2024
High-throughput transcriptome profiling indicates ribosomal RNAs to be associated with resistance to immunotherapy in non-small cell lung cancer (NSCLC)
Moutafi M, Bates K, Aung T, Milian R, Xirou V, Vathiotis I, Gavrielatou N, Angelakis A, Schalper K, Salichos L, Rimm D. High-throughput transcriptome profiling indicates ribosomal RNAs to be associated with resistance to immunotherapy in non-small cell lung cancer (NSCLC). Journal For ImmunoTherapy Of Cancer 2024, 12: e009039. PMID: 38857914, PMCID: PMC11168162, DOI: 10.1136/jitc-2024-009039.Peer-Reviewed Original ResearchConceptsNon-small cell lung cancerImmune checkpoint inhibitorsProgrammed cell death protein 1Associated with OSCell lung cancerTissue microarray spotsTissue microarrayValidation cohortLung cancerNon-small cell lung cancer treated with immune checkpoint inhibitorsAssociated with resistance to immunotherapyCell death protein 1Resistance to immunotherapyAssociated with PFSProgression-free survivalSecreted frizzled-related protein 2Cox proportional-hazards model analysisCheckpoint inhibitorsImmunotherapy strategiesTumor compartmentsRetrospective cohortDiscovery cohortLong-term benefitsPatientsCD68
2019
Closed system RT-qPCR as a potential companion diagnostic test for immunotherapy outcome in metastatic melanoma
Gupta S, McCann L, Chan YGY, Lai EW, Wei W, Wong PF, Smithy JW, Weidler J, Rhees B, Bates M, Kluger HM, Rimm DL. Closed system RT-qPCR as a potential companion diagnostic test for immunotherapy outcome in metastatic melanoma. Journal For ImmunoTherapy Of Cancer 2019, 7: 254. PMID: 31533832, PMCID: PMC6751819, DOI: 10.1186/s40425-019-0731-9.Peer-Reviewed Original ResearchMeSH KeywordsAgedAntineoplastic Agents, ImmunologicalB7-H1 AntigenBiomarkers, TumorCD8 AntigensFemaleFollow-Up StudiesGene Expression ProfilingHumansInterferon Regulatory Factor-1MaleMelanomaMiddle AgedMonitoring, ImmunologicPrognosisProgrammed Cell Death 1 Ligand 2 ProteinProgression-Free SurvivalReal-Time Polymerase Chain ReactionRetrospective StudiesReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSkin NeoplasmsConceptsCompanion diagnostic testsImmunotherapy outcomesMelanoma patientsClinical benefitAnti-PD-1 therapyImmune checkpoint inhibitor therapyMRNA expressionQuantitative immunofluorescenceDiagnostic testsCheckpoint inhibitor therapyReal-time quantitative reverse transcription polymerase chain reactionMetastatic melanoma patientsQuantitative reverse transcription polymerase chain reactionReverse transcription-polymerase chain reactionTranscription-polymerase chain reactionYale Pathology archivesParaffin-embedded tissue sectionsAdjuvant settingICI therapyOS associationInhibitor therapyBaseline variablesMetastatic melanomaPredictive biomarkersPolymerase chain reaction
2016
Non-malignant respiratory epithelial cells preferentially proliferate from resected non-small cell lung cancer specimens cultured under conditionally reprogrammed conditions
