2022
Tumors of the Diffuse Neuroendocrine and Gastroenteropancreatic System
Vosburgh E. Tumors of the Diffuse Neuroendocrine and Gastroenteropancreatic System. 2022, 1-10. DOI: 10.1002/9781119000822.hfcm083.pub2.Peer-Reviewed Original ResearchPeptide receptor radiotherapyMultiple endocrine neoplasiaDiffuse neuroendocrine systemClinical featuresHepatic metastasesNeuroendocrine tumorsGastroenteropancreatic systemNeuroendocrine systemInformed clinical careUnique clinical syndromeOngoing clinical trialsAbsence of symptomsCancer registry dataUnexplained incidenceReceptor radiotherapyClinical presentationRandomized trialsTherapeutic optionsClinical syndromeMultiple myelomaSomatostatin analoguesSpecific therapyRecent trialsSurvival resultsClinical trials
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 developmentAlleles of Insm1 determine whether RIP1-Tag2 mice produce insulinomas or nonfunctioning pancreatic neuroendocrine tumors
Kobayashi S, Contractor T, Vosburgh E, Du YN, Tang LH, Clausen R, Harris CR. Alleles of Insm1 determine whether RIP1-Tag2 mice produce insulinomas or nonfunctioning pancreatic neuroendocrine tumors. Oncogenesis 2019, 8: 16. PMID: 30796198, PMCID: PMC6386750, DOI: 10.1038/s41389-019-0127-1.Peer-Reviewed Original ResearchPancreatic neuroendocrine tumorsNeuroendocrine tumorsRIP1-Tag2 transgenic miceBeta-cell transcription factorsRIP1-Tag2 miceC57BL/6 genetic backgroundCell linesExpression of Insm1Stem cell markersLiver metastasesNonfunctioning tumorsB6 miceLarge tumorsMetastatic tumorsSevere diseaseRT2 miceAnimal modelsInsulinomaTransgenic miceCell transcription factorsInsulin productionGenetic backgroundTumorsHuman insulinomasCell markers
2017
Tumors of the Diffuse Neuroendocrine and Gastroenteropancreatic System
Vosburgh E. Tumors of the Diffuse Neuroendocrine and Gastroenteropancreatic System. 2017, 1-12. DOI: 10.1002/9781119000822.hfcm083.ChaptersDiffuse neuroendocrine systemClinical featuresNeuroendocrine tumorsGastroenteropancreatic systemProgression-free survival benefitNeuroendocrine systemMultiple endocrine neoplasia syndromeInformed clinical careUnique clinical syndromeFive-year survivalOngoing clinical trialsAbsence of symptomsCancer registry dataEndocrine neoplasia syndromeUnexplained incidenceSurvival benefitClinical presentationHepatic metastasesClinical syndromeMultiple myelomaSurvival resultsClinical trialsRegistry dataNeoplasia syndromeClinical care
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
Human Neuroendocrine Tumor Cell Lines as a Three-Dimensional Model for the Study of Human Neuroendocrine Tumor Therapy
Wong C, Vosburgh E, Levine AJ, Cong L, Xu EY. Human Neuroendocrine Tumor Cell Lines as a Three-Dimensional Model for the Study of Human Neuroendocrine Tumor Therapy. Journal Of Visualized Experiments 2012, 4218. PMID: 22929519, PMCID: PMC3486771, DOI: 10.3791/4218.Peer-Reviewed Original ResearchConceptsNeuroendocrine tumorsNET cell linesDrug treatmentCell linesMetastatic neuroendocrine tumorsMinority of patientsHuman neuroendocrine tumor cell linesNeuroendocrine Tumor TherapyNew therapeutic targetsBiology of NETsNeuroendocrine tumor cell linesSingle-drug effectsHuman NET cell linesLocalized diseaseNET patientsSurvival benefitSystemic therapyRare tumorDrug effectsImmunohistochemical techniquesTherapeutic targetAnimal modelsNET biologyTumor cell linesHuman malignanciesHeat 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
2010
A pilot genome-wide association study shows genomic variants enriched in the non-tumor cells of patients with well-differentiated neuroendocrine tumors of the ileum
Walsh KM, Choi M, Oberg K, Kulke MH, Yao JC, Wu C, Jurkiewicz M, Hsu LI, Hooshmand SM, Hassan M, Janson ET, Cunningham JL, Vosburgh E, Sackler RS, Lifton RP, DeWan AT, Hoh J. A pilot genome-wide association study shows genomic variants enriched in the non-tumor cells of patients with well-differentiated neuroendocrine tumors of the ileum. Endocrine Related Cancer 2010, 18: 171-180. PMID: 21139019, PMCID: PMC3221459, DOI: 10.1677/erc-10-0248.Peer-Reviewed Original ResearchMeSH KeywordsCase-Control StudiesCell DifferentiationCellsDNA Copy Number VariationsFemaleGenetic VariationGenome-Wide Association StudyHumansIleal NeoplasmsMaleMeta-Analysis as TopicMicroarray AnalysisNeoplasm StagingNeuroendocrine TumorsPilot ProjectsPolymorphism, Single NucleotideReview Literature as TopicConceptsLoss of heterozygosityDana-Farber Cancer InstituteTumor cellsMD Anderson Cancer CenterCarcinoid tumor cellsUppsala University HospitalPopulation-based controlsAnderson Cancer CenterCopy number variantsBonferroni-corrected levelBlood-derived DNACarcinoid cancerReal-time quantitative PCRCancer CenterNeuroendocrine tumorsUniversity HospitalNon-tumor cellsSerious conditionIndependent cohortCancer InstituteKb heterozygous deletionSmall sample sizePilot genome-wide association studyGenetic polymorphismsSingle nucleotide polymorphisms