2022
Pyruvate kinase M1 suppresses development and progression of prostate adenocarcinoma
Davidson S, Schmidt D, Heyman J, O'Brien J, Liu A, Israelsen W, Dayton T, Sehgal R, Bronson R, Freinkman E, Mak H, Fanelli G, Malstrom S, Bellinger G, Carracedo A, Pandolfi P, Courtney K, Jha A, DePinho R, Horner J, Thomas C, Cantley L, Loda M, Vander Heiden M. Pyruvate kinase M1 suppresses development and progression of prostate adenocarcinoma. Cancer Research 2022, 82: 2403-2416. PMID: 35584006, PMCID: PMC9256808, DOI: 10.1158/0008-5472.can-21-2352.Peer-Reviewed Original Research
2013
Depletion of a Putatively Druggable Class of Phosphatidylinositol Kinases Inhibits Growth of p53-Null Tumors
Emerling B, Hurov J, Poulogiannis G, Tsukazawa K, Choo-Wing R, Wulf G, Bell E, Shim H, Lamia K, Rameh L, Bellinger G, Sasaki A, Asara J, Yuan X, Bullock A, DeNicola G, Song J, Brown V, Signoretti S, Cantley L. Depletion of a Putatively Druggable Class of Phosphatidylinositol Kinases Inhibits Growth of p53-Null Tumors. Cell 2013, 155: 844-857. PMID: 24209622, PMCID: PMC4070383, DOI: 10.1016/j.cell.2013.09.057.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBreast NeoplasmsCell Line, TumorCell ProliferationCell RespirationCellular SenescenceEmbryo, MammalianGene Knockdown TechniquesGenes, LethalHeterograftsHumansMiceNeoplasm TransplantationPhosphotransferases (Alcohol Group Acceptor)Reactive Oxygen SpeciesSignal TransductionTumor Suppressor Protein p53ConceptsReactive oxygen speciesP53-null tumorsBreast cancer cell linesCancer cell linesBreast cancerType 2Druggable classesAbsence of p53Tumor formationInhibits growthCell linesCancerHomozygous deletionMiceTP53Oxygen speciesP53Enhanced levelsHigh levelsDramatic reductionXenograftsLittermatesTumorsSynthetic lethalityPKM2 Isoform-Specific Deletion Reveals a Differential Requirement for Pyruvate Kinase in Tumor Cells
Israelsen WJ, Dayton TL, Davidson SM, Fiske BP, Hosios AM, Bellinger G, Li J, Yu Y, Sasaki M, Horner JW, Burga LN, Xie J, Jurczak MJ, DePinho RA, Clish CB, Jacks T, Kibbey RG, Wulf GM, Di Vizio D, Mills GB, Cantley LC, Vander Heiden M. PKM2 Isoform-Specific Deletion Reveals a Differential Requirement for Pyruvate Kinase in Tumor Cells. Cell 2013, 155: 397-409. PMID: 24120138, PMCID: PMC3850755, DOI: 10.1016/j.cell.2013.09.025.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBase SequenceBreast NeoplasmsExonsFemaleGene DeletionGene Knockout TechniquesHeterograftsHumansIsoenzymesMammary Neoplasms, ExperimentalMiceMice, Inbred C57BLModels, MolecularMolecular Sequence DataMutagenesisMutationNeoplasm MetastasisNeoplasm TransplantationPyruvate KinaseRNA SplicingConceptsTumor cellsPKM2 expressionPKM1 expressionTumor formationMammary tumor formationTumor cell proliferationPyruvate kinase M2 isoformPyruvate kinase expressionBreast cancerNull tumorsHuman tumorsTumorsKinase expressionCell proliferationCell populationsPKM2 deletionPKM2 activityCancerPKM2Anabolic metabolismMetabolic requirementsPyruvate kinaseM2 isoformDifferent metabolic requirementsMetformin Decreases Glucose Oxidation and Increases the Dependency of Prostate Cancer Cells on Reductive Glutamine Metabolism
Fendt S, Bell E, Keibler M, Davidson S, Wirth G, Fiske B, Mayers J, Schwab M, Bellinger G, Csibi A, Patnaik A, Blouin M, Cantley L, Guarente L, Blenis J, Pollak M, Olumi A, Vander Heiden M, Stephanopoulos G. Metformin Decreases Glucose Oxidation and Increases the Dependency of Prostate Cancer Cells on Reductive Glutamine Metabolism. Cancer Research 2013, 73: 4429-4438. PMID: 23687346, PMCID: PMC3930683, DOI: 10.1158/0008-5472.can-13-0080.Peer-Reviewed Original ResearchConceptsProstate cancer cellsProstate cancerCancer cellsGlutamine metabolismReductive glutamine metabolismCancer cell proliferationPresence of metforminCancer cell linesGlucose oxidationCancer outcomesMouse modelAttenuated proliferationMetforminEpidemiology studiesCancerGlutamine anaplerosisCell proliferationPatientsCell linesProliferative defectMetabolismOutcomesProliferationCellsTumors
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