Sandra Canosa, MSc, CCRP
Molecular Biology Research AssistantCards
Contact Info
About
Titles
Molecular Biology Research Assistant
Biography
Mrs. Canosa’s scientific career encompasses more than two decades of biomedical research at Yale University and the Howard Hughes Medical Institute. She did her undergraduate studies in biology at the University of California, Santa Cruz before completing her Master’s in applied genomics at the University of Connecticut. As a research associate in the pathology labs of Yale School of Medicine, Mrs. Canosa has worked extensively with microarray expression profiling, genotyping, and DNA sequencing. In 2011, she joined the institution’s molecular diagnostics laboratory where she developed translational next generation sequencing assays and bioinformatics workflows for the Tumor Profiling Lab of the Yale Cancer Center. This work led to the laboratory's selection as a sequencing center for the NCI-MATCH clinical trial, and the creation of The Yale Clinical Molecular Pathology Laboratory, which supports clinical trials by offering custom assays for integral biomarkers, a function critical to Precision Medicine initiatives. Following the conclusion of that clinical trial, Mrs. Canosa was recruited to manage Yale Cancer Center's Clinical Research Support Laboratories in New Haven, where specimens for over 400 oncology clinical trials are processed.
Departments & Organizations
Education & Training
- MSc
- University of Connecticut, Applied Genomics (2010)
Research
Research at a Glance
Yale Co-Authors
Publications Timeline
Joseph Madri, MD/PhD
David Schoenfeld, MD, PhD
Karin Finberg, MD, PhD
Anita Huttner, MD
Bauer Sumpio, MD, PhD, FACS
Jeremy Kortmansky, MD
Publications
2023
NCI10066: a Phase 1/2 study of olaparib in combination with ramucirumab in previously treated metastatic gastric and gastroesophageal junction adenocarcinoma
Cecchini M, Cleary J, Shyr Y, Chao J, Uboha N, Cho M, Shields A, Pant S, Goff L, Spencer K, Kim E, Stein S, Kortmansky J, Canosa S, Sklar J, Swisher E, Radke M, Ivy P, Boerner S, Durecki D, Hsu C, LoRusso P, Lacy J. NCI10066: a Phase 1/2 study of olaparib in combination with ramucirumab in previously treated metastatic gastric and gastroesophageal junction adenocarcinoma. British Journal Of Cancer 2023, 130: 476-482. PMID: 38135713, PMCID: PMC10844282, DOI: 10.1038/s41416-023-02534-1.Peer-Reviewed Original ResearchCitationsAltmetric
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 ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH 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
2017
MMP-2: A modulator of neuronal precursor activity and cognitive and motor behaviors
Li Q, Michaud M, Shankar R, Canosa S, Schwartz M, Madri JA. MMP-2: A modulator of neuronal precursor activity and cognitive and motor behaviors. Behavioural Brain Research 2017, 333: 74-82. PMID: 28666838, DOI: 10.1016/j.bbr.2017.06.041.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsAnimals, NewbornCell MovementCell ProliferationCells, CulturedCognitionExploratory BehaviorGene Expression RegulationMatrix Metalloproteinase 2MiceMice, Inbred C57BLMice, KnockoutMotor ActivityNerve Tissue ProteinsNeural Stem CellsNeurogenesisOncogene Protein v-aktProliferating Cell Nuclear AntigenReceptors, CXCR4Spatial LearningConceptsNeural precursor cellsBroad substrate specificityNeurosphere formationAdherent neurospheresSecondary neurosphere formationNPC activitySubstrate specificityNPC numberCell surface moleculesZinc-containing enzymesAkt activationAbsence of MMP2Cell typesExtracellular matrixActivity assaysPrecursor cellsImportant roleNPC migrationMatrix metalloproteinase2Surface moleculesExpressionKO miceBioactive moleculesNestin expressionMMP2Analytical Validation of the Next-Generation Sequencing Assay for a Nationwide Signal-Finding Clinical Trial Molecular Analysis for Therapy Choice Clinical Trial
Lih CJ, Harrington RD, Sims DJ, Harper KN, Bouk CH, Datta V, Yau J, Singh RR, Routbort MJ, Luthra R, Patel KP, Mantha GS, Krishnamurthy S, Ronski K, Walther Z, Finberg KE, Canosa S, Robinson H, Raymond A, Le LP, McShane LM, Polley EC, Conley BA, Doroshow JH, Iafrate AJ, Sklar JL, Hamilton SR, Williams PM. Analytical Validation of the Next-Generation Sequencing Assay for a Nationwide Signal-Finding Clinical Trial Molecular Analysis for Therapy Choice Clinical Trial. Journal Of Molecular Diagnostics 2017, 19: 313-327. PMID: 28188106, PMCID: PMC5397672, DOI: 10.1016/j.jmoldx.2016.10.007.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsNext-generation sequencingNational Cancer Institute-Molecular AnalysisMultiple clinical laboratoriesParaffin-embedded clinical specimensTherapy Choice (NCI-MATCH) trialClinical Laboratory Improvement AmendmentsNext-generation sequencing assayPrecision medicine studiesStandard treatmentRefractory cancerClinical trialsBiopsy collectionClinical specimensPanel assayClinical useOverall sensitivityMedicine studiesPairwise concordanceReportable variantsCompliant useNGS assaysTrialsPrecision medicineCell linesClinical laboratories
2016
