2019
Two well-differentiated pancreatic neuroendocrine tumor mouse models
Wong C, Tang LH, Davidson C, Vosburgh E, Chen W, Foran DJ, Notterman DA, Levine AJ, Xu EY. Two well-differentiated pancreatic neuroendocrine tumor mouse models. Cell Death & Differentiation 2019, 27: 269-283. PMID: 31160716, PMCID: PMC7206057, DOI: 10.1038/s41418-019-0355-0.Peer-Reviewed Original ResearchConceptsMultiple endocrine neoplasia type 1Neuroendocrine tumorsMouse modelShort latencyPI3K/Akt/mTORPancreatic neuroendocrine tumorsPituitary neuroendocrine tumorsTumor mouse modelAkt/mTORMTOR inhibitor rapamycinCre-loxP systemNeuroendocrine cancerProlonged survivalProlonged latencyMEN1 patientsMouse insulin 1 promoterSame miceMen1 lossTherapeutic opportunitiesType 1Genetic syndromesPTEN lossEarly onsetTumorsTumor development
2016
Sexual dimorphism of liver metastasis by murine pancreatic neuroendocrine tumors is affected by expression of complement C5
Contractor T, Kobayashi S, da Silva E, Clausen R, Chan C, Vosburgh E, Tang LH, Levine AJ, Harris CR. Sexual dimorphism of liver metastasis by murine pancreatic neuroendocrine tumors is affected by expression of complement C5. Oncotarget 2016, 7: 30585-30596. PMID: 27105526, PMCID: PMC5058703, DOI: 10.18632/oncotarget.8874.Peer-Reviewed Original ResearchConceptsComplement C5Liver metastasesAdvanced tumorsNeuroendocrine tumorsMouse modelSmall primary tumorsPancreatic neuroendocrine tumorsTypes of tumorsSmall molecule antagonistsIntratumoral levelsPrimary tumorMale miceComplement C5aMetastasisTumorsMolecule antagonistsMiceHigh frequencySexual dimorphismHuman diseasesMalesFirst reportCD88CD68PMX53
2012
Heat shock protein 90 is a promising target for effective growth inhibition of gastrointestinal neuroendocrine tumors.
Gloesenkamp C, Nitzsche B, Lim A, Normant E, Vosburgh E, Schrader M, Ocker M, Scherübl H, Höpfner M. Heat shock protein 90 is a promising target for effective growth inhibition of gastrointestinal neuroendocrine tumors. International Journal Of Oncology 2012, 40: 1659-67. PMID: 22246317, DOI: 10.3892/ijo.2012.1328.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsApoptosisBenzoquinonesCell Cycle CheckpointsCell Line, TumorCell MovementCell ProliferationChick EmbryoChorioallantoic MembraneDose-Response Relationship, DrugFlow CytometryGastrointestinal NeoplasmsGene Expression ProfilingGene Expression Regulation, NeoplasticHSP90 Heat-Shock ProteinsHumansLactams, MacrocyclicNeuroendocrine TumorsPhosphatidylinositol 3-KinaseProtein Kinase InhibitorsProto-Oncogene Proteins c-aktReceptor, IGF Type 1Signal TransductionTOR Serine-Threonine KinasesConceptsShock protein 90IGF-1 receptorIPI-504Protein 90GEP-NETsNeuroendocrine tumorsHsp90 inhibitor IPI-504Heat shock protein 90Antiproliferative effectsGEP-NET cellsDose-dependent growth inhibitionGEP-NET treatmentPI3K/AKT/mTOR pathwayGastrointestinal neuroendocrine tumorsGastroenteropancreatic neuroendocrine tumorsAKT/mTOR pathwayCancer gene expressionAdditive antiproliferative effectsCell cycle arrestInnovative therapeutic approachesTyrosine kinase inhibitionGrowth inhibitionMechanism of actionGene expressionHsp90 inhibition