2015
Regulation of Glutamine Carrier Proteins by RNF5 Determines Breast Cancer Response to ER Stress-Inducing Chemotherapies
Jeon YJ, Khelifa S, Ratnikov B, Scott DA, Feng Y, Parisi F, Ruller C, Lau E, Kim H, Brill LM, Jiang T, Rimm DL, Cardiff RD, Mills GB, Smith JW, Osterman AL, Kluger Y, Ronai Z. Regulation of Glutamine Carrier Proteins by RNF5 Determines Breast Cancer Response to ER Stress-Inducing Chemotherapies. Cancer Cell 2015, 27: 354-369. PMID: 25759021, PMCID: PMC4356903, DOI: 10.1016/j.ccell.2015.02.006.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid Transport System AAmino Acid Transport System ASCAnimalsAntineoplastic AgentsApoptosisAutophagyBreast NeoplasmsCitric Acid CycleDNA-Binding ProteinsEndoplasmic ReticulumEndoplasmic Reticulum StressFemaleHumansMice, Inbred BALB CMice, Inbred C57BLMice, NudeMinor Histocompatibility AntigensPaclitaxelProteolysisSignal TransductionTOR Serine-Threonine KinasesUbiquitinationUbiquitin-Protein LigasesConceptsBreast cancerPyMT mammary tumorsTCA cycle componentsBreast cancer responseMDA-MB-231 cellsSLC1A5 expressionMammary tumorsCancer responseGlutamine dependencePositive prognosisER stressCell deathAltered metabolismTumor cellsCarrier proteinPaclitaxel responsivenessGln uptakeChemotherapyCycle componentsRegulationExpressionUbiquitinationCellsPrognosis
2014
Identification of proteomic biomarkers predicting prostate cancer aggressiveness and lethality despite biopsy-sampling error
Shipitsin M, Small C, Choudhury S, Giladi E, Friedlander S, Nardone J, Hussain S, Hurley AD, Ernst C, Huang YE, Chang H, Nifong TP, Rimm DL, Dunyak J, Loda M, Berman DM, Blume-Jensen P. Identification of proteomic biomarkers predicting prostate cancer aggressiveness and lethality despite biopsy-sampling error. British Journal Of Cancer 2014, 111: 1201-1212. PMID: 25032733, PMCID: PMC4453845, DOI: 10.1038/bjc.2014.396.Peer-Reviewed Original ResearchMeSH KeywordsActininAgedAlkyl and Aryl TransferasesArea Under CurveBiomarkers, TumorBiopsy, Fine-NeedleCullin ProteinsDNA-Binding ProteinsFollow-Up StudiesHSP70 Heat-Shock ProteinsHumansImage Processing, Computer-AssistedMaleMembrane ProteinsMiddle AgedMitochondrial ProteinsNeoplasm GradingNeoplasm StagingPhosphorylationProstateProstatic NeoplasmsProteomicsRibosomal Protein S6RNA-Binding Protein FUSROC CurveSelection BiasSmad2 ProteinSmad4 ProteinTissue Array AnalysisVoltage-Dependent Anion Channel 1Y-Box-Binding Protein 1ConceptsProstate cancer aggressivenessCancer aggressivenessLarge patient cohortLow Gleason gradePatient cohortTumor microarrayLethal outcomeProstatectomy samplesGleason gradeSignificant overtreatmentBiopsy interpretationProstatectomy tissuePatient samplesBiopsy testsProteomic biomarkersCancer biomarker discoveryExpert pathologistsMarker signaturesTumor heterogeneityBiomarkersAggressivenessProtein biomarkersBiomarker discoveryQuantitative proteomics approach
2013
TOP2A protein by quantitative immunofluorescence as a predictor of response to epirubicin in the neoadjuvant treatment of breast cancer
Moretti E, Desmedt C, Biagioni C, Regan MM, Oakman C, Larsimont D, Galardi F, Piccart-Gebhart M, Sotiriou C, Rimm DL, Di Leo A. TOP2A protein by quantitative immunofluorescence as a predictor of response to epirubicin in the neoadjuvant treatment of breast cancer. Future Oncology 2013, 9: 1477-1487. PMID: 24106899, DOI: 10.2217/fon.13.103.Peer-Reviewed Original ResearchConceptsPathologic complete responseBreast cancerQIF scoresQuantitative immunofluorescenceEstrogen receptor-negative breast cancerReceptor-negative breast cancerMultifactorial predictive modelKi-67 levelsPredictors of responseNegative predictive roleAnthracycline sensitivityNeoadjuvant epirubicinNeoadjuvant treatmentPretreatment biopsiesComplete responseHER2 statusPredictive biomarkersC quartilesHER2 gene statusPredictive roleTOP2A mRNAAbstractTextHost factorsTotal scoreGene status
2009
GOLPH3 modulates mTOR signalling and rapamycin sensitivity in cancer
