2018
Quantitative Spatial Profiling of PD-1/PD-L1 Interaction and HLA-DR/IDO-1 Predicts Improved Outcomes of Anti–PD-1 Therapies in Metastatic Melanoma
Johnson DB, Bordeaux J, Kim J, Vaupel C, Rimm DL, Ho TH, Joseph RW, Daud AI, Conry RM, Gaughan EM, Hernandez-Aya LF, Dimou A, Funchain P, Smithy J, Witte JS, McKee SB, Ko J, Wrangle J, Dabbas B, Tangri S, Lameh J, Hall J, Markowitz J, Balko JM, Dakappagari N. Quantitative Spatial Profiling of PD-1/PD-L1 Interaction and HLA-DR/IDO-1 Predicts Improved Outcomes of Anti–PD-1 Therapies in Metastatic Melanoma. Clinical Cancer Research 2018, 24: 5250-5260. PMID: 30021908, PMCID: PMC6214750, DOI: 10.1158/1078-0432.ccr-18-0309.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAntineoplastic Agents, ImmunologicalB7-H1 AntigenBiomarkers, TumorBiopsyCell Line, TumorFemaleHLA-DR AntigensHumansImmunohistochemistryIndoleamine-Pyrrole 2,3,-DioxygenaseMaleMelanomaMiddle AgedModels, BiologicalNeoplasm MetastasisNeoplasm StagingPrognosisProgrammed Cell Death 1 ReceptorProtein BindingRetreatmentTreatment OutcomeConceptsAnti-PD-1 responseHLA-DRValidation cohortPD-1/PD-L1PD-1 blockersPD-1 monotherapyPD-L1 expressionPretreatment tumor biopsiesProgression-free survivalSubset of patientsAcademic cancer centerBiomarkers of responseIndependent validation cohortClin Cancer ResImmunosuppression mechanismsClinical responseOverall survivalPD-L1Melanoma patientsCancer CenterTreatment outcomesTumor biopsiesDiscovery cohortPatientsIndividual biomarkersPatient-derived conditionally reprogrammed cells maintain intra-tumor genetic heterogeneity
Correa BRS, Hu J, Penalva LOF, Schlegel R, Rimm DL, Galante PAF, Agarwal S. Patient-derived conditionally reprogrammed cells maintain intra-tumor genetic heterogeneity. Scientific Reports 2018, 8: 4097. PMID: 29511269, PMCID: PMC5840339, DOI: 10.1038/s41598-018-22427-1.Peer-Reviewed Original ResearchConceptsDrug target identificationNon-small cell lung cancerCancer cell biologyIntra-tumor genetic heterogeneityDrug discovery effortsMutant-allele tumor heterogeneity (MATH) scoreCell biologyWhole-exome sequencingCell heterogeneityNumber variationsPatient-derived cell culturesDiscovery effortsCR cellsCancer cell linesIntra-tumoral heterogeneityGenetic heterogeneityCell linesExome sequencingTarget identificationCell lung cancerLung cancer modelBiologyCell culturesMolecular characteristicsPrimary cultures
2013
Construction and Analysis of Multiparameter Prognostic Models for Melanoma Outcome
Rothberg BE, Rimm DL. Construction and Analysis of Multiparameter Prognostic Models for Melanoma Outcome. Methods In Molecular Biology 2013, 1102: 227-258. PMID: 24258982, PMCID: PMC3912557, DOI: 10.1007/978-1-62703-727-3_13.Peer-Reviewed Original ResearchConceptsAdjuvant regimensNegative sentinel lymph node biopsyAdverse risk-benefit ratioPrognostic modelStage II melanoma patientsSentinel lymph node biopsyConventional clinicopathologic criteriaLymph node biopsyStage II melanomaMelanoma-specific survivalWide local excisionRisk-benefit ratioKi-67 assaysTumor molecular profilesComposite prognostic indicesMost patientsNode biopsyLocal excisionMelanoma patientsPrognostic indexRisk stratificationClinicopathologic criteriaMelanoma outcomesPrognostic biomarkerIndependent cohort
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 tissueChapter 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
2008
Genomic analysis of estrogen cascade reveals histone variant H2A.Z associated with breast cancer progression
