2019
Reversion and non-reversion mechanisms of resistance (MoR) to PARP inhibitor (PARPi) or platinum chemotherapy (chemotx) in patients (pts) with BRCA1/2 -mutant metastatic breast cancer (MBC).
Waks A, Cohen O, Kochupurakkal B, Kim D, Wander S, Buendia-Buendia J, Helvie K, Matulonis U, Krop I, Tolaney S, Winer E, D'Andrea A, Shapiro G, Lin N, Wagle N. Reversion and non-reversion mechanisms of resistance (MoR) to PARP inhibitor (PARPi) or platinum chemotherapy (chemotx) in patients (pts) with BRCA1/2 -mutant metastatic breast cancer (MBC). Journal Of Clinical Oncology 2019, 37: 1085-1085. DOI: 10.1200/jco.2019.37.15_suppl.1085.Peer-Reviewed Original ResearchFork protectionRAD51 fociHomologous recombinationWhole-exome sequencingReplication fork protectionDNA end resectionPARP inhibitorsReversion mutationsIntact homologous recombinationEnd resectionGenomic dataBRCA1/2 proteinsMetastatic tumor biopsiesExome sequencingMutationsGenesResponse/resistanceGermline DNAWES analysisIntrinsic resistanceReversionSequencingProteinDNAAlterations
2014
Phosphorylation of ETS1 by Src Family Kinases Prevents Its Recognition by the COP1 Tumor Suppressor
Lu G, Zhang Q, Huang Y, Song J, Tomaino R, Ehrenberger T, Lim E, Liu W, Bronson RT, Bowden M, Brock J, Krop IE, Dillon DA, Gygi SP, Mills GB, Richardson AL, Signoretti S, Yaffe MB, Kaelin WG. Phosphorylation of ETS1 by Src Family Kinases Prevents Its Recognition by the COP1 Tumor Suppressor. Cancer Cell 2014, 26: 222-234. PMID: 25117710, PMCID: PMC4169234, DOI: 10.1016/j.ccr.2014.06.026.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsBinding SitesFemaleHCT116 CellsHEK293 CellsHumansMiceMice, Inbred NODMice, SCIDMolecular Sequence DataNeoplasm TransplantationPhosphorylationProtein BindingProto-Oncogene Protein c-ets-1Proto-Oncogene Protein c-ets-2Src-Family KinasesTriple Negative Breast NeoplasmsTumor BurdenUbiquitinationUbiquitin-Protein LigasesConceptsSrc family kinasesFamily kinasesTumor suppressorPhosphorylation of ETS1Ubiquitin ligase componentTumor suppressor proteinAnchorage-independent growthNeighboring tyrosine residueCOP1 substratesRegulatory phosphorylationSpecific serineThreonine residuesSrc familySuppressor proteinTyrosine residuesETS1Breast cancer cellsPhosphorylationCancer cellsNeoplastic growthKinaseSuppressorProteinOncoproteinResidues
2005
HIN-1, an Inhibitor of Cell Growth, Invasion, and AKT Activation
Krop I, Parker MT, Bloushtain-Qimron N, Porter D, Gelman R, Sasaki H, Maurer M, Terry MB, Parsons R, Polyak K. HIN-1, an Inhibitor of Cell Growth, Invasion, and AKT Activation. Cancer Research 2005, 65: 9659-9669. PMID: 16266985, DOI: 10.1158/0008-5472.can-05-1663.Peer-Reviewed Original ResearchConceptsTumor suppressor functionHIN-1Suppressor functionMitogen-induced phosphorylationCell growthPotential tumor suppressor functionAnchorage-independent cell growthCell cycle reentryActivation of AktCell cycle arrestActivates AktRetinoblastoma proteinHIN-1 geneGrowth arrestAkt activationRb phosphorylationApparent cell cycle arrestLigand-binding studiesCell migrationCycle arrestPhosphorylationAktEpithelial cellsProteinPotent inhibitor