2020
Acquired Resistance to HER2-Targeted Therapies Creates Vulnerability to ATP Synthase Inhibition
Gale M, Li Y, Cao J, Liu ZZ, Holmbeck MA, Zhang M, Lang SM, Wu L, Do Carmo M, Gupta S, Aoshima K, DiGiovanna MP, Stern DF, Rimm DL, Shadel GS, Chen X, Yan Q. Acquired Resistance to HER2-Targeted Therapies Creates Vulnerability to ATP Synthase Inhibition. Cancer Research 2020, 80: 524-535. PMID: 31690671, PMCID: PMC7002225, DOI: 10.1158/0008-5472.can-18-3985.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic Combined Chemotherapy ProtocolsApoptosisBreast NeoplasmsCell ProliferationDrug Resistance, NeoplasmEnzyme InhibitorsFemaleHumansMiceMice, Inbred NODMice, SCIDMitochondrial Proton-Translocating ATPasesOligomycinsReceptor, ErbB-2TrastuzumabTumor Cells, CulturedXenograft Model Antitumor AssaysConceptsResistant cellsHER2-Targeted TherapyTrastuzumab-resistant tumorsNew therapeutic strategiesNovel potential targetDrug-free mediumAntibody therapySynthase inhibitionLow doseTherapeutic strategiesTrastuzumabBreast tumorsHER2TherapyAcquired ResistanceTumorsPotential targetMitochondrial respirationCellsSelective dependencyInhibitionMinimal changesNovel vulnerabilitiesATP synthase inhibitionOligomycin A
2019
Reanalysis of the NCCN PD-L1 companion diagnostic assay study for lung cancer in the context of PD-L1 expression findings in triple-negative breast cancer
Rimm DL, Han G, Taube JM, Yi ES, Bridge JA, Flieder DB, Homer R, Roden AC, Hirsch FR, Wistuba II, Pusztai L. Reanalysis of the NCCN PD-L1 companion diagnostic assay study for lung cancer in the context of PD-L1 expression findings in triple-negative breast cancer. Breast Cancer Research 2019, 21: 72. PMID: 31196152, PMCID: PMC6567382, DOI: 10.1186/s13058-019-1156-6.Peer-Reviewed Original ResearchConceptsPD-L1 expressionImmune cell PD-L1 expressionLung cancerImmune cellsTriple-negative breast cancerEasy scoring methodCompanion diagnostic testsPD-L1Immune therapyBreast cancerImmunohistochemical testsBetter outcomesLarger studyTumor cellsDiagnostic testsCancerExpression findingsCellsExpressionPoor agreementScoring methodTherapyTrials
2018
Tumor-specific MHC-II expression drives a unique pattern of resistance to immunotherapy via LAG-3/FCRL6 engagement
Johnson DB, Nixon MJ, Wang Y, Wang DY, Castellanos E, Estrada MV, Ericsson-Gonzalez PI, Cote CH, Salgado R, Sanchez V, Dean PT, Opalenik SR, Schreeder DM, Rimm DL, Kim JY, Bordeaux J, Loi S, Horn L, Sanders ME, Ferrell PB, Xu Y, Sosman JA, Davis RS, Balko JM. Tumor-specific MHC-II expression drives a unique pattern of resistance to immunotherapy via LAG-3/FCRL6 engagement. JCI Insight 2018, 3: e120360. PMID: 30568030, PMCID: PMC6338319, DOI: 10.1172/jci.insight.120360.Peer-Reviewed Original ResearchMeSH KeywordsAdaptive ImmunityAnimalsAntibodies, NeutralizingAntigens, CDBreast NeoplasmsCD4-Positive T-LymphocytesCell Line, TumorHistocompatibility Antigens Class IIHLA-DR AntigensHumansImmunotherapyKiller Cells, NaturalLigandsLymphocyte Activation Gene 3 ProteinMiceProgrammed Cell Death 1 ReceptorReceptors, Antigen, T-CellReceptors, Cell SurfaceT-LymphocytesTumor MicroenvironmentConceptsMHC-II expressionT cellsAnti-PD-1 therapyTumor cellsPD-1 pathwayTumor-intrinsic factorsPD-1-targeted immunotherapiesMHC-II receptorsDurable responsesPD-1Immune activationImmunotherapy targetPreclinical modelsLAG-3TumorsUnique patternMHCEnhanced expressionInhibitory functionAdaptive resistanceNovel inhibitory functionImmunotherapyPatientsContext-dependent mechanismsCells
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 KinasesUbiquitin-Protein LigasesUbiquitinationConceptsBreast cancerPyMT mammary tumorsTCA cycle componentsBreast cancer responseMDA-MB-231 cellsSLC1A5 expressionMammary tumorsCancer responseGlutamine dependencePositive prognosisER stressCell deathAltered metabolismTumor cellsCarrier proteinPaclitaxel responsivenessGln uptakeChemotherapyCycle componentsRegulationExpressionUbiquitinationCellsPrognosis
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
2011
A Pathway for the Control of Anoikis Sensitivity by E-Cadherin and Epithelial-to-Mesenchymal Transition