Scott KL, Kabbarah O, Liang MC, Ivanova E, Anagnostou V, Wu J, Dhakal S, Wu M, Chen S, Feinberg T, Huang J, Saci A, Widlund HR, Fisher DE, Xiao Y, Rimm DL, Protopopov A, Wong KK, Chin L. GOLPH3 modulates mTOR signalling and rapamycin sensitivity in cancer. Nature 2009, 459: 1085-1090. PMID: 19553991, PMCID: PMC2753613, DOI: 10.1038/nature08109.Peer-Reviewed Original ResearchConceptsTarget of rapamycinTrans-Golgi networkHuman cancersGenome-wide copy number analysisCopy number analysisRetromer complexGolgi proteinsHuman cancer cellsRapamycin sensitivityNew oncogeneGOLPH3Integrative analysisPotent oncogeneGenomic profilesBiochemical dataCancer cellsFunction studiesNumber analysisYeastSolid tumor typesCell sizeOncogeneMTORRapamycinMTOR inhibitors
2008
Expression patterns and prognostic value of Bag-1 and Bcl-2 in breast cancer
Nadler Y, Camp RL, Giltnane JM, Moeder C, Rimm DL, Kluger HM, Kluger Y. Expression patterns and prognostic value of Bag-1 and Bcl-2 in breast cancer. Breast Cancer Research 2008, 10: r35. PMID: 18430249, PMCID: PMC2397537, DOI: 10.1186/bcr1998.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAntineoplastic AgentsBiomarkers, TumorBreast NeoplasmsDNA-Binding ProteinsDrug Resistance, NeoplasmFemaleFluorescent Antibody TechniqueFollow-Up StudiesGene Expression Regulation, NeoplasticHumansImmunohistochemistryKaplan-Meier EstimateLymphatic MetastasisMiddle AgedPredictive Value of TestsPrognosisProportional Hazards ModelsProtein Array AnalysisProto-Oncogene Proteins c-bcl-2Receptors, EstrogenReceptors, ProgesteroneTranscription FactorsTreatment OutcomeConceptsNode-positive subsetHER2/neuProgesterone receptorBreast cancerEstrogen receptorBcl-2 expressionBAG-1 expressionImproved survivalBcl-2Anti-apoptotic mediator Bcl-2Breast tumorsSteroid receptor positivitySubset of patientsBAG-1Antihormonal therapyFavorable prognosisReceptor positivityMultivariable analysisPathological variablesEntire cohortPrognostic valuePrognostic markerImproved outcomesLarge cohortClinical development
2005
Integrative genomic analyses identify MITF as a lineage survival oncogene amplified in malignant melanoma
Garraway LA, Widlund HR, Rubin MA, Getz G, Berger AJ, Ramaswamy S, Beroukhim R, Milner DA, Granter SR, Du J, Lee C, Wagner SN, Li C, Golub TR, Rimm DL, Meyerson ML, Fisher DE, Sellers WR. Integrative genomic analyses identify MITF as a lineage survival oncogene amplified in malignant melanoma. Nature 2005, 436: 117-122. PMID: 16001072, DOI: 10.1038/nature03664.Peer-Reviewed Original ResearchMeSH KeywordsCell Line, TumorCell LineageCell SurvivalChromosomes, Human, Pair 3Disease ProgressionDNA-Binding ProteinsGene AmplificationGene DosageGene Expression Regulation, NeoplasticGenomicsHumansIn Situ Hybridization, FluorescenceMelanomaMicrophthalmia-Associated Transcription FactorOncogenesPolymerase Chain ReactionPolymorphism, Single NucleotideTranscription FactorsConceptsMITF gene expressionDNA amplification eventsIntegrative genomic analysisLineage-survival oncogenePossible drug targetsGenomics effortsGenomic analysisGenetic dataGene expressionMelanoma formationAmplification eventsMelanoma genesDrug targetsCancer cell linesGenetic alterationsCell linesMITFMelanoma cellsHuman melanomaMalignant melanomaGenesMelanomaOncogeneExpressionCells
2003
Loss of Smad Signaling in Human Colorectal Cancer Is Associated with Advanced Disease and Poor Prognosis
Xie W, Rimm DL, Lin Y, Shih WJ, Reiss M. Loss of Smad Signaling in Human Colorectal Cancer Is Associated with Advanced Disease and Poor Prognosis. The Cancer Journal 2003, 9: 302-312. PMID: 12967141, DOI: 10.1097/00130404-200307000-00013.Peer-Reviewed Original ResearchConceptsColorectal cancerHuman colorectal cancerAdvanced diseasePoor prognosisHuman colorectal cancer specimensAdvanced stage diseasePresence of lymphLymph node metastasisColorectal cancer specimensShorter overall survivalClinical outcome informationOverall survivalNode metastasisClinical behaviorReceptor defectCancer specimensTissue microarrayAnimal studiesCancerSmad signalingOutcome informationPhosphorylated Smad2DiseaseSmad activationSmad2Tissue 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
2002
Alterations of Smad signaling in human breast carcinoma are associated with poor outcome: a tissue microarray study.
