2016
Copy Number Changes Are Associated with Response to Treatment with Carboplatin, Paclitaxel, and Sorafenib in Melanoma
Wilson MA, Zhao F, Khare S, Roszik J, Woodman SE, D'Andrea K, Wubbenhorst B, Rimm DL, Kirkwood JM, Kluger HM, Schuchter LM, Lee SJ, Flaherty KT, Nathanson KL. Copy Number Changes Are Associated with Response to Treatment with Carboplatin, Paclitaxel, and Sorafenib in Melanoma. Clinical Cancer Research 2016, 22: 374-382. PMID: 26307133, PMCID: PMC4821426, DOI: 10.1158/1078-0432.ccr-15-1162.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic Combined Chemotherapy ProtocolsCarboplatinDisease-Free SurvivalDNA Copy Number VariationsDNA Mutational AnalysisDouble-Blind MethodGenes, rasHumansMelanomaMutationNeoplasm StagingNiacinamidePaclitaxelPhenylurea CompoundsProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-metSorafenibTreatment OutcomeConceptsProgression-free survivalGene copy gainOverall survivalImproved progression-free survivalCopy gainImproved overall survivalGenomic alterationsCancer Genome Atlas (TCGA) datasetImproved treatment responseClinical outcomesMET amplificationV600KCCND1 amplificationTreatment responseMelanoma pathogenesisV600E mutationCurrent FDAPretreatment samplesBRAF geneTumor samplesPatientsSorafenibTherapyTumorsAtlas dataset
2009
Association of constitutively activated hepatocyte growth factor receptor (Met) with resistance to a dual EGFR/Her2 inhibitor in non-small-cell lung cancer cells
Agarwal S, Zerillo C, Kolmakova J, Christensen JG, Harris LN, Rimm DL, DiGiovanna MP, Stern DF. Association of constitutively activated hepatocyte growth factor receptor (Met) with resistance to a dual EGFR/Her2 inhibitor in non-small-cell lung cancer cells. British Journal Of Cancer 2009, 100: 941-949. PMID: 19240716, PMCID: PMC2661782, DOI: 10.1038/sj.bjc.6604937.Peer-Reviewed Original ResearchConceptsEpidermal growth factor receptorEGFR/HER2 inhibitorsNSCLC cell linesDual EGFR/HER2 inhibitorsGrowth factor receptorMET inhibitorsHER2 inhibitorsUse of EGFREGFR tyrosine kinase inhibitorsCell lung cancer cellsFactor receptorMajority of patientsTreatment of NSCLCCell lung carcinomaTyrosine kinase inhibitorsPotential therapeutic advantagesSubset of tumorsLung cancer cellsCell linesCurrent clinical useReceptor TKTumor cell growthHepatocyte growth factor receptorMaximal growth inhibitionImportant molecular targetChapter 1 The Function, Proteolytic Processing, and Histopathology of Met in Cancer
Hanna JA, Bordeaux J, Rimm DL, Agarwal S. Chapter 1 The Function, Proteolytic Processing, and Histopathology of Met in Cancer. Advances In Cancer Research 2009, 103: 1-23. PMID: 19854350, DOI: 10.1016/s0065-230x(09)03001-2.Peer-Reviewed Original ResearchConceptsHepatocyte growth factorExpression of METLocalization of MetClinicopathological characteristicsMET receptor tyrosine kinaseTherapeutic targetCancer typesReceptor tyrosine kinasesCancer treatmentGrowth factorCancer cellsCell proliferationMetSProteolytic processingHistopathologyCancerTyrosine kinaseRecent studiesImproper regulationNuclear localizationAntibodies
2007
Definition of a direct extracellular interaction between Met and E‐cadherin
Reshetnikova G, Troyanovsky S, Rimm DL. Definition of a direct extracellular interaction between Met and E‐cadherin. Cell Biology International 2007, 31: 366-373. PMID: 17336101, DOI: 10.1016/j.cellbi.2007.01.022.Peer-Reviewed Original ResearchConceptsBT-549 cellsE-cadherinCadherin-dependent cell-cell contactsHT-29 cellsE-cadherin interactsHepatocyte growth factorCell-cell adhesionCell-cell contactCross-linking studiesDirect extracellular interactionTyrosine kinase receptor expressionExtracellular interactionsMolecular mechanismsExtracellular domainIntracellular compartmentsPhysical interactionCellular presentationFirst evidenceGrowth factorCellsBT-549HT-29ExpressionReceptor expressionMetSAntibody validation by quantitative analysis of protein expression using expression of Met in breast cancer as a model
Pozner-Moulis S, Cregger M, Camp RL, Rimm DL. Antibody validation by quantitative analysis of protein expression using expression of Met in breast cancer as a model. Laboratory Investigation 2007, 87: 251-260. PMID: 17260003, DOI: 10.1038/labinvest.3700515.Peer-Reviewed Original ResearchConceptsExpression of METPrognostic valueBreast cancerProtein expressionShorter disease-specific survivalDisease-specific survivalInvasive breast cancerHepatocyte growth factor receptorGrowth factor receptorNeck carcinomaAssessment of reproducibilityIntracellular domainTissue microarrayPotential biomarkersCell line controlAntibody validationNuclear MetCancerFactor receptorAntibodiesMetSMet receptorVariable resultsReceptorsCompartmental analysis
