2021
BRCA1 Protein Expression Predicts Survival in Glioblastoma Patients from an NRG Oncology RTOG Cohort
Vassilakopoulou M, Won M, Curran WJ, Souhami L, Prados MD, Langer CJ, Rimm DL, Hanna JA, Neumeister VM, Melian E, Diaz AZ, Atkins JN, Komarnicky LT, Schultz CJ, Howard SP, Zhang P, Dicker AP, Knisely JPS. BRCA1 Protein Expression Predicts Survival in Glioblastoma Patients from an NRG Oncology RTOG Cohort. Oncology 2021, 99: 580-588. PMID: 33957633, PMCID: PMC8491475, DOI: 10.1159/000516168.Peer-Reviewed Original ResearchConceptsBRCA1 protein expressionTensin homolog (PTEN) tumor suppressor geneProtein expressionTumor suppressor geneQuantitative protein analysisDNA repairGenetic profiling studiesMolecular markersSuppressor geneProtein analysisProfiling studiesBRCA1 expressionSitu hybridizationExpression levelsTumor formationCommon malignant brain tumorCancer cellsTissue microarrayGlioblastoma tumorsExpressionPre-temozolomide eraGlioblastoma patients
2017
Calcium Sensor, NCS-1, Promotes Tumor Aggressiveness and Predicts Patient Survival
Moore LM, England A, Ehrlich BE, Rimm DL. Calcium Sensor, NCS-1, Promotes Tumor Aggressiveness and Predicts Patient Survival. Molecular Cancer Research 2017, 15: 942-952. PMID: 28275088, PMCID: PMC5500411, DOI: 10.1158/1541-7786.mcr-16-0408.Peer-Reviewed Original ResearchConceptsBreast cancer cellsNCS-1Breast cancer patient cohortsNCS-1 expressionLymph node statusCancer cellsShorter survival rateIndependent breast cancer cohortsCancer patient cohortsBreast cancer cohortMB-231 breast cancer cellsPaclitaxel-induced cell deathAggressive tumor phenotypeNeuronal model systemClinical outcomesClinicopathologic featuresNeuronal calcium sensor-1Node statusPatient cohortProgesterone receptorWorse outcomesBreast cancerCalcium-binding proteinsCancer cohortEstrogen receptor
2016
Non-malignant respiratory epithelial cells preferentially proliferate from resected non-small cell lung cancer specimens cultured under conditionally reprogrammed conditions
Gao B, Huang C, Kernstine K, Pelekanou V, Kluger Y, Jiang T, Peters-Hall JR, Coquelin M, Girard L, Zhang W, Huffman K, Oliver D, Kinose F, Haura E, Teer JK, Rix U, Le AT, Aisner DL, Varella-Garcia M, Doebele RC, Covington KR, Hampton OA, Doddapaneni HV, Jayaseelan JC, Hu J, Wheeler DA, Shay JW, Rimm DL, Gazdar A, Minna JD. Non-malignant respiratory epithelial cells preferentially proliferate from resected non-small cell lung cancer specimens cultured under conditionally reprogrammed conditions. Oncotarget 2016, 5: 11114-11126. PMID: 28052041, PMCID: PMC5355251, DOI: 10.18632/oncotarget.14366.Peer-Reviewed Original ResearchMeSH KeywordsA549 CellsAdultAgedAged, 80 and overBase SequenceCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationCells, CulturedCoculture TechniquesDNA Copy Number VariationsDNA Mutational AnalysisEpithelial CellsFemaleGene Expression ProfilingGenetic Predisposition to DiseaseHumansLung NeoplasmsMaleMiddle AgedMutationRespiratory MucosaTumor Cells, CulturedConceptsNon-small cell lung cancerRespiratory epithelial cellsNon-malignant lungCell lung cancerCRC culturesLung cancerEpithelial cellsResected non-small cell lung cancerPrimary lung cancerNon-malignant samplesLung epithelial cellsRho-kinase inhibitorNon-malignant cellsPrimary NSCLCPrimary tumorDiploid patternOriginal tumorTumor specimensTumor tissueTumorsKinase inhibitorsCancerCancer cellsMRNA expression profilesSmall subpopulationOncogenic 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
