2021
Programmed Death-Ligand 1 Tumor Proportion Score and Overall Survival From First-Line Pembrolizumab in Patients With Nonsquamous Versus Squamous NSCLC
Doroshow DB, Wei W, Gupta S, Zugazagoitia J, Robbins C, Adamson B, Rimm DL. Programmed Death-Ligand 1 Tumor Proportion Score and Overall Survival From First-Line Pembrolizumab in Patients With Nonsquamous Versus Squamous NSCLC. Journal Of Thoracic Oncology 2021, 16: 2139-2143. PMID: 34455068, PMCID: PMC8612948, DOI: 10.1016/j.jtho.2021.07.032.Peer-Reviewed Original ResearchConceptsPD-L1 tumor proportion scoreTumor proportion scoreHigh PD-L1 tumor proportion scoreOverall survivalNonsquamous histologySquamous NSCLCNonsquamous NSCLCPredictive biomarkersProportion scoreDeath ligand 1 (PD-L1) tumor proportion scoreElectronic health record-derived databaseFirst-line pembrolizumab therapyPD-1 expression levelsPD-L1 expression levelsCommunity oncology clinicsMedian OS differenceSingle-agent pembrolizumabImmune checkpoint inhibitorsImproved overall survivalMedian overall survivalPrimary end pointFirst-line pembrolizumabFirst-line therapyPD-L1 expressionPD-L1 testing
2016
Oncogenic EGFR Represses the TET1 DNA Demethylase to Induce Silencing of Tumor Suppressors in Cancer Cells
Forloni M, Gupta R, Nagarajan A, Sun LS, Dong Y, Pirazzoli V, Toki M, Wurtz A, Melnick MA, Kobayashi S, Homer RJ, Rimm DL, Gettinger SJ, Politi K, Dogra SK, Wajapeyee N. Oncogenic EGFR Represses the TET1 DNA Demethylase to Induce Silencing of Tumor Suppressors in Cancer Cells. Cell Reports 2016, 16: 457-471. PMID: 27346347, PMCID: PMC4945411, DOI: 10.1016/j.celrep.2016.05.087.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaAdenocarcinoma of LungAntineoplastic AgentsBrain NeoplasmsCCAAT-Enhancer-Binding ProteinsCell Line, TumorCpG IslandsDNA MethylationDrug Screening Assays, AntitumorErbB ReceptorsGene Expression Regulation, NeoplasticGene SilencingGlioblastomaHumansLung NeoplasmsMAP Kinase Signaling SystemMixed Function OxygenasesMutationOncogenesProtein Kinase InhibitorsProto-Oncogene ProteinsTranscription, GeneticTumor Suppressor ProteinsUp-RegulationConceptsOncogenic epidermal growth factor receptorMethylation-mediated transcriptional silencingEpidermal growth factor receptorTumor suppressorTranscriptional silencingActive DNA demethylationCancer cellsFamily member 1TET1 knockdownDNA demethylaseDNA demethylationTranscription factorsGrowth factor receptorEctopic expressionCytoplasmic localizationGlioblastoma tumor growthLung cancer cellsTET1 expressionFunctional roleSuppressorFactor receptorMember 1TET1SilencingLung cancer samples
2013
A Prospective, Multi-Institutional Diagnostic Trial to Determine Pathologist Accuracy in Estimation of Percentage of Malignant Cells
Viray H, Li K, Long TA, Vasalos P, Bridge JA, Jennings LJ, Halling KC, Hameed M, Rimm DL. A Prospective, Multi-Institutional Diagnostic Trial to Determine Pathologist Accuracy in Estimation of Percentage of Malignant Cells. Archives Of Pathology & Laboratory Medicine 2013, 137: 1545-9. PMID: 24168492, DOI: 10.5858/arpa.2012-0561-cp.Peer-Reviewed Original ResearchConceptsFalse-negative test resultsMalignant cellsMulti-institutional studyColon tissue specimensCriterion standardPatient careTissue specimensTumor tissueDiagnostic trialPathologists' accuracyGenetic alterationsNuclear countsPathologist estimationEstimation of percentageVisual estimationCurrent studyCellsTesting failures
2012
Quantitative Assessment of Effect of Preanalytic Cold Ischemic Time on Protein Expression in Breast Cancer Tissues
Neumeister VM, Anagnostou V, Siddiqui S, England AM, Zarrella ER, Vassilakopoulou M, Parisi F, Kluger Y, Hicks DG, Rimm DL. Quantitative Assessment of Effect of Preanalytic Cold Ischemic Time on Protein Expression in Breast Cancer Tissues. Journal Of The National Cancer Institute 2012, 104: 1815-1824. PMID: 23090068, PMCID: PMC3514166, DOI: 10.1093/jnci/djs438.Peer-Reviewed Original ResearchMeSH KeywordsA Kinase Anchor ProteinsBiomarkers, TumorBiopsy, Large-Core NeedleBreast NeoplasmsCold IschemiaConfounding Factors, EpidemiologicFalse Negative ReactionsFemaleFixativesFluorescent Antibody TechniqueFormaldehydeGene Expression Regulation, NeoplasticHumansHypoxia-Inducible Factor 1, alpha SubunitKi-67 AntigenMastectomy, SegmentalMatched-Pair AnalysisMinor Histocompatibility AntigensProspective StudiesProto-Oncogene ProteinsReceptor, ErbB-2Receptors, EstrogenReceptors, ProgesteroneResearch DesignTime FactorsConceptsCold ischemic timeIschemic timeBreast cancer tissuesEstrogen receptorCancer tissuesLoss of antigenicityBreast cancer resectionProtein expressionCore needle biopsyCompanion diagnostic testsConditions of hypoxiaFalse-negative resultsBreast cancer biomarkersCancer resectionProgesterone receptorNeedle biopsyRecent guidelinesCold ischemiaBreast cancerTissue microarrayEvidence of lossQuantitative immunofluorescenceDiagnostic testsAntigenicityAQUA method
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
Antibody 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
Automated Quantitative Analysis of HDM2 Expression in Malignant Melanoma Shows Association with Early-Stage Disease and Improved Outcome
Berger AJ, Camp RL, DiVito KA, Kluger HM, Halaban R, Rimm DL. Automated Quantitative Analysis of HDM2 Expression in Malignant Melanoma Shows Association with Early-Stage Disease and Improved Outcome. Cancer Research 2004, 64: 8767-8772. PMID: 15574789, DOI: 10.1158/0008-5472.can-04-1384.Peer-Reviewed Original ResearchConceptsMurine double minute 2Double minute 2Protein expressionMalignant melanomaMinute 2Early-stage diseaseTissue microarray cohortPotential tissue biomarkersCutaneous malignant melanomaValuable prognostic toolNormal skin samplesSkin cancer deathsMicroarray cohortAdvanced melanomaMetastatic lesionsCancer deathPrimary melanomaImproved outcomesExpression of HDM2Tissue biomarkersPrognostic toolBetter outcomesMelanoma lesionsAggressive natureMelanoma
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 outcomes