Xie W, Mertens JC, Reiss DJ, Rimm DL, Camp RL, Haffty BG, Reiss M. Alterations of Smad signaling in human breast carcinoma are associated with poor outcome: a tissue microarray study. Cancer Research 2002, 62: 497-505. PMID: 11809701.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBreast NeoplasmsCell DivisionCell LineDNA-Binding ProteinsFemaleGenes, BRCA1Genes, BRCA2Germ-Line MutationHeterozygoteHumansImmunohistochemistryKeratinocytesMammary Glands, AnimalMiceMice, Inbred BALB CPhosphorylationPregnancyPrognosisSignal TransductionSmad2 ProteinSmad3 ProteinSmad4 ProteinTrans-ActivatorsTransforming Growth Factor betaTumor Cells, CulturedConceptsHuman breast cancer cell linesBreast cancer cell linesHuman breast carcinomaBreast cancerCancer cell linesBreast carcinomaCell linesStage II breast cancerAxillary lymph node metastasisHuman breast cancer developmentHER2/neu expressionSmad signalingParticular histological subtypeProgesterone receptor expressionLymph node metastasisShorter overall survivalTGF-beta type II receptorTissue microarray studyBreast carcinoma specimensBreast cancer developmentTransgenic mouse modelHuman breast cancerHereditary breast cancerTGF-beta receptor signalingGrowth factor-beta signaling
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
Beta- and gamma-catenin mutations, but not E-cadherin inactivation, underlie T-cell factor/lymphoid enhancer factor transcriptional deregulation in gastric and pancreatic cancer.
Caca K, Kolligs FT, Ji X, Hayes M, Qian J, Yahanda A, Rimm DL, Costa J, Fearon ER. Beta- and gamma-catenin mutations, but not E-cadherin inactivation, underlie T-cell factor/lymphoid enhancer factor transcriptional deregulation in gastric and pancreatic cancer. Molecular Cancer Research 1999, 10: 369-76. PMID: 10392898.Peer-Reviewed Original ResearchMeSH KeywordsAdenomatous Polyposis Coli ProteinAmino Acid SequenceAnimalsBeta CateninCadherinsCytoskeletal ProteinsDesmoplakinsDNA-Binding ProteinsGamma CateninGene Expression Regulation, NeoplasticHMGB ProteinsHumansLymphoid Enhancer-Binding Factor 1Molecular Sequence DataMutagenesisPancreatic NeoplasmsStomach NeoplasmsTCF Transcription FactorsTrans-ActivatorsTranscription Factor 7-Like 1 ProteinTranscription FactorsTranscription, GeneticTumor Cells, CulturedConceptsPhosphorylation sitesMutant proteinsGlycogen synthase kinase 3beta phosphorylation sitesGlycogen synthase kinase-3betaFactor transcription factorsPotential phosphorylation sitesSynthase kinase-3betaTCF transcriptional activityE-cadherin inactivationNH2-terminal deletionsRole of APCImportant binding partnerSerine 28TCF transcriptionTranscriptional deregulationT-cell factorBinding partnerTranscription factorsAPC proteinKinase-3betaTranscriptional activityNH2 terminusAdenomatous polyposis coli (APC) mutationsCell adhesionPancreatic cancer lines
1997
Transcriptional defects underlie loss of E-cadherin expression in breast cancer.
Ji X, Woodard AS, Rimm DL, Fearon ER. Transcriptional defects underlie loss of E-cadherin expression in breast cancer. Molecular Cancer Research 1997, 8: 773-8. PMID: 9218871.Peer-Reviewed Original ResearchMeSH KeywordsAntimetabolites, AntineoplasticAzacitidineBreast NeoplasmsCadherinsCloning, MolecularDecitabineDNA MethylationDNA-Binding ProteinsGene Expression Regulation, NeoplasticHumansPromoter Regions, GeneticTrans-ActivatorsTranscription Factor AP-2Transcription FactorsTranscription, GeneticTumor Cells, CulturedConceptsE-cad expressionBreast cancerEpithelial cancersHuman breast cancer cell linesMost breast cancersDifferent epithelial cancersBreast cancer cell linesMajority of cancersE-cadherin expressionCancer cell linesCell adhesion moleculeProgression eventsCancerAdhesion moleculesTumor heterogeneityE-cadherinFunctional assaysCell linesSomatic mutationsE-cad geneGene expression differencesExpressionPromoter activityGene expressionReporter gene constructs