2010
PMCA2 regulates apoptosis during mammary gland involution and predicts outcome in breast cancer
VanHouten J, Sullivan C, Bazinet C, Ryoo T, Camp R, Rimm DL, Chung G, Wysolmerski J. PMCA2 regulates apoptosis during mammary gland involution and predicts outcome in breast cancer. Proceedings Of The National Academy Of Sciences Of The United States Of America 2010, 107: 11405-11410. PMID: 20534448, PMCID: PMC2895115, DOI: 10.1073/pnas.0911186107.Peer-Reviewed Original ResearchConceptsPMCA2 expressionBreast cancerT47D breast cancer cellsIntracellular calcium levelsBreast cancer progressionBreast cancer cellsEpithelial cell apoptosisPoor outcomeIntracellular calciumCalcium levelsMammary gland involutionCancer progressionCell apoptosisCancer cellsMammary involutionApoptosisGland involutionCancerMammary epithelial cell apoptosisOutcomesPMCA2Triggers apoptosisApical surfaceExpressionOverexpression
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 inhibitorsChapter 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
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 region
2006
Reciprocal regulation of RhoA and RhoC characterizes the EMT and identifies RhoC as a prognostic marker of colon carcinoma
Bellovin DI, Simpson KJ, Danilov T, Maynard E, Rimm DL, Oettgen P, Mercurio AM. Reciprocal regulation of RhoA and RhoC characterizes the EMT and identifies RhoC as a prognostic marker of colon carcinoma. Oncogene 2006, 25: 6959-6967. PMID: 16715134, DOI: 10.1038/sj.onc.1209682.Peer-Reviewed Original ResearchMeSH KeywordsBiomarkers, TumorCadherinsCell Line, TumorColonic NeoplasmsEnzyme ActivationEpithelial CellsHumansImmunohistochemistryImmunoprecipitationNeoplasm InvasivenessPrognosisPromoter Regions, GeneticProto-Oncogene Protein c-ets-1Reverse Transcriptase Polymerase Chain ReactionRho GTP-Binding ProteinsRhoA GTP-Binding ProteinRhoC GTP-Binding ProteinRNA, Small InterferingTranscription, GeneticConceptsColon carcinomaRhoC expressionPrognostic markerRhoC protein expressionE-cadherinET-1 binding sitesClinical outcomesPoor outcomeColon cancer cellsColorectal tumorsET-1Colon cancerUse of shRNAMesenchymal transitionExpression correlatesCarcinomaAberrant expressionHigh expressionProtein expressionCancer cellsMesenchymal characteristicsEMTSubsequent activationReciprocal regulationCell migration
2005
β1,6-Branched Oligosaccharides Are Increased in Lymph Node Metastases and Predict Poor Outcome in Breast Carcinoma
Handerson T, Camp R, Harigopal M, Rimm D, Pawelek J. β1,6-Branched Oligosaccharides Are Increased in Lymph Node Metastases and Predict Poor Outcome in Breast Carcinoma. Clinical Cancer Research 2005, 11: 2969-2973. PMID: 15837749, DOI: 10.1158/1078-0432.ccr-04-2211.Peer-Reviewed Original ResearchConceptsLymph node metastasisPrimary tumorNode metastasisPoor outcomeBreast carcinomaNode-positive primary tumorsPatient-matched primary tumorsNode-negative tumorsBreast carcinoma metastasisPatient ageNodal metastasisTumor sizeRisk factorsNuclear gradeCarcinoma metastasisTissue microarrayBlinded observersMyeloid cellsMetastasisMultivariate analysisTumor progressionTumorsSystemic migrationCancer cellsLectin histochemistry