2006
Met, the Hepatocyte Growth Factor Receptor, Localizes to the Nucleus in Cells at Low Density
Pozner-Moulis S, Pappas DJ, Rimm DL. Met, the Hepatocyte Growth Factor Receptor, Localizes to the Nucleus in Cells at Low Density. Cancer Research 2006, 66: 7976-7982. PMID: 16912172, DOI: 10.1158/0008-5472.can-05-4335.Peer-Reviewed Original Research
2004
β‐Catenin and p53 analyses of a breast carcinoma tissue microarray
Chung GG, Zerkowski MP, Ocal IT, Dolled‐Filhart M, Kang JY, Psyrri A, Camp RL, Rimm DL. β‐Catenin and p53 analyses of a breast carcinoma tissue microarray. Cancer 2004, 100: 2084-2092. PMID: 15139049, DOI: 10.1002/cncr.20232.Peer-Reviewed Original Research
2003
Tissue microarray‐based studies of patients with lymph node negative breast carcinoma show that met expression is associated with worse outcome but is not correlated with epidermal growth factor family receptors
Ocal I, Dolled‐Filhart M, D'Aquila TG, Camp RL, Rimm DL. Tissue microarray‐based studies of patients with lymph node negative breast carcinoma show that met expression is associated with worse outcome but is not correlated with epidermal growth factor family receptors. Cancer 2003, 97: 1841-1848. PMID: 12673709, DOI: 10.1002/cncr.11335.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaBiomarkers, TumorBreast NeoplasmsCohort StudiesErbB ReceptorsFemaleGene Expression Regulation, NeoplasticHepatocyte Growth FactorHumansImmunoenzyme TechniquesKi-67 AntigenLymph NodesLymphatic MetastasisNeoplasm StagingPrognosisProto-Oncogene Proteins c-metReceptor, ErbB-2Receptors, EstrogenReceptors, Fibroblast Growth FactorReceptors, ProgesteroneSurvival RateConceptsLymph node negative breast carcinomaEpidermal growth factor receptorNode-negative breast carcinomaNegative breast carcinomaHER-2Breast carcinomaSet of patientsReceptor tyrosine kinasesGrowth factor receptorReceptor statusTumor sizeWorse outcomesEpidermal growth factor family receptorsProgesterone receptor expression levelsTissue microarray-based studyFamily receptorsHormone receptor statusFactor receptorGroup of patientsIndependent predictive valueExpression levelsReceptor expression levelsUnique staining patternStudy cohortTissue microarray technologyTissue 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 outcomes
1999
Met expression is associated with poor outcome in patients with axillary lymph node negative breast carcinoma
Camp R, Rimm E, Rimm D. Met expression is associated with poor outcome in patients with axillary lymph node negative breast carcinoma. Cancer 1999, 86: 2259-2265. PMID: 10590366, DOI: 10.1002/(sici)1097-0142(19991201)86:11<2259::aid-cncr13>3.0.co;2-2.Peer-Reviewed Original ResearchConceptsAxillary lymph node negative breast carcinomaLymph node negative breast carcinomaExpression of METNode-negative breast carcinomaNegative breast carcinomaBreast carcinomaMET expressionMetastatic diseaseRelative riskNegative invasive ductal carcinomaLow Met expressionMET-negative patientsIndependent predictive valueIndependent prognostic markerUseful prognostic indicatorInvasive ductal carcinomaStandard immunoperoxidase techniqueHigh MET expressionHepatocyte growth factorActivation of METAxillary lymphNegative patientsPatient agePrognostic factorsAggressive disease
1998
Expression of c‐met is a strong independent prognostic factor in breast carcinoma
Ghoussoub R, Dillon D, D'Aquila T, Rimm E, Fearon E, Rimm D. Expression of c‐met is a strong independent prognostic factor in breast carcinoma. Cancer 1998, 82: 1513-1520. PMID: 9554529, DOI: 10.1002/(sici)1097-0142(19980415)82:8<1513::aid-cncr13>3.0.co;2-7.Peer-Reviewed Original ResearchConceptsBreast carcinomaIndependent predictorsStrong independent prognostic factorCox proportional hazards modelGrowth factorIndependent prognostic factorLymph node statusSubset of patientsInvasive ductal carcinomaUseful prognostic markerProportional hazards modelBreast tumor specimensHepatocyte growth factorNegative patientsPrognostic factorsAggressive diseaseDuctal carcinomaNode statusPrognostic valuePrognostic markerTumor specimensHazards modelPatientsPredictive valueSurvival rate