Gao B, Huang C, Kernstine K, Pelekanou V, Kluger Y, Jiang T, Peters-Hall JR, Coquelin M, Girard L, Zhang W, Huffman K, Oliver D, Kinose F, Haura E, Teer JK, Rix U, Le AT, Aisner DL, Varella-Garcia M, Doebele RC, Covington KR, Hampton OA, Doddapaneni HV, Jayaseelan JC, Hu J, Wheeler DA, Shay JW, Rimm DL, Gazdar A, Minna JD. Non-malignant respiratory epithelial cells preferentially proliferate from resected non-small cell lung cancer specimens cultured under conditionally reprogrammed conditions. Oncotarget 2016, 5: 11114-11126. PMID: 28052041, PMCID: PMC5355251, DOI: 10.18632/oncotarget.14366.Peer-Reviewed Original ResearchMeSH KeywordsA549 CellsAdultAgedAged, 80 and overBase SequenceCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationCells, CulturedCoculture TechniquesDNA Copy Number VariationsDNA Mutational AnalysisEpithelial CellsFemaleGene Expression ProfilingGenetic Predisposition to DiseaseHumansLung NeoplasmsMaleMiddle AgedMutationRespiratory MucosaTumor Cells, CulturedConceptsNon-small cell lung cancerRespiratory epithelial cellsNon-malignant lungCell lung cancerCRC culturesLung cancerEpithelial cellsResected non-small cell lung cancerPrimary lung cancerNon-malignant samplesLung epithelial cellsRho-kinase inhibitorNon-malignant cellsPrimary NSCLCPrimary tumorDiploid patternOriginal tumorTumor specimensTumor tissueTumorsKinase inhibitorsCancerCancer cellsMRNA expression profilesSmall subpopulationRAS/MAPK Activation Is Associated with Reduced Tumor-Infiltrating Lymphocytes in Triple-Negative Breast Cancer: Therapeutic Cooperation Between MEK and PD-1/PD-L1 Immune Checkpoint Inhibitors
Loi S, Dushyanthen S, Beavis PA, Salgado R, Denkert C, Savas P, Combs S, Rimm DL, Giltnane JM, Estrada MV, Sánchez V, Sanders ME, Cook RS, Pilkinton MA, Mallal SA, Wang K, Miller VA, Stephens PJ, Yelensky R, Doimi FD, Gómez H, Ryzhov SV, Darcy PK, Arteaga CL, Balko JM. RAS/MAPK Activation Is Associated with Reduced Tumor-Infiltrating Lymphocytes in Triple-Negative Breast Cancer: Therapeutic Cooperation Between MEK and PD-1/PD-L1 Immune Checkpoint Inhibitors. Clinical Cancer Research 2016, 22: 1499-1509. PMID: 26515496, PMCID: PMC4794351, DOI: 10.1158/1078-0432.ccr-15-1125.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsB7-H1 AntigenBiomarkersCell Line, TumorDisease Models, AnimalDisease ProgressionFemaleGene Expression ProfilingHumansImmunomodulationImmunophenotypingLymphocytes, Tumor-InfiltratingMiceMitogen-Activated Protein KinasesMortalityPhenotypeProgrammed Cell Death 1 ReceptorProtein Kinase InhibitorsRas ProteinsSignal TransductionTranscriptomeTriple Negative Breast NeoplasmsConceptsTriple-negative breast cancerTumor-infiltrating lymphocytesImmune checkpoint inhibitorsResidual diseaseNeoadjuvant chemotherapyBreast cancerPD-L1Checkpoint inhibitorsMHC expressionMouse modelPD-1/PD-L1 immune checkpoint inhibitorsPD-L1 immune checkpoint inhibitorsPresence of TILsPD-1/PD-L1Low tumor-infiltrating lymphocytesPD-L1/PDAntitumor immune responseRAS/MAPK activationCell-surface MHC expressionMAPK activationImproved survivalImproved prognosisPredictive biomarkersClinical trialsImmune response
2015
PLEKHA5 as a Biomarker and Potential Mediator of Melanoma Brain Metastasis
Jilaveanu LB, Parisi F, Barr ML, Zito CR, Cruz-Munoz W, Kerbel RS, Rimm DL, Bosenberg MW, Halaban R, Kluger Y, Kluger HM. PLEKHA5 as a Biomarker and Potential Mediator of Melanoma Brain Metastasis. Clinical Cancer Research 2015, 21: 2138-2147. PMID: 25316811, PMCID: PMC4397107, DOI: 10.1158/1078-0432.ccr-14-0861.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overBiomarkers, TumorBrain NeoplasmsCell Line, TumorFemaleFluorescent Antibody TechniqueGene Expression ProfilingHumansImage Processing, Computer-AssistedIntracellular Signaling Peptides and ProteinsMaleMelanomaMiddle AgedNeoplasm InvasivenessTissue Array AnalysisTranscriptomeYoung AdultConceptsCell line modelsBlood-brain barrierBrain metastasesGene expression profilesGene expression profilingExpression profilingExpression profilesPLEKHA5Brain metastasis-free survivalA375P cellsQuantitative immunofluorescenceEarly brain metastasisMelanoma brain metastasesMetastasis-free survivalProfile of patientsPotential mediatorsProtein levelsMetastatic melanoma casesEarly developmentMelanoma cellsKnockdownDecrease proliferationBBB transmigrationExtracerebral sitesMetastatic sites
