2005
Quantitative insitu cancer proteomics: molecular pathology comes of age with automated tissue microarray analysis
Dolled-Filhart MP, Rimm DL, Stroobant P. Quantitative insitu cancer proteomics: molecular pathology comes of age with automated tissue microarray analysis. Personalized Medicine 2005, 2: 291-300. PMID: 29788575, DOI: 10.2217/17410541.2.4.291.Peer-Reviewed Original ResearchProtein expression analysisExpression analysisProtein expressionPotential future therapeutic developmentsHigh-throughput methodAutomated Quantitative AnalysisMicroarray analysisTarget discoverySitu protein expressionTissue microarray analysisFluorescence microscopyFuture therapeutic developmentMicroarrayTissue microarrayNew targetsDynamic rangeDiscovery toolMolecular pathologyTherapeutic developmentUnparalleled opportunityUnique roleMicroscope slidesTumor samplesExpressionNovel prognostic marker
2004
Macrophage Colony-Stimulating Factor-1 Receptor Expression Is Associated with Poor Outcome in Breast Cancer by Large Cohort Tissue Microarray Analysis
Kluger HM, Dolled-Filhart M, Rodov S, Kacinski BM, Camp RL, Rimm DL. Macrophage Colony-Stimulating Factor-1 Receptor Expression Is Associated with Poor Outcome in Breast Cancer by Large Cohort Tissue Microarray Analysis. Clinical Cancer Research 2004, 10: 173-177. PMID: 14734466, DOI: 10.1158/1078-0432.ccr-0699-3.Peer-Reviewed Original ResearchConceptsNode-positive patientsNode-negative patientsNode-positive casesCSF-1R expressionBreast cancerNodal statusOverall survivalPoor outcomeIpsilateral breast cancer recurrenceInvasive breast cancerNonmetastatic breast cancerPredictors of survivalNode-negative casesLarger tumor sizeSmall cohort studiesBreast cancer recurrenceCSF-1RTissue microarray analysisMacrophage colony-stimulating factor 1 receptorFactor 1 receptorTransmembrane tyrosine kinase receptorTyrosine kinase receptorsCohort studyColony-stimulating factor 1 receptorNodal involvement
2003
Tissue microarray analysis of hepatocyte growth factor/Met pathway components reveals a role for Met, matriptase, and hepatocyte growth factor activator inhibitor 1 in the progression of node-negative breast cancer.
Kang JY, Dolled-Filhart M, Ocal IT, Singh B, Lin CY, Dickson RB, Rimm DL, Camp RL. Tissue microarray analysis of hepatocyte growth factor/Met pathway components reveals a role for Met, matriptase, and hepatocyte growth factor activator inhibitor 1 in the progression of node-negative breast cancer. Cancer Research 2003, 63: 1101-5. PMID: 12615728.Peer-Reviewed Original ResearchConceptsHepatocyte growth factor activator inhibitor-1Breast carcinomaSeries of proteasesNode-negative breast cancerHigh-level expressionNode-negative breast carcinomaHGF/MET pathwayIndependent prognostic valueBreast cancer progressionPoor patient outcomesTissue microarray analysisPathway componentsMicroarray analysisExtracellular domainActivator inhibitor-1Expression of HGFOverexpression of METMet receptorHepatocyte growth factorCancer progressionMatriptasePrognostic valueBreast markersPatient followPatient outcomesTissue microarray analysis of signal transducers and activators of transcription 3 (Stat3) and phospho-Stat3 (Tyr705) in node-negative breast cancer shows nuclear localization is associated with a better prognosis.
Dolled-Filhart M, Camp RL, Kowalski DP, Smith BL, Rimm DL. Tissue microarray analysis of signal transducers and activators of transcription 3 (Stat3) and phospho-Stat3 (Tyr705) in node-negative breast cancer shows nuclear localization is associated with a better prognosis. Clinical Cancer Research 2003, 9: 594-600. PMID: 12576423.Peer-Reviewed Original ResearchMeSH KeywordsAcute-Phase ProteinsBiomarkersBreast NeoplasmsCell NucleusDNA-Binding ProteinsFemaleHumansImmunohistochemistryLymphatic MetastasisMultivariate AnalysisPhosphorylationPhosphotyrosinePrognosisProportional Hazards ModelsSTAT3 Transcription FactorSurvival AnalysisTime FactorsTrans-ActivatorsConceptsNode-negative breast cancerBreast cancerCytoplasmic expressionNuclear expressionOverall survivalReceptor stainingPrognostic markerPhospho-STAT3Breast cancer tissue microarrayEstrogen receptor stainingProgesterone receptor stainingNode-negative tumorsLarge retrospective studyIndependent prognostic markerBreast cancer specimensTissue microarray analysisCancer tissue microarrayShort-term survivalTranscription 3Breast cancer tumorsHER2 stainingBetter prognosisRetrospective studyRole of STAT3Signal transducerFrequent alterations of Smad signaling in human head and neck squamous cell carcinomas: a tissue microarray analysis.
Xie W, Bharathy S, Kim D, Haffty BG, Rimm DL, Reiss M. Frequent alterations of Smad signaling in human head and neck squamous cell carcinomas: a tissue microarray analysis. Oncology Research Featuring Preclinical And Clinical Cancer Therapeutics 2003, 14: 61-73. PMID: 14649540, DOI: 10.3727/000000003108748612.Peer-Reviewed Original ResearchConceptsNeck squamous cell carcinomaSquamous cell carcinomaCell carcinomaHNSCC specimensTGF-beta type II receptorTGF-beta/Smad signalingTissue microarray analysisTGF-beta/SmadProgression of HNSCCCell linesType II receptorHuman SCC linesDistant recurrenceTGF-beta signalingFrequent cancerCell cycle arrestPatient outcomesMetastatic spreadTissue microarrayHNSCCII receptorsSmall seriesEvidence of lossSCC linesActivation of Smad
2001
Tissue microarray analysis of beta-catenin in colorectal cancer shows nuclear phospho-beta-catenin is associated with a better prognosis.
Chung GG, Provost E, Kielhorn EP, Charette LA, Smith BL, Rimm DL. Tissue microarray analysis of beta-catenin in colorectal cancer shows nuclear phospho-beta-catenin is associated with a better prognosis. Clinical Cancer Research 2001, 7: 4013-20. PMID: 11751495.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBeta CateninCadherinsCell LineCell NucleusColorectal NeoplasmsCytoplasmCytoskeletal ProteinsDogsGene Expression Regulation, NeoplasticHumansImmunohistochemistryNeoplasm StagingOligonucleotide Array Sequence AnalysisPhosphoproteinsPrognosisProportional Hazards ModelsRecombinant ProteinsReproducibility of ResultsSurvival RateTrans-ActivatorsTransfectionTreatment OutcomeConceptsOverall survivalNuclear expressionColorectal cancerSeries of patientsColorectal cancer specimensTissue microarray analysisMajority of cancersBetter prognosisClinical outcomesClinicopathological factorsImproved survivalCancer specimensTissue microarrayImmunohistochemical analysisMembranous stainingColorectal tumorigenesisCytoplasmic stainingMultivariate analysisSignificant associationCancerAdenomatous polyposis coli (APC) geneNuclear stainingBeta-catenin overexpressionOnly stageSurvival