Hua S, Kallen CB, Dhar R, Baquero MT, Mason CE, Russell BA, Shah PK, Liu J, Khramtsov A, Tretiakova MS, Krausz TN, Olopade OI, Rimm DL, White KP. Genomic analysis of estrogen cascade reveals histone variant H2A.Z associated with breast cancer progression. Molecular Systems Biology 2008, 4: msb200825. PMID: 18414489, PMCID: PMC2394496, DOI: 10.1038/msb.2008.25.Peer-Reviewed Original ResearchConceptsHistone variant H2A.ZVariant H2A.ZBreast cancer progressionTranscription factor-binding sitesTranscriptional regulatory cascadeCancer progressionGenome tiling arraysWhole-genome mappingFactor-binding sitesRegulatory cascadeTiling arraysChromatin immunoprecipitationGenome mappingGenomic analysisH2A.Z levelsRNA interferenceGene targetsGene expressionEpigenetic factorsMicroarray screeningH2A.ZCell proliferationLymph node metastasisBreast cancer survivalHigh expression
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
2001
Parathyroid hormone-related protein maintains mammary epithelial fate and triggers nipple skin differentiation during embryonic breast development
Foley J, Dann P, Hong J, Cosgrove J, Dreyer B, Rimm D, Dunbar M, Philbrick W, Wysolmerski J. Parathyroid hormone-related protein maintains mammary epithelial fate and triggers nipple skin differentiation during embryonic breast development. Development 2001, 128: 513-525. PMID: 11171335, DOI: 10.1242/dev.128.4.513.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBeta CateninCell DifferentiationCell LineageCytoskeletal ProteinsDNA-Binding ProteinsEpidermal CellsEpidermisEpithelial CellsFemaleGene Expression Regulation, DevelopmentalHistocytochemistryLymphoid Enhancer-Binding Factor 1Mammary Glands, AnimalMiceMice, KnockoutMice, TransgenicModels, BiologicalNipplesParathyroid Hormone-Related ProteinProteinsReceptor, Parathyroid Hormone, Type 1Receptors, Parathyroid HormoneSignal TransductionTrans-ActivatorsTranscription FactorsTransgenesConceptsPTH/PTHrP receptorCell fateHormone-related proteinMammary epithelial cell fateMammary mesenchymeCell fate decisionsEpithelial cell fatePTHrP receptorEmbryonic mammary glandMesenchymal cellsType I PTH/PTHrP receptorEmbryonic mammary developmentMammary epithelial cellsParathyroid hormone-related proteinEpithelial cellsEpithelial fateEpidermal fateFate decisionsEpithelial morphogenesisAbsence of PTHrPMesenchymal expressionVentral epidermisProper developmentSkin differentiationCombination of loss
1999
PECAM-1 (CD31) functions as a reservoir for and a modulator of tyrosine-phosphorylated β-catenin
Ilan N, Mahooti S, Rimm D, Madri J. PECAM-1 (CD31) functions as a reservoir for and a modulator of tyrosine-phosphorylated β-catenin. Journal Of Cell Science 1999, 112: 3005-3014. PMID: 10462517, DOI: 10.1242/jcs.112.18.3005.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBeta CateninCattleCells, CulturedCytoskeletal ProteinsEndothelial Growth FactorsEndothelium, VascularGene ExpressionHumansIn Vitro TechniquesLymphokinesModels, BiologicalNeovascularization, PhysiologicPhosphorylationPlatelet Endothelial Cell Adhesion Molecule-1Protein-Tyrosine KinasesTrans-ActivatorsTransfectionTyrosineVascular Endothelial Growth Factor AVascular Endothelial Growth FactorsConceptsTyrosine phosphorylationBeta-catenin tyrosine phosphorylationBeta-catenin nuclear translocationAdherens junction formationProtein tyrosine kinasesPECAM-1 functionsTyrosine phosphorylation levelsCell-cell contactSW480 colon carcinoma cellsEndothelial cell-cell contactsCatenin functionVascular endothelial growth factorCell adhesion moleculeTranscriptional factorsPECAM-1Colon carcinoma cellsTyrosine kinaseGamma cateninMajor substrateJunctional proteinsCytoplasmic levelsPhosphorylation levelsNuclear translocationΒ-cateninCatenin