2020
Enhancer Reprogramming Confers Dependence on Glycolysis and IGF Signaling in KMT2D Mutant Melanoma
Maitituoheti M, Keung E, Tang M, Yan L, Alam H, Han G, Singh A, Raman A, Terranova C, Sarkar S, Orouji E, Amin S, Sharma S, Williams M, Samant N, Dhamdhere M, Zheng N, Shah T, Shah A, Axelrad J, Anvar N, Lin Y, Jiang S, Chang E, Ingram D, Wang W, Lazar A, Lee M, Muller F, Wang L, Ying H, Rai K. Enhancer Reprogramming Confers Dependence on Glycolysis and IGF Signaling in KMT2D Mutant Melanoma. Cell Reports 2020, 33: 108293. PMID: 33086062, PMCID: PMC7649750, DOI: 10.1016/j.celrep.2020.108293.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCarrier ProteinsCell Line, TumorDNA-Binding ProteinsFemaleGenes, Tumor SuppressorGlucoseGlycolysisHistone MethyltransferasesHistone-Lysine N-MethyltransferaseHumansInsulinIntercellular Signaling Peptides and ProteinsMaleMelanomaMiceMice, Inbred C57BLMice, NudeMyeloid-Lymphoid Leukemia ProteinNeoplasm ProteinsReceptor, IGF Type 1Regulatory Sequences, Nucleic AcidSignal TransductionXenograft Model Antitumor AssaysConceptsKMT2D-deficient cellsInsulin growth factorEnhancer reprogrammingIGF1R-AktMelanocyte-specific deletionMutant melanomaMouse modelTumor typesTherapeutic interventionsPharmacological inhibitionPathway inhibitorPotent tumor suppressorIGF signalingGrowth factorMelanomaPooled RNAi screensSomatic point mutationsTumor suppressorKey metabolic pathwaysFrequent lossGlycolysisGlycolysis enzymesTumorigenesisGlycolysis pathwayMetabolic pathways
2016
Mechanism of Insulin Action
White M. Mechanism of Insulin Action. 2016, 114-132. DOI: 10.1002/9781118924853.ch8.Peer-Reviewed Original ResearchInsulin-like signalingGenome-wide association studiesInsulin-like peptidesClassical insulin target tissuesInsulin-like growth factor 2Receptor tyrosine kinasesSimilar receptor tyrosine kinasesEnvironmental signalsHuman genomeInsulin target tissuesGenetic lociPancreatic β-cellsInsulin signalTyrosine kinaseAssociation studiesRelease of nutrientsConflicting signalsGrowth factor 2IGF signalingAnimal growthFactor 1Factor 2Insulin-like growth factor-1Β-cellsGenes
2009
The IRS2 Gly1057Asp Variant Is Associated With Human Longevity
Barbieri M, Rizzo M, Papa M, Boccardi V, Esposito A, White M, Paolisso G. The IRS2 Gly1057Asp Variant Is Associated With Human Longevity. The Journals Of Gerontology Series A 2009, 65A: 282-286. PMID: 19887537, DOI: 10.1093/gerona/glp154.Peer-Reviewed Original ResearchConceptsInsulin receptor substrate 2Gene polymorphismsYears of ageIGF-1 signalingß-cell functionInsulin-like growth factor-1 signalingIrs2 branchInsulin resistanceInsulin sensitivityMetabolic covariatesGly1057Asp variantIRS2 geneExtreme old ageLarge population groupsInternal medicineC participantsOlder ageHuman longevityCommon polymorphismsIGF signalingInsulinFurther studiesPopulation groupsAgeWhole population
2006
The relationship of insulin-like growth factor-II, insulin-like growth factor binding protein-3, and estrogen receptor-alpha expression to disease progression in epithelial ovarian cancer.
Lu L, Katsaros D, Wiley A, de la Longrais I, Risch HA, Puopolo M, Yu H. The relationship of insulin-like growth factor-II, insulin-like growth factor binding protein-3, and estrogen receptor-alpha expression to disease progression in epithelial ovarian cancer. Clinical Cancer Research 2006, 12: 1208-1214. PMID: 16489075, DOI: 10.1158/1078-0432.ccr-05-1801.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overBiomarkers, TumorDisease ProgressionEpithelial CellsEstrogen Receptor alphaFemaleGene Expression Regulation, NeoplasticHumansInsulin-Like Growth Factor Binding Protein 3Insulin-Like Growth Factor IIMiddle AgedNeoplasm StagingOvarian NeoplasmsReverse Transcriptase Polymerase Chain ReactionRNA, NeoplasmSurvival AnalysisConceptsIGF-II expressionEstrogen receptor alpha expressionReceptor alpha expressionEpithelial ovarian cancerIGF-IIDisease progressionOvarian cancerInsulin-like growth factor (IGF) systemPrimary epithelial ovarian cancerProtein 3Insulin-like growth factorIGF signalingHigh IGF-IILarge residual lesionExpression of estrogenInsulin-like growth factor IIIGFBP-3 expressionEffects of IGFOvarian cancer treatmentGrowth factor systemFresh tumor specimensGrowth factor IIQuantitative reverse transcription PCRIGFBP-3Serous histology
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