2022
Comprehensive Analysis of Metabolic Isozyme Targets in Cancer
Marczyk M, Gunasekharan V, Casadevall D, Qing T, Foldi J, Sehgal R, Shan NL, Blenman KRM, O'Meara TA, Umlauf S, Surovtseva YV, Muthusamy V, Rinehart J, Perry RJ, Kibbey R, Hatzis C, Pusztai L. Comprehensive Analysis of Metabolic Isozyme Targets in Cancer. Cancer Research 2022, 82: 1698-1711. PMID: 35247885, PMCID: PMC10883296, DOI: 10.1158/0008-5472.can-21-3983.Peer-Reviewed Original ResearchConceptsPotential therapeutic targetAcetyl-CoA carboxylase 1Therapeutic targetCancer typesCell linesBreast cancer viabilityPatient-derived xenograftsNovel metabolic targetsCorresponding cell linesExpression patternsDrug treatmentMatching normal tissuesRelated commentaryTumor growthMalignant transformationSmall molecule inhibitionCancer viabilityCancer Cell Line EncyclopediaNormal tissuesMetabolic vulnerabilitiesCarboxylase 1Anticancer therapyCellular changesCell proliferationMetabolic reprogramming
2020
Endocrine-Exocrine Signaling Drives Obesity-Associated Pancreatic Ductal Adenocarcinoma
Chung KM, Singh J, Lawres L, Dorans KJ, Garcia C, Burkhardt DB, Robbins R, Bhutkar A, Cardone R, Zhao X, Babic A, Vayrynen SA, Dias Costa A, Nowak JA, Chang DT, Dunne RF, Hezel AF, Koong AC, Wilhelm JJ, Bellin MD, Nylander V, Gloyn AL, McCarthy MI, Kibbey RG, Krishnaswamy S, Wolpin BM, Jacks T, Fuchs CS, Muzumdar MD. Endocrine-Exocrine Signaling Drives Obesity-Associated Pancreatic Ductal Adenocarcinoma. Cell 2020, 181: 832-847.e18. PMID: 32304665, PMCID: PMC7266008, DOI: 10.1016/j.cell.2020.03.062.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCarcinogenesisCarcinoma, Pancreatic DuctalCell LineCell Line, TumorCell Transformation, NeoplasticDisease Models, AnimalDisease ProgressionEndocrine CellsExocrine GlandsFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, Inbred C57BLMutationObesityPancreatic NeoplasmsSignal TransductionTumor MicroenvironmentConceptsPancreatic ductal adenocarcinomaPDAC progressionDuctal adenocarcinomaMajor modifiable risk factorModifiable risk factorsBeta cell expressionObesity-associated changesAutochthonous mouse modelPancreatic ductal tumorigenesisDriver gene mutationsPeptide hormone cholecystokininRisk factorsPDAC developmentMouse modelObesityHormone cholecystokininOncogenic KrasCell expressionTumor microenvironmentDietary inductionCancer developmentGene mutationsReversible roleMurine samplesProgression
2019
N-acyl taurines are endogenous lipid messengers that improve glucose homeostasis
Grevengoed TJ, Trammell SAJ, McKinney MK, Petersen N, Cardone RL, Svenningsen JS, Ogasawara D, Nexøe-Larsen CC, Knop FK, Schwartz TW, Kibbey RG, Cravatt BF, Gillum MP. N-acyl taurines are endogenous lipid messengers that improve glucose homeostasis. Proceedings Of The National Academy Of Sciences Of The United States Of America 2019, 116: 24770-24778. PMID: 31740614, PMCID: PMC6900532, DOI: 10.1073/pnas.1916288116.Peer-Reviewed Original ResearchMeSH KeywordsAmidohydrolasesAmino Acid SubstitutionAnimalsBlood GlucoseDisease Models, AnimalEatingEthanolaminesFemaleGlucagonGlucagon-Like Peptide 1Glucose Tolerance TestHumansInjections, IntravenousInsulinIslets of LangerhansMaleMetabolic SyndromeMiceMice, TransgenicMiddle AgedOleic AcidsPostprandial PeriodReceptors, G-Protein-CoupledTaurineConceptsFatty acid amide hydrolaseGLP-1 secretionPostprandial glucose regulationN-acyl taurinesBioactive fatty acid amidesEndogenous lipid messengersGlucagon secretionGlucose toleranceInsulin sensitivityUnique metabolic profileFood intakeGLP-1Peripheral tissuesMouse modelGlucose homeostasisLipid messengersGlucose regulationMetabolic diseasesAmide hydrolaseFunctional polymorphismsConcurrent elevationSubstantial elevationMetabolic profileFatty acid amidesMiceChildhood Pancreatitis and Risk for Incident Diabetes in Adulthood
Bendor CD, Bardugo A, Zucker I, Cukierman-Yaffe T, Lutski M, Derazne E, Shohat T, Mosenzon O, Tzur D, Sapir A, Pinhas-Hamiel O, Kibbey RG, Raz I, Afek A, Gerstein HC, Tirosh A, Twig G. Childhood Pancreatitis and Risk for Incident Diabetes in Adulthood. Diabetes Care 2019, 43: 145-151. PMID: 31694859, PMCID: PMC7011197, DOI: 10.2337/dc19-1562.Peer-Reviewed Original ResearchConceptsIsraeli National Diabetes RegistryIncident diabetesAcute pancreatitisNormal pancreatic functionUnexposed groupPancreatic functionOdds ratioChildhood pancreatitisIncident type 2 diabetesNational Diabetes RegistryPopulation-based studyType 2 diabetesDiagnosis of diabetesLogistic regression analysisYears of ageBaseline BMINormal BMIDiabetes RegistryRisk factorsPancreatitisCase subjectsSociodemographic confoundersDiabetesYounger ageFurther adjustment