2022
A Distinct Chromatin State Drives Therapeutic Resistance in Invasive Lobular Breast Cancer.
Nardone A, Qiu X, Spisak S, Nagy Z, Feiglin A, Feit A, Cohen Feit G, Xie Y, Font-Tello A, Guarducci C, Hermida-Prado F, Syamala S, Lim K, Munoz Gomez M, Pun M, Cornwell M, Liu W, Ors A, Mohammed H, Cejas P, Brock JB, Freedman ML, Winer EP, Fu X, Schiff R, Long HW, Metzger Filho O, Jeselsohn R. A Distinct Chromatin State Drives Therapeutic Resistance in Invasive Lobular Breast Cancer. Cancer Research 2022, 82: 3673-3686. PMID: 35950920, PMCID: PMC9588703, DOI: 10.1158/0008-5472.can-21-3186.Peer-Reviewed Original ResearchConceptsInvasive lobular breast cancerInvasive ductal cancerLobular breast cancerTamoxifen resistanceBreast cancerInferior long-term outcomesTumor progressionLong-term outcomesBreast cancer subtypesPotential therapeutic avenuesDuctal cancerClinical findingsPoor outcomeReceptor axisClinical trialsDisease progressionPatient outcomesPreclinical modelsClinical investigationRelated commentaryTherapeutic avenuesCancer subtypesTherapeutic resistanceCancerClinical samples
2018
Allele-Specific Chromatin Recruitment and Therapeutic Vulnerabilities of ESR1 Activating Mutations
Jeselsohn R, Bergholz JS, Pun M, Cornwell M, Liu W, Nardone A, Xiao T, Li W, Qiu X, Buchwalter G, Feiglin A, Abell-Hart K, Fei T, Rao P, Long H, Kwiatkowski N, Zhang T, Gray N, Melchers D, Houtman R, Liu XS, Cohen O, Wagle N, Winer EP, Zhao J, Brown M. Allele-Specific Chromatin Recruitment and Therapeutic Vulnerabilities of ESR1 Activating Mutations. Cancer Cell 2018, 33: 173-186.e5. PMID: 29438694, PMCID: PMC5813700, DOI: 10.1016/j.ccell.2018.01.004.Peer-Reviewed Original ResearchConceptsChromatin recruitmentLigand-independent functionsER mutationsPro-metastatic phenotypeGenetic screenTranscriptional networksTranscriptional programsWild-type ERTherapeutic vulnerabilitiesPotential therapeutic targetMutationsMutantsDomain mutationsLigand-binding domain mutationsActivating mutationsTherapeutic targetTherapy resistanceUnique recruitmentRecruitmentGenetic vulnerabilityCancer modelGenesBreast cancer modelERPhenotype
2016
Response and resistance to BET bromodomain inhibitors in triple-negative breast cancer
Shu S, Lin CY, He HH, Witwicki RM, Tabassum DP, Roberts JM, Janiszewska M, Jin Huh S, Liang Y, Ryan J, Doherty E, Mohammed H, Guo H, Stover DG, Ekram MB, Peluffo G, Brown J, D’Santos C, Krop I, Dillon D, McKeown M, Ott C, Qi J, Ni M, Rao P, Duarte M, Wu S, Chiang C, Anders L, Young R, Winer E, Letai A, Barry W, Carroll J, Long H, Brown M, Shirley Liu X, Meyer C, Bradner J, Polyak K. Response and resistance to BET bromodomain inhibitors in triple-negative breast cancer. Nature 2016, 529: 413-417. PMID: 26735014, PMCID: PMC4854653, DOI: 10.1038/nature16508.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAzepinesBinding, CompetitiveCasein Kinase IICell Cycle ProteinsCell Line, TumorCell ProliferationChromatinDrug Resistance, NeoplasmEpigenesis, GeneticFemaleGene Expression Regulation, NeoplasticGenome, HumanHumansMediator Complex Subunit 1MiceNuclear ProteinsPhosphorylationPhosphoserineProtein BindingProtein Phosphatase 2Protein Structure, TertiaryProteomicsTranscription FactorsTranscription, GeneticTriazolesTriple Negative Breast NeoplasmsXenograft Model Antitumor Assays