Kumar S, Park SH, Cieply B, Schupp J, Killiam E, Zhang F, Rimm DL, Frisch SM. A Pathway for the Control of Anoikis Sensitivity by E-Cadherin and Epithelial-to-Mesenchymal Transition. Molecular And Cellular Biology 2011, 31: 4036-4051. PMID: 21746881, PMCID: PMC3187352, DOI: 10.1128/mcb.01342-10.Peer-Reviewed Original ResearchConceptsRegulation of anoikisE-cadherin complexMesenchymal transitionE-cadherinAnoikis sensitivityNuclear localizationInappropriate matrixAnoikis resistanceApoptotic responseOncogenic EMTAnoikisNRAGECellular sensitivityNovel pathwayUnknown mechanismAnkyrinEpithelial cellsEMTPathwayP14ARFCellsTbx2ComplexesGenesCytoplasm
2007
Melanophages reside in hypermelanotic, aberrantly glycosylated tumor areas and predict improved outcome in primary cutaneous malignant melanoma
Handerson T, Berger A, Harigopol M, Rimm D, Nishigori C, Ueda M, Miyoshi E, Taniguchi N, Pawelek J. Melanophages reside in hypermelanotic, aberrantly glycosylated tumor areas and predict improved outcome in primary cutaneous malignant melanoma. Journal Of Cutaneous Pathology 2007, 34: 679-686. PMID: 17696914, DOI: 10.1111/j.1600-0560.2006.00681.x.Peer-Reviewed Original ResearchConceptsCutaneous malignant melanomaPrimary cutaneous malignant melanomaImproved outcomesMalignant melanomaMelanoma cellsAnti-tumor roleMelanoma tissue microarrayFollow-upWorse outcomesPatient outcomesPoor survivalTissue microarrayBetter outcomesMyeloid cellsImmune systemMelanophagesTumor areaMelanomaCancer cellsMelanoma biologyOutcomesAberrant glycosylationCell typesCellsTumor regionDefinition 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 expressionMetS
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
2002
Quantitative examination of mechanophysical tumor cell enrichment in fine‐needle aspiration specimens
Ernst LM, Rimm DL. Quantitative examination of mechanophysical tumor cell enrichment in fine‐needle aspiration specimens. Cancer 2002, 96: 275-279. PMID: 12378594, DOI: 10.1002/cncr.10746.Peer-Reviewed Original ResearchConceptsFine-needle aspirationBreast carcinomaMalignant cellsSurgical excisionHistologic sectionsDiagnostic fine needle aspirationNontumor cellsSurgical excision specimensChi-square testTumor cell enrichmentExcision specimensFNA specimensCurrent studyFNA specimenCarcinomaCDNA microarrayRepresentative slidesNonmalignant cellsThinPrep preparationsTotal cellsTissue sectionsCell enrichmentTumorsExcisionCells
1997
Of Membrane Stability and Mosaics: The Spectrin Cytoskeleton
Morrow J, Rimm D, Kennedy S, Cianci C, Sinard J, Weed S. Of Membrane Stability and Mosaics: The Spectrin Cytoskeleton. 1997, 485-540. DOI: 10.1002/cphy.cp140111.Peer-Reviewed Original ResearchNon-erythroid cellsMembrane skeletonRed cell membrane skeletonSpectrin membrane skeletonCell membrane skeletonErythrocyte membrane skeletonMembrane organizersProtein 4.1Spectrin cytoskeletonAdhesion proteinsCytoskeletal elementsSpectrin skeletonMembrane stabilityMosaic modelSpectrinProteinCellsDematinDynaminStomatinPallidinCytoskeletonAnkyrinAdducinTropomodulin
1996
Expression of a candidate cadherin in T lymphocytes.
Cepek KL, Rimm DL, Brenner MB. Expression of a candidate cadherin in T lymphocytes. Proceedings Of The National Academy Of Sciences Of The United States Of America 1996, 93: 6567-6571. PMID: 8692857, PMCID: PMC39065, DOI: 10.1073/pnas.93.13.6567.Peer-Reviewed Original ResearchConceptsCell adhesion eventsV8 protease digestionHuman T-cell leukemic cell lineT-cell leukemic cell lineCytoplasmic domainHomotypic adhesion moleculeCadherinLeukemic cell linesAdhesion eventsMolecular massProtease digestionHomotypic adhesionHeterotypic adhesionE-cadherinPeptide mapsSpeciesCell linesEpithelial cellsWider roleMucosal epithelial cellsAdhesion moleculesIntestinal intraepithelial T lymphocytesPan-cadherinCellsSolid tissues
1989
Structure-Function Studies of the Actin Filament System of Acanthamoeba
Pollard T, Magnus K, Doberstein S, Goldschmidt-Clermont P, Kaiser D, Machesky L, Maciver S, Rimm D, Wachsstock D. Structure-Function Studies of the Actin Filament System of Acanthamoeba. Springer Series In Biophysics 1989, 3: 271-279. DOI: 10.1007/978-3-642-73925-5_50.Peer-Reviewed Original ResearchRegulatory proteinsActin polymerizationEssential protein componentsActin filament systemStructure-function studiesMajor functional classesMechanism of actionActin systemAccessory proteinsProtein componentsPrimary structureFilament systemCellular levelProteinCytoplasmic matrixOverall mechanismCellsMechanismFunctional classAssemblyAcanthamoeba