Featured Publications
Activation state-specific monoclonal antibody detects tyrosine phosphorylated p185neu/erbB-2 in a subset of human breast tumors overexpressing this receptor.
DiGiovanna MP, Stern DF. Activation state-specific monoclonal antibody detects tyrosine phosphorylated p185neu/erbB-2 in a subset of human breast tumors overexpressing this receptor. Cancer Research 1995, 55: 1946-55. PMID: 7728765.Peer-Reviewed Original ResearchConceptsHuman breast tumorsBreast tumorsPrimary human breast tumorsPoor patient prognosisSubset of tumorsEpidermal growth factor receptorGrowth factor receptorPatient prognosisImmunohistochemical stainingNeu/ErbBTumor samplesTumorsMonoclonal antibodiesHuman tumorsFactor receptorRelated receptorsReceptorsP185Polyclonal antibodiesAntibodiesErbBRelated epidermal growth factor receptorSubsetTyrosine phosphoproteinsPrognosisAntiserum raised against a synthetic phosphotyrosine-containing peptide selectively recognizes p185neu/erbB-2 and the epidermal growth factor receptor.
Bangalore L, Tanner AJ, Laudano AP, Stern DF. Antiserum raised against a synthetic phosphotyrosine-containing peptide selectively recognizes p185neu/erbB-2 and the epidermal growth factor receptor. Proceedings Of The National Academy Of Sciences Of The United States Of America 1992, 89: 11637-11641. PMID: 1280833, PMCID: PMC50608, DOI: 10.1073/pnas.89.23.11637.Peer-Reviewed Original Research
2020
Acquired Resistance to HER2-Targeted Therapies Creates Vulnerability to ATP Synthase Inhibition
Gale M, Li Y, Cao J, Liu ZZ, Holmbeck MA, Zhang M, Lang SM, Wu L, Do Carmo M, Gupta S, Aoshima K, DiGiovanna MP, Stern DF, Rimm DL, Shadel GS, Chen X, Yan Q. Acquired Resistance to HER2-Targeted Therapies Creates Vulnerability to ATP Synthase Inhibition. Cancer Research 2020, 80: 524-535. PMID: 31690671, PMCID: PMC7002225, DOI: 10.1158/0008-5472.can-18-3985.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic Combined Chemotherapy ProtocolsApoptosisBreast NeoplasmsCell ProliferationDrug Resistance, NeoplasmEnzyme InhibitorsFemaleHumansMiceMice, Inbred NODMice, SCIDMitochondrial Proton-Translocating ATPasesOligomycinsReceptor, ErbB-2TrastuzumabTumor Cells, CulturedXenograft Model Antitumor AssaysConceptsResistant cellsHER2-Targeted TherapyTrastuzumab-resistant tumorsNew therapeutic strategiesNovel potential targetDrug-free mediumAntibody therapySynthase inhibitionLow doseTherapeutic strategiesTrastuzumabBreast tumorsHER2TherapyAcquired ResistanceTumorsPotential targetMitochondrial respirationCellsSelective dependencyInhibitionMinimal changesNovel vulnerabilitiesATP synthase inhibitionOligomycin A
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 Research
2003
Gene expression profiling of ErbB receptor and ligand-dependent transcription
Amin DN, Perkins AS, Stern DF. Gene expression profiling of ErbB receptor and ligand-dependent transcription. Oncogene 2003, 23: 1428-1438. PMID: 14973552, DOI: 10.1038/sj.onc.1207257.Peer-Reviewed Original ResearchConceptsGene expression profilingExpression profilingInfluences gene transcriptionLigand-dependent transcriptionLigand-independent activationTranscriptional targetsGene transcriptionBreast cancerGene expressionMolecular mechanismsSame cell lineReceptor homodimersOligonucleotide arraysBreast cancer cellsUnidentified targetsErbB receptorsOverexpression of ErbB2GenesCancer cellsCell linesTranscriptionErbB4 receptorsErbB2ErbBClinical outcomes
1997
Cripto Enhances the Tyrosine Phosphorylation of Shc and Activates Mitogen-activated Protein Kinase (MAPK) in Mammary Epithelial Cells*
Kannan S, De Santis M, Lohmeyer M, David J, Smith G, Hynes N, Seno M, Brandt R, Bianco C, Persico G, Kenney N, Normanno N, Martinez-Lacaci I, Ciardiello F, Stern D, Gullick W, Salomon D. Cripto Enhances the Tyrosine Phosphorylation of Shc and Activates Mitogen-activated Protein Kinase (MAPK) in Mammary Epithelial Cells*. Journal Of Biological Chemistry 1997, 272: 3330-3335. PMID: 9013573, DOI: 10.1074/jbc.272.6.3330.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBinding, CompetitiveBreast NeoplasmsCalcium-Calmodulin-Dependent Protein KinasesEnzyme ActivationEpidermal Growth FactorEpitheliumFemaleGPI-Linked ProteinsGrowth SubstancesHumansIntercellular Signaling Peptides and ProteinsMammary Glands, AnimalMembrane GlycoproteinsMiceMitogen-Activated Protein Kinase 1Neoplasm ProteinsPhosphorylationProtein-Tyrosine KinasesSrc Homology DomainsTumor Cells, CulturedTyrosineConceptsTyrosine phosphorylationHC-11 cellsMammary epithelial cellsErb BCripto-1Ras/Raf/MEK/MAPK pathwayTyrosine kinaseRaf/MEK/MAPK pathwayMitogen-activated protein kinase activityMEK/MAPK pathwayHC-11 mouse mammary epithelial cellsEpithelial cellsMouse mammary epithelial cellsProtein kinase activityTyrosine-phosphorylated ShcReceptor tyrosine kinasesDifferent human breast cancer cell linesSKBR-3 breast cancer cellsType 1 receptor tyrosine kinasesEGF-like growth factorHuman breast cancer cell linesEpidermal growth factor (EGF) familyBreast cancer cell linesActivates MitogenGrowth factor family