2014
Markers of Epithelial to Mesenchymal Transition in Association with Survival in Head and Neck Squamous Cell Carcinoma (HNSCC)
Pectasides E, Rampias T, Sasaki C, Perisanidis C, Kouloulias V, Burtness B, Zaramboukas T, Rimm D, Fountzilas G, Psyrri A. Markers of Epithelial to Mesenchymal Transition in Association with Survival in Head and Neck Squamous Cell Carcinoma (HNSCC). PLOS ONE 2014, 9: e94273. PMID: 24722213, PMCID: PMC3983114, DOI: 10.1371/journal.pone.0094273.Peer-Reviewed Original ResearchMeSH KeywordsAutomationBiomarkers, TumorCarcinoma, Squamous CellCohort StudiesEpithelial-Mesenchymal TransitionFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHead and Neck NeoplasmsHumansImage Processing, Computer-AssistedImmunohistochemistryKaplan-Meier EstimateMaleMultivariate AnalysisNeoplasm MetastasisPhenotypePrognosisProportional Hazards ModelsSquamous Cell Carcinoma of Head and NeckTreatment OutcomeConceptsProgression-free survivalSquamous cell carcinomaOverall survivalCell carcinomaE-cadherinPrimary squamous cell carcinomaNeck squamous cell carcinomaHigh-risk HNSCCKaplan-Meier analysisNovel therapeutic approachesMesenchymal transition phenotypeHigh metastatic potentialLow E-cadherinImproved OSInferior OSIndependent predictorsPoor prognosisCarcinoma prognosisClinicopathological parametersInclusion criteriaTherapeutic approachesTransition phenotypeMetastatic potentialMesenchymal transitionProtein expression analysis
2012
Gene expression array analysis to determine tissue of origin of carcinoma of unknown primary
Dolled‐Filhart M, Rimm DL. Gene expression array analysis to determine tissue of origin of carcinoma of unknown primary. Cancer Cytopathology 2012, 121: 129-135. PMID: 22927160, DOI: 10.1002/cncy.21228.Peer-Reviewed Original ResearchMeSH KeywordsBiomarkers, TumorCell LineageGene Expression ProfilingGenetic TestingHumansNeoplasms, Unknown PrimaryOligonucleotide Array Sequence AnalysisPrognosisConceptsTissue of originIn situ measurement of miR-205 in malignant melanoma tissue supports its role as a tumor suppressor microRNA
Hanna JA, Hahn L, Agarwal S, Rimm DL. In situ measurement of miR-205 in malignant melanoma tissue supports its role as a tumor suppressor microRNA. Laboratory Investigation 2012, 92: 1390-1397. PMID: 22890556, PMCID: PMC3460033, DOI: 10.1038/labinvest.2012.119.Peer-Reviewed Original ResearchMeSH KeywordsAgedAnalysis of VarianceBiomarkers, TumorCell Line, TumorFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGp100 Melanoma AntigenHumansIn Situ HybridizationMaleMelanomaMicroRNAsMiddle AgedPrognosisRetrospective StudiesReverse Transcriptase Polymerase Chain ReactionRNA, NeoplasmS100 ProteinsSkin NeoplasmsTissue Array AnalysisConceptsMiR-205 levelsMiR-205 expressionMiR-205Shorter melanoma-specific survivalMelanoma-specific survivalMalignant melanoma tissuesPrimary melanoma specimensTypes of cancerImmunofluorescent assessmentBreslow depthAggressive tumorsWorse outcomesPrimary melanomaTumor suppressor miRNADiscovery cohortMelanoma specimensMultivariate analysisMelanoma tissuesQuantitative immunofluorescenceTumorsLow expressionHuman tumorsUse of miRNAsSuppressor miRNAAQUA method
