2020
KMT2D Deficiency Impairs Super-Enhancers to Confer a Glycolytic Vulnerability in Lung Cancer
Alam H, Tang M, Maitituoheti M, Dhar S, Kumar M, Han C, Ambati C, Amin S, Gu B, Chen T, Lin Y, Chen J, Muller F, Putluri N, Flores E, DeMayo F, Baseler L, Rai K, Lee M. KMT2D Deficiency Impairs Super-Enhancers to Confer a Glycolytic Vulnerability in Lung Cancer. Cancer Cell 2020, 37: 599-617.e7. PMID: 32243837, PMCID: PMC7178078, DOI: 10.1016/j.ccell.2020.03.005.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinoma of LungAnimalsAntimetabolitesApoptosisBiomarkers, TumorCell ProliferationDeoxyglucoseDNA-Binding ProteinsEnhancer Elements, GeneticGene Expression Regulation, NeoplasticGlycolysisHistone-Lysine N-MethyltransferaseHistonesHumansLung NeoplasmsMiceMice, KnockoutMice, NudeMutationMyeloid-Lymphoid Leukemia ProteinNeoplasm ProteinsPeriod Circadian ProteinsPrognosisTumor Cells, CulturedXenograft Model Antitumor AssaysConceptsLung cancerLung-specific lossHuman lung cancer cellsExpression of Per2Lung cancer cellsHistone methyltransferase KMT2DLung tumor suppressorTumor suppressive roleMultiple glycolytic genesLung tumorigenesisEpigenetic modifiersPharmacological inhibitionTherapeutic vulnerabilitiesGlycolytic inhibitorCancerCancer cellsKMT2DFunction mutationsTumor suppressorPer2GlycolysisGlycolytic genesMutationsMiceMolecular and clonal evolution in recurrent metastatic gliosarcoma
Anderson K, Tan A, Parkinson J, Back M, Kastelan M, Newey A, Brewer J, Wheeler H, Hudson A, Amin S, Johnson K, Barthel F, Verhaak R, Khasraw M. Molecular and clonal evolution in recurrent metastatic gliosarcoma. Molecular Case Studies 2020, 6: a004671. PMID: 31896544, PMCID: PMC6996521, DOI: 10.1101/mcs.a004671.Peer-Reviewed Original ResearchConceptsFirst recurrenceExtracranial metastasesIntracranial tumorsFrontal lobeRight iliac boneLeft frontal lobeOrigin of metastasesFrontal recurrenceMetastatic gliosarcomaConcurrent radiotherapyFurther surgeryFurther recurrenceRecurrent tumorsMetastatic tumorsIliac boneMetastasisRecurrenceTumorsMesenchymal typeSurgeryClonal relationshipRadiotherapyGliosarcomaMolecular profilePelvic bones
2018
An in vivo screen identifies PYGO2 as a driver for metastatic prostate cancer
Lu X, Pan X, Wu C, Zhao D, Feng S, Zang Y, Lee R, Khadka S, Amin S, Jin E, Shang X, Deng P, Luo Y, Morgenlander W, Weinrich J, Lu X, Jiang S, Chang Q, Navone N, Troncoso P, DePinho R, Wang Y. An in vivo screen identifies PYGO2 as a driver for metastatic prostate cancer. Cancer Research 2018, 78: canres.3564.2017. PMID: 29769196, PMCID: PMC6381393, DOI: 10.1158/0008-5472.can-17-3564.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiomarkers, TumorCarcinogenesisCell Line, TumorDisease ProgressionGene Expression Regulation, NeoplasticHEK293 CellsHumansIntracellular Signaling Peptides and ProteinsLymph NodesMaleMiceMice, NudeNeoplasm GradingOncogenesPC-3 CellsProstatic NeoplasmsTranscriptional ActivationUp-RegulationWnt Signaling PathwayConceptsProstate cancer progressionDepth functional analysisCancer progressionWnt/β-catenin signalingCancer cell invasionΒ-catenin signalingFunctional genomicsProstate cancerTranscriptional activationCopy number aberrationsTranscriptomic datasetsFinger 2New oncogenePygo2's functionFunctional driversFunctional analysisLymph nodesImpairs tumor progressionChromosomal instabilityPutative oncogeneCell invasionNumber aberrationsPositive hitsAmplification/overexpressionOncogene