Multiomic characterization of pancreatic cancer-associated macrophage polarization reveals deregulated metabolic programs driven by the GM-CSF–PI3K pathway
Boyer S, Lee H, Steele N, Zhang L, Sajjakulnukit P, Andren A, Ward M, Singh R, Basrur V, Zhang Y, Nesvizhskii A, di Magliano M, Halbrook C, Lyssiotis C. Multiomic characterization of pancreatic cancer-associated macrophage polarization reveals deregulated metabolic programs driven by the GM-CSF–PI3K pathway. ELife 2022, 11: e73796. PMID: 35156921, PMCID: PMC8843093, DOI: 10.7554/elife.73796.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell Line, TumorCell Transformation, NeoplasticGene Expression ProfilingGranulocyte-Macrophage Colony-Stimulating FactorHumansMetabolic Networks and PathwaysMetabolomicsMiceMice, Inbred C57BLPancreatic NeoplasmsProteomicsSignal TransductionTranscription FactorsTumor-Associated MacrophagesConceptsTumor-educated macrophagesSingle-cell RNA sequencing datasetsCancer cellsMultiomics characterizationRNA sequencing datasetsTumor-associated macrophagesPI3K-Akt pathwayPI3K pathwayMetabolic programsSequencing datasetsGene expressionMetabolic crosstalkFunction of TAMsCell typesK pathwayGM-CSFGranulocyte-macrophage colony-stimulating factorTumor promotingModel systemEpithelial cellsPathwayColony-stimulating factorMetabolic signaturesMutant KrasMalignant epithelial cellsA large-scale analysis of targeted metabolomics data from heterogeneous biological samples provides insights into metabolite dynamics
Lee HJ, Kremer DM, Sajjakulnukit P, Zhang L, Lyssiotis CA. A large-scale analysis of targeted metabolomics data from heterogeneous biological samples provides insights into metabolite dynamics. Metabolomics 2019, 15: 103. PMID: 31289941, PMCID: PMC6616221, DOI: 10.1007/s11306-019-1564-8.Peer-Reviewed Original ResearchAbnormal oxidative metabolism in a quiet genomic background underlies clear cell papillary renal cell carcinoma
Xu J, Reznik E, Lee HJ, Gundem G, Jonsson P, Sarungbam J, Bialik A, Sanchez-Vega F, Creighton CJ, Hoekstra J, Zhang L, Sajjakulnukit P, Kremer D, Tolstyka Z, Casuscelli J, Stirdivant S, Tang J, Schultz N, Jeng P, Dong Y, Su W, Cheng EH, Russo P, Coleman JA, Papaemmanuil E, Chen YB, Reuter VE, Sander C, Kennedy SR, Hsieh JJ, Lyssiotis CA, Tickoo SK, Hakimi AA. Abnormal oxidative metabolism in a quiet genomic background underlies clear cell papillary renal cell carcinoma. ELife 2019, 8: e38986. PMID: 30924768, PMCID: PMC6459676, DOI: 10.7554/elife.38986.Peer-Reviewed Original ResearchMeSH KeywordsAerobiosisCarcinoma, Renal CellCell RespirationHistocytochemistryHumansImmunohistochemistryKidney NeoplasmsMetabolic Networks and PathwaysOxidation-ReductionConceptsClear cell papillary renal cell carcinomaMtDNA-encoded proteinsPapillary renal cell carcinomaMetabolic phenotypeRenal cell carcinomaNuclear genomeDistinct metabolic phenotypesMitochondrial DNACell carcinomaRespiratory metabolismGenomic sequencingMolecular phenotypesAbnormal oxidative metabolismSugar alcohol sorbitolPresence of glycogenStudy of cancerMajority of cancersOncogenic alterationsPhenotypeOxidative stressOxidative metabolismCytoplasmic clarityDriver lesionsImmunohistochemical stainingKidney tumors