2011
Proinvasion Metastasis Drivers in Early-Stage Melanoma Are Oncogenes
Scott KL, Nogueira C, Heffernan TP, van Doorn R, Dhakal S, Hanna JA, Min C, Jaskelioff M, Xiao Y, Wu CJ, Cameron LA, Perry SR, Zeid R, Feinberg T, Kim M, Woude G, Granter SR, Bosenberg M, Chu GC, DePinho RA, Rimm DL, Chin L. Proinvasion Metastasis Drivers in Early-Stage Melanoma Are Oncogenes. Cancer Cell 2011, 20: 92-103. PMID: 21741599, PMCID: PMC3176328, DOI: 10.1016/j.ccr.2011.05.025.Peer-Reviewed Original ResearchMeSH KeywordsAcid PhosphataseAnimalsCell LineageConserved SequenceEvolution, MolecularGene Expression ProfilingGene Expression Regulation, NeoplasticGenomeHumansIsoenzymesKaplan-Meier EstimateMelanomaMiceNeoplasm InvasivenessNeoplasm MetastasisNeoplasm StagingOncogenesPhosphorylationReproducibility of ResultsSkin NeoplasmsTartrate-Resistant Acid PhosphataseTissue Array AnalysisConceptsFunctional genetic screensGenetic screenGlobal transcriptomeMetastatic potentialSuch genesGenomic evidenceExpression selectionTranscriptomic profilesHuman melanoma tissuesMetastasis driverCell invasionKey pathwaysOncogenic capabilitiesMelanoma tissuesGenesHuman melanomaHuman primary melanomasTranscriptomeMouse modelSpontaneous metastasisOncogeneEnhancerACP5PathwayInvasionTargeting Androgen Receptor in Estrogen Receptor-Negative Breast Cancer
Ni M, Chen Y, Lim E, Wimberly H, Bailey ST, Imai Y, Rimm DL, Liu XS, Brown M. Targeting Androgen Receptor in Estrogen Receptor-Negative Breast Cancer. Cancer Cell 2011, 20: 119-131. PMID: 21741601, PMCID: PMC3180861, DOI: 10.1016/j.ccr.2011.05.026.Peer-Reviewed Original ResearchMeSH KeywordsAndrogensAnilidesAnimalsBeta CateninBreast NeoplasmsCell Line, TumorCell ProliferationDihydrotestosteroneFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHepatocyte Nuclear Factor 3-alphaHumansMiceNitrilesReceptor, ErbB-2Receptors, AndrogenReceptors, EstrogenSignal TransductionTosyl CompoundsTranscriptional ActivationUp-RegulationWnt ProteinsXenograft Model Antitumor AssaysConceptsAndrogen receptorBreast cancerEstrogen receptorER-/HER2Estrogen receptor-negative breast cancerReceptor-negative breast cancerBreast cancer growthER- breast tumorsPotential therapeutic approachTumor cell growthAndrogen-regulated gene expressionEndocrine therapyER statusTherapeutic approachesAR cistromeBreast tumorsCancer growthDirect transcriptional inductionCancerHER2Ligand-dependent activationReceptorsSpecific targetingTumorsCell growth
2010
In Situ Identification of Putative Cancer Stem Cells by Multiplexing ALDH1, CD44, and Cytokeratin Identifies Breast Cancer Patients with Poor Prognosis
Neumeister V, Agarwal S, Bordeaux J, Camp RL, Rimm DL. In Situ Identification of Putative Cancer Stem Cells by Multiplexing ALDH1, CD44, and Cytokeratin Identifies Breast Cancer Patients with Poor Prognosis. American Journal Of Pathology 2010, 176: 2131-2138. PMID: 20228222, PMCID: PMC2861079, DOI: 10.2353/ajpath.2010.090712.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAldehyde DehydrogenaseAldehyde Dehydrogenase 1 FamilyBreast NeoplasmsFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansHyaluronan ReceptorsIsoenzymesKeratinsMiddle AgedNeoplastic Stem CellsPrognosisRetinal DehydrogenaseRetrospective StudiesConceptsCancer stem cellsPutative cancer stem cellsBreast cancerIdentifies high-risk patientsPresence of CSCsNode-positive patientsHigh-risk patientsBreast cancer patientsAggressive tumor behaviorParaffin-embedded breast cancer tissuesBreast cancer tissuesFlow cytometric studyStem cellsMean followNodal statusRisk patientsTumor persistenceCD44 positivityPoor prognosisPrognostic valueTumor sizeHistological gradeALDH1 positivityCancer patientsWorse outcomes
