2023
Assessment of the Impact of Alternative Fixatives on HER2 Detection in Breast Cancer and Gastric Cancer Tumor Specimens
Feng W, Inoue R, Kuwata T, Niikura N, Fujii S, Kumaki N, Honda K, Xu L, Goetz A, Gaule P, Cogswell J, Rimm D, McGee R. Assessment of the Impact of Alternative Fixatives on HER2 Detection in Breast Cancer and Gastric Cancer Tumor Specimens. Applied Immunohistochemistry & Molecular Morphology 2023, 31: 339-345. PMID: 37093713, PMCID: PMC10155692, DOI: 10.1097/pai.0000000000001126.Peer-Reviewed Original ResearchConceptsNeutral buffered formalinNegative percentage agreementPositive percentage agreementOverall percentage agreementBreast cancerPercentage agreementHER2 statusHuman epidermal growth factor receptor 2 (HER2) statusEpidermal growth factor receptor 2 statusTumor samplesCell linesGastric cancer tumorsGastric cancer cell linesTumor tissue samplesClinical trial sitesCancer cell linesHER2 testingTumor specimensReal-world settingTumor tissueCancer tumorsBuffered formalinSitu hybridization assaysType of fixativeCentral laboratory
2018
Patient-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
2011
Differential expression of arrestins is a predictor of breast cancer progression and survival
Michal AM, Peck AR, Tran TH, Liu C, Rimm DL, Rui H, Benovic JL. Differential expression of arrestins is a predictor of breast cancer progression and survival. Breast Cancer Research And Treatment 2011, 130: 791-807. PMID: 21318602, PMCID: PMC3156829, DOI: 10.1007/s10549-011-1374-9.Peer-Reviewed Original ResearchConceptsBreast cancer progressionBreast cancerCancer progressionArrestin2 expressionLuminal linesMyoepithelial cellsNormal human breast tissueMetastatic breast cancerLymph node metastasisPoor clinical outcomeIndependent prognostic markerPrimary breast tumorsBreast cancer cell linesG protein-coupled receptorsArrestin2 levelsPositive lymphCancer cell linesHazard ratioHuman breast tissueProtein-coupled receptorsNode metastasisClinical outcomesDuctal carcinomaTumor sizeNuclear grade
2007
High HSP90 Expression Is Associated with Decreased Survival in Breast Cancer
Pick E, Kluger Y, Giltnane JM, Moeder C, Camp RL, Rimm DL, Kluger HM. High HSP90 Expression Is Associated with Decreased Survival in Breast Cancer. Cancer Research 2007, 67: 2932-2937. PMID: 17409397, DOI: 10.1158/0008-5472.can-06-4511.Peer-Reviewed Original ResearchConceptsHigh HSP90 expressionBreast cancerHER2/neuHSP90 expressionEstrogen receptorHigh HER2/neuCell linesEarly-stage breast cancerHER2/neu expressionHuman tumorsLymph node involvementPrimary breast cancerSubset of patientsPopulation of patientsIndependent prognostic markerHigh nuclear gradeBreast cancer cell linesBreast cancer progressionCy5-conjugated antibodiesCancer cell linesNode involvementPathologic variablesPrognostic roleMultivariable analysisProspective study
2005
Using a Xenograft Model of Human Breast Cancer Metastasis to Find Genes Associated with Clinically Aggressive Disease
Kluger HM, Lev D, Kluger Y, McCarthy MM, Kiriakova G, Camp RL, Rimm DL, Price JE. Using a Xenograft Model of Human Breast Cancer Metastasis to Find Genes Associated with Clinically Aggressive Disease. Cancer Research 2005, 65: 5578-5587. PMID: 15994930, DOI: 10.1158/0008-5472.can-05-0108.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBreast NeoplasmsCell AdhesionCell Growth ProcessesCell Line, TumorDisease Models, AnimalFemaleGene Expression ProfilingHumansImmunohistochemistryMiceMice, NudeMultivariate AnalysisNeoplasm InvasivenessNeoplasm MetastasisNeoplasm TransplantationOligonucleotide Array Sequence AnalysisPredictive Value of TestsReproducibility of ResultsTissue Array AnalysisTransplantation, HeterologousConceptsBreast cancerXenograft modelHuman breast cancer metastasisLymph node involvementLymph node metastasisChemokine ligand 1Human breast cancer cell linesBreast cancer metastasisLeukocyte protease inhibitorBreast cancer cell linesBreast cancer tissuesHSP-70 expressionHeat shock protein 70Cancer cell linesShock protein 70Identification of genesNode involvementNode metastasisAggressive diseaseClinicopathologic variablesPrimary tumorPrognostic markerNovel therapiesCDNA microarray analysisCancer tissuesIntegrative 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
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
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
1995
Frequent alterations in E-cadherin and alpha- and beta-catenin expression in human breast cancer cell lines.
Pierceall W, Woodard A, Morrow J, Rimm D, Fearon E. Frequent alterations in E-cadherin and alpha- and beta-catenin expression in human breast cancer cell lines. Oncogene 1995, 11: 1319-26. PMID: 7478552.Peer-Reviewed Original ResearchMeSH KeywordsAlpha CateninBase SequenceBeta CateninBlotting, SouthernBlotting, WesternBreast NeoplasmsCadherinsCytoskeletal ProteinsFemaleGene DeletionGene ExpressionHumansMolecular Sequence DataMutationOligodeoxyribonucleotidesPolymerase Chain ReactionPolymorphism, Single-Stranded ConformationalReceptor, ErbB-2RibonucleasesTrans-ActivatorsTumor Cells, CulturedConceptsAlpha-catenin proteinE-cadherin transcriptE-cadherinE-cadherin expressionBeta-catenin expressionCell linesBreast cancer cell linesEpithelial cell-cell interactionsCancer cell linesBeta-catenin proteinCancer-derived cell linesMembrane cytoskeletal proteinsCell-cell interactionsBreast cancer-derived cell linesE-cadherin geneHuman breast cancer-derived cell linesLoss of functionTransmembrane proteinAdherens junctionsCytoskeletal matrixCadherin proteinCytoskeletal proteinsTranscript levelsFrequent alterationsSequence alterations