Featured Publications
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
2023
Decoding the obesity–cancer connection: lessons from preclinical models of pancreatic adenocarcinoma
Ruiz C, Garcia C, Jacox J, Lawres L, Muzumdar M. Decoding the obesity–cancer connection: lessons from preclinical models of pancreatic adenocarcinoma. Life Science Alliance 2023, 6: e202302228. PMID: 37648285, PMCID: PMC10474221, DOI: 10.26508/lsa.202302228.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaCarcinogenesisCell Transformation, NeoplasticHumansObesityPancreatic NeoplasmsConceptsPancreatic adenocarcinomaPreclinical modelsObesity-cancer connectionObesity-associated cancersMicrobial dysbiosisHormone dysregulationEarly progressionRisk factorsWorldwide prevalencePancreatic tumorigenesisObesityPreclinical modelingCancer typesCancer developmentTumor cellsAdenocarcinomaTumor initiationCancerMetabolic stateCellular metabolismNovel strategyDysbiosisInflammationTherapyPrevalence