2009
Residual breast cancers after conventional therapy display mesenchymal as well as tumor-initiating features
Creighton CJ, Li X, Landis M, Dixon JM, Neumeister VM, Sjolund A, Rimm DL, Wong H, Rodriguez A, Herschkowitz JI, Fan C, Zhang X, He X, Pavlick A, Gutierrez MC, Renshaw L, Larionov AA, Faratian D, Hilsenbeck SG, Perou CM, Lewis MT, Rosen JM, Chang JC. Residual breast cancers after conventional therapy display mesenchymal as well as tumor-initiating features. Proceedings Of The National Academy Of Sciences Of The United States Of America 2009, 106: 13820-13825. PMID: 19666588, PMCID: PMC2720409, DOI: 10.1073/pnas.0905718106.Peer-Reviewed Original ResearchConceptsBreast cancerConventional treatmentHigh tumor-initiating potentialResidual breast cancerBreast cancer patientsCell surface antigen profileLong-term survivalHuman breast tumorsBreast cancer cellsTumor-initiating cellsTumor-initiating potentialEndocrine therapyGene expression signaturesCancer patientsTumor cell populationClinical significanceMolecular subtypesTherapeutic strategiesMesenchymal markersMetalloproteinase-2Breast tumorsSubpopulation of cellsAntigen profileMesenchymal featuresTumor tissueAnalysis of Drosophila Segmentation Network Identifies a JNK Pathway Factor Overexpressed in Kidney Cancer
Liu J, Ghanim M, Xue L, Brown CD, Iossifov I, Angeletti C, Hua S, Nègre N, Ludwig M, Stricker T, Al-Ahmadie HA, Tretiakova M, Camp RL, Perera-Alberto M, Rimm DL, Xu T, Rzhetsky A, White KP. Analysis of Drosophila Segmentation Network Identifies a JNK Pathway Factor Overexpressed in Kidney Cancer. Science 2009, 323: 1218-1222. PMID: 19164706, PMCID: PMC2756524, DOI: 10.1126/science.1157669.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsApoptosisCarcinoma, Renal CellCell LineCompound Eye, ArthropodDrosophila melanogasterDrosophila ProteinsEmbryo, NonmammalianFushi Tarazu Transcription FactorsGene Expression ProfilingGene Regulatory NetworksHomeodomain ProteinsHumansJanus KinasesKidneyKidney NeoplasmsMolecular Sequence DataNervous SystemNuclear ProteinsPhosphoprotein PhosphatasesPhosphorylationRepressor ProteinsSignal TransductionTranscription FactorsTranscription, GeneticConceptsTranscription factorsClear cell renal cell carcinomaCell renal cell carcinomaKey transcription factorDrosophila segmentation networkConserved roleEmbryonic segmentationDrosophila melanogasterUbiquitin E3JNK signalingDependent apoptosisSPOPRenal cell carcinomaSPOP expressionKidney cancerTumor necrosis factorNew roleDrosophilaMelanogasterPuckeredGenesSignalingOverexpressedIdentificationApoptosis
2008
A Decade of Tissue Microarrays: Progress in the Discovery and Validation of Cancer Biomarkers
Camp RL, Neumeister V, Rimm DL. A Decade of Tissue Microarrays: Progress in the Discovery and Validation of Cancer Biomarkers. Journal Of Clinical Oncology 2008, 26: 5630-5637. PMID: 18936473, DOI: 10.1200/jco.2008.17.3567.Peer-Reviewed Original Research
2007
Dr. David Rimm is interviewed by Feras Akbik.
