Featured Publications
Loss of CHD1 Promotes Heterogeneous Mechanisms of Resistance to AR-Targeted Therapy via Chromatin Dysregulation
Zhang Z, Zhou C, Li X, Barnes S, Deng S, Hoover E, Chen C, Lee Y, Zhang Y, Wang C, Metang L, Wu C, Tirado C, Johnson N, Wongvipat J, Navrazhina K, Cao Z, Choi D, Huang C, Linton E, Chen X, Liang Y, Mason C, de Stanchina E, Abida W, Lujambio A, Li S, Lowe S, Mendell J, Malladi V, Sawyers C, Mu P. Loss of CHD1 Promotes Heterogeneous Mechanisms of Resistance to AR-Targeted Therapy via Chromatin Dysregulation. Cancer Cell 2020, 37: 584-598.e11. PMID: 32220301, PMCID: PMC7292228, DOI: 10.1016/j.ccell.2020.03.001.Peer-Reviewed Original ResearchMeSH KeywordsAndrogen AntagonistsAnimalsApoptosisBiomarkers, TumorCell ProliferationChromatinDNA HelicasesDNA-Binding ProteinsDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHigh-Throughput Screening AssaysHumansMaleMiceProstatic Neoplasms, Castration-ResistantReceptors, AndrogenRNA, Small InterferingTranscription FactorsTumor Cells, CulturedXenograft Model Antitumor AssaysConceptsAntiandrogen resistanceChromatin dysregulationCHD1 lossProstate cancerGenomic copy number alterationsRNA-seq analysisResistance to hormonal therapyCopy number alterationsAR-targeted therapiesMetastatic prostate cancerATAC-seqClosed chromatinRNA-seqTranscriptional plasticityTranscription factorsFunctional screeningTranscriptomic changesMechanisms of resistanceHormone therapyLineage programsChromatinCHD1Global changeIntegrated analysisTherapyAn allelic series of miR-17∼92–mutant mice uncovers functional specialization and cooperation among members of a microRNA polycistron
Han Y, Vidigal J, Mu P, Yao E, Singh I, González A, Concepcion C, Bonetti C, Ogrodowski P, Carver B, Selleri L, Betel D, Leslie C, Ventura A. An allelic series of miR-17∼92–mutant mice uncovers functional specialization and cooperation among members of a microRNA polycistron. Nature Genetics 2015, 47: 766-775. PMID: 26029871, PMCID: PMC4485521, DOI: 10.1038/ng.3321.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisB-LymphocytesCarcinogenesisCells, CulturedEyelidsGene FrequencyGenes, LethalGenome-Wide Association StudyIntellectual DisabilityLimb Deformities, CongenitalMaleMice, 129 StrainMice, Inbred C57BLMice, TransgenicMicrocephalyMicroRNAsMultigene FamilyMutationTracheoesophageal Fistula
2012
Intact p53-Dependent Responses in miR-34–Deficient Mice
Concepcion C, Han Y, Mu P, Bonetti C, Yao E, D'Andrea A, Vidigal J, Maughan W, Ogrodowski P, Ventura A. Intact p53-Dependent Responses in miR-34–Deficient Mice. PLOS Genetics 2012, 8: e1002797. PMID: 22844244, PMCID: PMC3406012, DOI: 10.1371/journal.pgen.1002797.Peer-Reviewed Original ResearchConceptsMiR-34 familyMiR-34 expressionP53 pathwayP53-induced cell cycle arrestP53-independent functionsP53-dependent responseCell cycle arrestMiR-34Potential tumor suppressorExpression of membersP53-deficient miceP53-independentFamily of miRNAsP53 functionCycle arrestTumor suppressorMicroRNA familyCellular proliferation in vitroHuman cancersProliferation in vitroP53Brains of miceMicroRNAsNormal developmentMice