2017
CDK4/6 inhibition triggers anti-tumour immunity
Goel S, DeCristo MJ, Watt AC, BrinJones H, Sceneay J, Li BB, Khan N, Ubellacker JM, Xie S, Metzger-Filho O, Hoog J, Ellis MJ, Ma CX, Ramm S, Krop IE, Winer EP, Roberts TM, Kim HJ, McAllister SS, Zhao JJ. CDK4/6 inhibition triggers anti-tumour immunity. Nature 2017, 548: 471-475. PMID: 28813415, PMCID: PMC5570667, DOI: 10.1038/nature23465.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigen PresentationBiological MimicryBreast NeoplasmsCell Cycle CheckpointsCell Line, TumorCell ProliferationCyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6Disease Models, AnimalFemaleHumansInterferonsMicePhosphorylationProtein Kinase InhibitorsRepressor ProteinsRNA, Double-StrandedSignal TransductionT-Lymphocytes, RegulatoryTranscriptomeViruses
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
2008
Short Preoperative Treatment With Erlotinib Inhibits Tumor Cell Proliferation in Hormone Receptor–Positive Breast Cancers
Guix M, de Matos Granja N, Meszoely I, Adkins TB, Wieman BM, Frierson KE, Sanchez V, Sanders ME, Grau AM, Mayer IA, Pestano G, Shyr Y, Muthuswamy S, Calvo B, Krontiras H, Krop IE, Kelley MC, Arteaga CL. Short Preoperative Treatment With Erlotinib Inhibits Tumor Cell Proliferation in Hormone Receptor–Positive Breast Cancers. Journal Of Clinical Oncology 2008, 26: 897-906. PMID: 18180460, DOI: 10.1200/jco.2007.13.5939.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAnimalsAntineoplastic AgentsBiomarkers, TumorBreast NeoplasmsCell ProliferationChemotherapy, AdjuvantErbB ReceptorsErlotinib HydrochlorideFemaleHumansImmunohistochemistryIn Situ Nick-End LabelingKi-67 AntigenMiceMice, NudeMiddle AgedNeoadjuvant TherapyNeoplasm StagingNeoplasms, Hormone-DependentProtein Kinase InhibitorsProtein-Tyrosine KinasesQuinazolinesReceptor, ErbB-2Receptors, EstrogenReceptors, ProgesteroneSignal TransductionTandem Mass SpectrometryTreatment OutcomeXenograft Model Antitumor AssaysConceptsTumor cell proliferationBreast cancerPreoperative treatmentCell proliferationHormone receptor-positive breast cancerP-S6P-AktEpidermal growth factor receptor (EGFR) tyrosine kinase inhibitor erlotinibHormone receptor-positive cancersReceptor-positive breast cancerHuman epidermal growth factor receptor 2Epidermal growth factor receptor 2ER-positive breast cancerP-EGFRTyrosine kinase inhibitor erlotinibTriple-negative breast cancerP-MAPKImmediate preoperative periodUntreated breast cancerGrowth factor receptor 2Day of surgeryInvasive breast cancerReceptor-positive cancersTriple-negative cancersKinase inhibitor erlotinib