Rimm D. Dr. David Rimm is interviewed by Feras Akbik. The Yale Journal Of Biology And Medicine 2007, 80: 183-5. PMID: 18449386, PMCID: PMC2347361.Peer-Reviewed Original ResearchMeSH KeywordsAlgorithmsBiomarkersDiagnosis, Computer-AssistedGene Expression ProfilingPathologySoftwareTissue Array AnalysisConceptsAutomated Quantitative AnalysisLack of Extracellular Signal-Regulated Kinase Mitogen-Activated Protein Kinase Signaling Shows a New Type of Melanoma
Shields JM, Thomas NE, Cregger M, Berger AJ, Leslie M, Torrice C, Hao H, Penland S, Arbiser J, Scott G, Zhou T, Bar-Eli M, Bear JE, Der CJ, Kaufmann WK, Rimm DL, Sharpless NE. Lack of Extracellular Signal-Regulated Kinase Mitogen-Activated Protein Kinase Signaling Shows a New Type of Melanoma. Cancer Research 2007, 67: 1502-1512. PMID: 17308088, DOI: 10.1158/0008-5472.can-06-3311.Peer-Reviewed Original ResearchConceptsMitogen-activated protein kinaseERK activationB-RafERK activityMitogen-Activated Protein Kinase SignalingSignal-regulated kinase kinaseN-RASERK MAPK cascadeProtein Kinase SignalingPrimary human melanocytesRNA expression profilesCell linesEpithelial-mesenchymal transformationDistinct melanoma subtypeMAPK cascadeKinase kinaseExtracellular signalsTranscriptional targetsKinase signalingProtein kinaseExpression profilesEpithelial markersMelanoma cell linesRAS/RAFPrimary human tumors
2005
Automated Quantitative Analysis (AQUA) of In Situ Protein Expression, Antibody Concentration, and Prognosis
McCabe A, Dolled-Filhart M, Camp RL, Rimm DL. Automated Quantitative Analysis (AQUA) of In Situ Protein Expression, Antibody Concentration, and Prognosis. Journal Of The National Cancer Institute 2005, 97: 1808-1815. PMID: 16368942, DOI: 10.1093/jnci/dji427.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAntibodies, NeoplasmBiomarkers, TumorCell Line, TumorConfidence IntervalsEnzyme-Linked Immunosorbent AssayFemaleFluorescent Antibody TechniqueGene Expression ProfilingGene Expression Regulation, NeoplasticHumansImmunohistochemistryMaleMiddle AgedNeoplasmsOdds RatioPredictive Value of TestsPrognosisProtein Array AnalysisReceptor, ErbB-2Receptors, EstrogenSurvival AnalysisTreatment OutcomeTumor Suppressor Protein p53ConceptsDisease-specific mortalityHigh HER2 expressionHER2 expressionAntibody concentrationsHigh expressionPoor survivalRelative riskTissue microarrayCumulative disease-specific survivalBiomarker expressionLong-term survival dataLow expressionHER2 antibodyX-tile programDisease-specific survivalLow HER2 expressionKaplan-Meier methodBreast cancer patientsExpression of HER2Higher antibody concentrationsLow antibody concentrationsConcentration of antibodyCancer patientsPatient outcomesSitu protein expressionCoexpression of β1,6-N-Acetylglucosaminyltransferase V Glycoprotein Substrates Defines Aggressive Breast Cancers with Poor Outcome
