2016
Oncogenic 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
2009
DNA Hypermethylation of ESR1 and PGR in Breast Cancer: Pathologic and Epidemiologic Associations
Gaudet MM, Campan M, Figueroa JD, Yang XR, Lissowska J, Peplonska B, Brinton LA, Rimm DL, Laird PW, Garcia-Closas M, Sherman ME. DNA Hypermethylation of ESR1 and PGR in Breast Cancer: Pathologic and Epidemiologic Associations. Cancer Epidemiology Biomarkers & Prevention 2009, 18: 3036-3043. PMID: 19861523, PMCID: PMC2783691, DOI: 10.1158/1055-9965.epi-09-0678.Peer-Reviewed Original ResearchConceptsBreast cancerPopulation-based case-control studyBreast cancer risk factorsPromoter CLevels of ERalphaPR-negative tumorsInvasive breast cancerCancer risk factorsCase-control studyPercentage of tumorsNegative breast cancerTumor tissue coresImproved risk predictionLower ERalphaTumor characteristicsPR expressionProgesterone receptorEpidemiologic associationRisk factorsInverse associationDNA hypermethylationPR levelsMost tumorsReceptor silencingTumors
2005
Hypercalcemia of Malignancy due to Ectopic Transactivation of the Parathyroid Hormone Gene
VanHouten JN, Yu N, Rimm D, Dotto J, Arnold A, Wysolmerski JJ, Udelsman R. Hypercalcemia of Malignancy due to Ectopic Transactivation of the Parathyroid Hormone Gene. The Journal Of Clinical Endocrinology & Metabolism 2005, 91: 580-583. PMID: 16263810, DOI: 10.1210/jc.2005-2095.Peer-Reviewed Original ResearchMeSH KeywordsAgedDNA MethylationDNA, NeoplasmFatal OutcomeFemaleGene ExpressionHumansHypercalcemiaHyperparathyroidismNeuroendocrine TumorsPancreatic NeoplasmsParathyroid GlandsParathyroid Hormone-Related ProteinPromoter Regions, GeneticReverse Transcriptase Polymerase Chain ReactionTranscriptional Activation
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