2017
Systematic Drug Screening Identifies Tractable Targeted Combination Therapies in Triple-Negative Breast Cancer
Wali VB, Langdon CG, Held MA, Platt JT, Patwardhan GA, Safonov A, Aktas B, Pusztai L, Stern DF, Hatzis C. Systematic Drug Screening Identifies Tractable Targeted Combination Therapies in Triple-Negative Breast Cancer. Cancer Research 2017, 77: 566-578. PMID: 27872098, PMCID: PMC5582957, DOI: 10.1158/0008-5472.can-16-1901.Peer-Reviewed Original ResearchConceptsTriple-negative breast cancerTNBC cell linesPairwise drug combinationsClinical translationAggressive diseaseCombination therapyBreast cancerPreclinical proofDrug combinationsCombination treatmentInvestigational drugsSingle agentSensitivity patternCell sensitivityCell linesTherapyApoptotic activityAnticancer activityDownregulated genesMitogenic signalingCrizotinibBlockadeClinicAgentsCancer
2008
Direct resequencing of the complete ERBB2 coding sequence reveals an absence of activating mutations in ERBB2 amplified breast cancer
Zito CI, Riches D, Kolmakova J, Simons J, Egholm M, Stern DF. Direct resequencing of the complete ERBB2 coding sequence reveals an absence of activating mutations in ERBB2 amplified breast cancer. Genes Chromosomes And Cancer 2008, 47: 633-638. PMID: 18418848, PMCID: PMC6668724, DOI: 10.1002/gcc.20566.Peer-Reviewed Original ResearchRegulation of the Rad53 protein kinase in signal amplification by oligomer assembly and disassembly
Jia-Lin Ma N, Stern DF. Regulation of the Rad53 protein kinase in signal amplification by oligomer assembly and disassembly. Cell Cycle 2008, 7: 808-817. PMID: 18239457, DOI: 10.4161/cc.7.6.5595.Peer-Reviewed Original ResearchConceptsRad53 activationDNA damageOligomer assemblyRad53 kinase activityRad53 protein kinaseAbsence of Mec1DNA damage responseSignal transduction processesMammalian Chk2Autophosphorylation activityGenetic requirementsCheckpoint responseChk2 activationDamage responseEffector kinaseProtein kinaseKinase activityRad53Forms oligomersTransduction processesSCD domainsInduced oligomerizationOligomer formationOligomerizationChk2
2006
Formation of Neu/ErbB2-induced mammary tumors is unaffected by loss of ErbB4
Jackson-Fisher AJ, Bellinger G, Shum E, Duong JK, Perkins AS, Gassmann M, Muller W, Kent Lloyd KC, Stern DF. Formation of Neu/ErbB2-induced mammary tumors is unaffected by loss of ErbB4. Oncogene 2006, 25: 5664-5672. PMID: 16652155, DOI: 10.1038/sj.onc.1209574.Peer-Reviewed Original ResearchConceptsClinical studiesMammary tumorsMammary glandSimilar latency periodHistology of tumorsLoss of ERBB4Epidermal growth factor receptorTumor suppressorGrowth factor receptorLung metastasesBreast cancerErbb4 allelesMMTV-NeuLatency periodNull miceTumorsReceptor tyrosine kinasesFactor receptorErbB4ErbB familyCancerMiceTyrosine kinaseTissue culture analysisGland
2005
The Plk1 Polo Box Domain Mediates a Cell Cycle and DNA Damage Regulated Interaction with Chk2
Tsvetkov LM, Tsekova RT, Xu X, Stern DF. The Plk1 Polo Box Domain Mediates a Cell Cycle and DNA Damage Regulated Interaction with Chk2. Cell Cycle 2005, 4: 602-610. PMID: 15876876, DOI: 10.4161/cc.4.4.1599.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCatalytic DomainCell CycleCell Cycle ProteinsCell DivisionCell SeparationCheckpoint Kinase 2DNA DamageDNA RepairG2 PhaseGenetic VectorsGlutathione TransferaseHeLa CellsHumansImmunoblottingImmunoprecipitationIn Vitro TechniquesMitosisPhosphorylationProtein BindingProtein KinasesProtein Serine-Threonine KinasesProtein Structure, TertiaryProto-Oncogene ProteinsSignal TransductionConceptsPlk1 polo-box domainDNA damage checkpointPolo-box domainPolo-like kinase 1Eukaryotic proteinsDamage checkpointMitotic regulationBox domainRegulated interactionPlk1 activityProtein kinaseSignaling cascadesChk2Kinase 1Tumor suppressorCell cycleDNA damageS phasePlk1M phaseMitosisMultiple processesPotential mechanismsPhosphorylatesKinaseInteraction of Chromatin-associated Plk1 and Mcm7*
Tsvetkov L, Stern DF. Interaction of Chromatin-associated Plk1 and Mcm7*. Journal Of Biological Chemistry 2005, 280: 11943-11947. PMID: 15654075, DOI: 10.1074/jbc.m413514200.Peer-Reviewed Original ResearchMeSH KeywordsCell Cycle ProteinsCells, CulturedChromatinDNA DamageDNA ReplicationDNA-Binding ProteinsHumansImmunoprecipitationMinichromosome Maintenance Complex Component 3Minichromosome Maintenance Complex Component 7MitosisNuclear ProteinsPhosphorylationProtein KinasesProtein Serine-Threonine KinasesProto-Oncogene ProteinsTranscription FactorsConceptsPolo-box domainEndogenous Plk1Mcm2-7 protein complexPBD of Plk1DNA damage checkpointMultifunctional protein kinaseInteraction of chromatinFull-length Plk1Soluble chromatin fractionMinichromosome maintenance proteinsChromosome segregationMitotic exitDamage checkpointPlk1 interactsMitotic structuresProtein complexesMitotic entryDNA replicationChromatin fractionProtein kinaseMitotic eventsMaintenance proteinsCell cyclePlk1MCM7