Endometrial carcinoma as the presenting malignancy in an 18-year-old patient with Li-Fraumeni syndrome
Clark M, Menderes G, Azodi M, Finberg K, Canosa S, Parkash V. Endometrial carcinoma as the presenting malignancy in an 18-year-old patient with Li-Fraumeni syndrome. Gynecologic Oncology 2016, 141: 183-184. DOI: 10.1016/j.ygyno.2016.04.473.Peer-Reviewed Original ResearchCitations
2013
Modeling the Neurovascular Niche: Unbiased Transcriptome Analysis of the Murine Subventricular Zone in Response to Hypoxic Insult
Li Q, Canosa S, Flynn K, Michaud M, Krauthammer M, Madri JA. Modeling the Neurovascular Niche: Unbiased Transcriptome Analysis of the Murine Subventricular Zone in Response to Hypoxic Insult. PLOS ONE 2013, 8: e76265. PMID: 24146847, PMCID: PMC3795763, DOI: 10.1371/journal.pone.0076265.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsConceptsSubventricular zoneRepair/recoveryChronic hypoxiaPremature infant populationMurine subventricular zoneEarly intervention approachesNeurodevelopmental handicapPremature infantsNeurovascular nicheHypoxic insultCD1 miceInfant populationMotor responsivenessCNS tissueDisease severityMRNA expressionUnbiased transcriptome analysisDifferent behavioral parametersNeural functionMouse strainsDifferential responseHypoxiaHypoxic conditionsRange of responsivenessIntervention approachesCD44 regulates vascular endothelial barrier integrity via a PECAM-1 dependent mechanism
Flynn KM, Michaud M, Canosa S, Madri JA. CD44 regulates vascular endothelial barrier integrity via a PECAM-1 dependent mechanism. Angiogenesis 2013, 16: 689-705. PMID: 23504212, DOI: 10.1007/s10456-013-9346-9.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsConceptsEndothelial cellsVascular permeabilityPlatelet endothelial cell adhesion molecule-1 expressionCell adhesion molecule-1 expressionAdhesion molecule-1 expressionDependent mechanismCD44 KO miceEndothelial cell adhesion molecule-1 expressionVascular endothelial barrier integrityLoss of CD44Molecule-1 expressionMatrix metalloprotease expressionCD44-deficient miceVascular barrier functionEndothelial junction proteinsEndothelial barrier integrityProlonged permeabilityC57BL/6 WTVasoactive challengeWT statusBarrier integrityWT counterpartsVascular integrityEvans blueBarrier functionModeling the neurovascular niche: unbiased transcriptome analysis of the murine subventricular zone in response to hypoxic insult
PLoS One. 2013 Oct 11;8(10)Peer-Reviewed Original Research
2011
GSK-3β: a signaling pathway node modulating neural stem cell and endothelial cell interactions
Li Q, Michaud M, Canosa S, Kuo A, Madri JA. GSK-3β: a signaling pathway node modulating neural stem cell and endothelial cell interactions. Angiogenesis 2011, 14: 173-185. PMID: 21253820, DOI: 10.1007/s10456-011-9201-9.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsMeSH KeywordsAminophenolsAnimalsBasic Helix-Loop-Helix Transcription FactorsBeta CateninBrainCell CommunicationCell DifferentiationCell MovementCell ProliferationEndothelial CellsEnzyme ActivationGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHypoxia-Inducible Factor 1, alpha SubunitIntercellular Signaling Peptides and ProteinsMaleMaleimidesMiceMice, Inbred C57BLNeovascularization, PhysiologicNeural Stem CellsNeurogenesisPhosphorylationPhosphoserineReceptor Cross-TalkSignal TransductionSolubilitySpecies SpecificityConceptsNeural stem cellsNotch-1 expressionHIF-1αGSK-3βSDF-1III-tubulinStem cellsPremature infant populationMicrovascular endothelial cellsGSK-3β activationCD1 levelsEndothelial cell interactionsNeurogenic areasVascular proliferationInfant populationGSK-3β inhibitorTherapeutic potentialSVZ tissueGreater angiogenesisHIF-2αMouse strainsΒ-catenin participatesEndothelial cellsReciprocal modulation
2006
PECAM-1 Affects GSK-3β-Mediated β-Catenin Phosphorylation and Degradation
Biswas P, Canosa S, Schoenfeld D, Schoenfeld J, Li P, Cheas LC, Zhang J, Cordova A, Sumpio B, Madri JA. PECAM-1 Affects GSK-3β-Mediated β-Catenin Phosphorylation and Degradation. American Journal Of Pathology 2006, 169: 314-324. PMID: 16816383, PMCID: PMC1698776, DOI: 10.2353/ajpath.2006.051112.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsMeSH KeywordsAnimalsBeta CateninBlotting, WesternCapillary PermeabilityCells, CulturedEndothelial CellsFluorescent Antibody TechniqueGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHistamineHistamine AgentsHumansMiceModels, BiologicalPhosphatidylinositol 3-KinasesPhosphorylationPlatelet Endothelial Cell Adhesion Molecule-1Proto-Oncogene Proteins c-aktReceptors, HistamineSignal TransductionConceptsAdherens junctionsSerine phosphorylationSrc homology 2 domainBeta-catenin expression levelsAdherens junction componentsSerine phosphorylation levelEndothelial cellsΒ-catenin phosphorylationPECAM-1Cell biological responsesCytoplasmic domainSHP-2Proteosomal degradationGSK-3betaDynamic regulatorJunction componentsPhosphorylation levelsPhosphorylationEndothelial cell adhesion molecule-1Expression levelsGSK-3βBiological responsesEndothelial barrier permeabilityMice exhibitCell adhesion molecule-1