Siddiqui SF, Pawelek J, Handerson T, Lin CY, Dickson RB, Rimm DL, Camp RL. Coexpression of β1,6-N-Acetylglucosaminyltransferase V Glycoprotein Substrates Defines Aggressive Breast Cancers with Poor Outcome. Cancer Epidemiology Biomarkers & Prevention 2005, 14: 2517-2523. PMID: 16284372, DOI: 10.1158/1055-9965.epi-05-0464.Peer-Reviewed Original ResearchConceptsSubstrate proteinsEpidermal growth factor receptorGrowth factor receptorLAMP-1Glycoprotein substratesFactor receptorComplex oligosaccharide side chainsN-cadherin expressionTumor progressionOligosaccharide side chainsBeta1 integrin expressionGnT-VN-cadherinUnsupervised hierarchical clusteringN-acetylglucosaminyltransferaseMatriptaseDistinct clustersProteinProtein expressionTumor metastasisExpressionHigh expressionAggressive breast cancerLow expressionSide chainsEvaluating the Expression and Prognostic Value of TRAIL-R1 and TRAIL-R2 in Breast Cancer
McCarthy MM, Sznol M, DiVito KA, Camp RL, Rimm DL, Kluger HM. Evaluating the Expression and Prognostic Value of TRAIL-R1 and TRAIL-R2 in Breast Cancer. Clinical Cancer Research 2005, 11: 5188-5194. PMID: 16033835, DOI: 10.1158/1078-0432.ccr-05-0158.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overBreast NeoplasmsCase-Control StudiesFemaleFollow-Up StudiesGene Expression ProfilingHumansMiddle AgedMultivariate AnalysisOligonucleotide Array Sequence AnalysisPrognosisReceptors, TNF-Related Apoptosis-Inducing LigandReceptors, Tumor Necrosis FactorSurvival AnalysisConceptsEarly-stage breast cancerTRAIL-R2 expressionBreast cancerPrognostic valueTRAIL-R2TRAIL-R1Normal breast specimensTumor necrosis factor-related apoptosis-inducing ligand receptor 1Lymph node involvementSubset of patientsBreast cancer patientsIndependent prognostic markerTRAIL-R1 expressionNormal breast epitheliumTRAIL receptor expressionLigand receptor 1Apoptosis-inducing ligand receptor 1Adjuvant treatmentNode involvementNodal statusPathologic variablesTumor sizeCancer patientsClinical trialsPrognostic markerUsing a Xenograft Model of Human Breast Cancer Metastasis to Find Genes Associated with Clinically Aggressive Disease
Kluger HM, Lev D, Kluger Y, McCarthy MM, Kiriakova G, Camp RL, Rimm DL, Price JE. Using a Xenograft Model of Human Breast Cancer Metastasis to Find Genes Associated with Clinically Aggressive Disease. Cancer Research 2005, 65: 5578-5587. PMID: 15994930, DOI: 10.1158/0008-5472.can-05-0108.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBreast NeoplasmsCell AdhesionCell Growth ProcessesCell Line, TumorDisease Models, AnimalFemaleGene Expression ProfilingHumansImmunohistochemistryMiceMice, NudeMultivariate AnalysisNeoplasm InvasivenessNeoplasm MetastasisNeoplasm TransplantationOligonucleotide Array Sequence AnalysisPredictive Value of TestsReproducibility of ResultsTissue Array AnalysisTransplantation, HeterologousConceptsBreast cancerXenograft modelHuman breast cancer metastasisLymph node involvementLymph node metastasisChemokine ligand 1Human breast cancer cell linesBreast cancer metastasisLeukocyte protease inhibitorBreast cancer cell linesBreast cancer tissuesHSP-70 expressionHeat shock protein 70Cancer cell linesShock protein 70Identification of genesNode involvementNode metastasisAggressive diseaseClinicopathologic variablesPrimary tumorPrognostic markerNovel therapiesCDNA microarray analysisCancer tissues