasmsHumansIntracranial HemorrhagesMemantineMiddle AgedMyxomaTreatment OutcomeConceptsAtrial myxomaSporadic tumorsExtra-cardiac complicationsMetastatic cardiac myxomaMajority of tumorsDissemination of tumorsIntracranial hemorrhagic lesionsWhole-exome sequencingAutosomal dominant conditionConclusionsOur patientsSporadic myxomasInvasive tumor cellsParenchymal metastasesCardiac myxomaCase reportClinical behaviorHemorrhagic lesionsAneurysm formationBenign neoplasmsMyxomaSporadic lesionsVascular wallCarney complexTumorsGermline mutations
2005
Enhanced Susceptibility to Endotoxic Shock and Impaired STAT3 Signaling in CD31-Deficient Mice
Carrithers M, Tandon S, Canosa S, Michaud M, Graesser D, Madri JA. Enhanced Susceptibility to Endotoxic Shock and Impaired STAT3 Signaling in CD31-Deficient Mice. American Journal Of Pathology 2005, 166: 185-196. PMID: 15632011, PMCID: PMC1602311, DOI: 10.1016/s0002-9440(10)62243-2.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCells, CulturedDisease SusceptibilityDNA-Binding ProteinsEndothelium, VascularFemaleFlow CytometryGene Expression RegulationLipopolysaccharidesMiceMice, Inbred C57BLMice, KnockoutPlatelet Endothelial Cell Adhesion Molecule-1Pulmonary CirculationShock, SepticSpleenSTAT3 Transcription FactorTrans-ActivatorsTumor Necrosis Factor-alphaVanadatesConceptsCD31-deficient miceAcute phase responseSeptic shockEndothelial integritySerum tumor necrosis factor alphaTumor necrosis factor alphaEndothelial cellsCell adhesion molecule-1Necrosis factor alphaAdhesion molecule-1Endothelial cell adhesion molecule-1Wild-type controlsIL-6Endotoxic shockMCP-1Neutrophil transmigrationPhase responseMCP-5Factor alphaImmune stimuliVascular permeabilityInterferon gammaKnockout miceMolecule-1STAT3 Signaling
2003
Elevated glucose inhibits VEGF-A–mediated endocardial cushion formation
Enciso JM, Gratzinger D, Camenisch TD, Canosa S, Pinter E, Madri JA. Elevated glucose inhibits VEGF-A–mediated endocardial cushion formation. Journal Of Cell Biology 2003, 160: 605-615. PMID: 12591918, PMCID: PMC2173755, DOI: 10.1083/jcb.200209014.Peer-Reviewed Original ResearchMeSH KeywordsAngiogenesis Inducing AgentsAnimalsCell MovementCell SizeCells, CulturedCulture TechniquesDipeptidesEmbryo, MammalianEndocardial Cushion DefectsFemaleGlucoseHeartMaleMatrix Metalloproteinase 2MiceMorphogenesisMyocardiumPlatelet Endothelial Cell Adhesion Molecule-1Protease InhibitorsRecombinant Fusion ProteinsVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1ConceptsEpithelial-mesenchymal transformationEndocardial cushion formationPlatelet endothelial cell adhesion molecule-1Cushion formationPECAM-1-positive endothelial cellsSingle cell motilityMMP-2 expressionMorphogenesis resultsHigh glucose-induced inhibitionCell motilityEndothelial cellsBlocks invasionMatrix metalloproteinase-2 expressionEndocardial cellsExtracellular matrixLack of invasionEndothelial cell adhesion molecule-1Mesenchymal cellsMyocardial VEGFMMP-2 inductionMetalloproteinase-2 expressionVEGF-A165ExpressionGrowth factorVascular endothelial growth factor