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
2018
Adaptive and Reversible Resistance to Kras Inhibition in Pancreatic Cancer Cells
Chen PY, Muzumdar M, Dorans KJ, Robbins R, Bhutkar A, Del Rosario A, Mertins P, Qiao J, Schafer AC, Gertler F, Carr S, Jacks T. Adaptive and Reversible Resistance to Kras Inhibition in Pancreatic Cancer Cells. Cancer Research 2018, 78: 985-1002. PMID: 29279356, PMCID: PMC5837062, DOI: 10.1158/0008-5472.can-17-2129.Peer-Reviewed Original ResearchConceptsMurine PDAC cellsPDAC cellsNontranscriptional mechanismsKRAS inhibitorsGlobal phosphoproteomic profilingActivated KRASHallmark genetic alterationsTranscriptional changesPhosphoproteomic profilingCell signalingCell statesPathway componentsTumor-initiating capacityPancreatic ductal adenocarcinomaTemporal controlGenetic alterationsCell morphologyMechanistic directionsKras expressionKrasCellsProliferative kineticsInhibitorsNovel KRAS inhibitorsAdherence properties
2013
Targeting the HGF/c-MET Pathway in Hepatocellular Carcinoma
Goyal L, Muzumdar MD, Zhu AX. Targeting the HGF/c-MET Pathway in Hepatocellular Carcinoma. Clinical Cancer Research 2013, 19: 2310-2318. PMID: 23388504, PMCID: PMC4583193, DOI: 10.1158/1078-0432.ccr-12-2791.Peer-Reviewed Original ResearchConceptsAdvanced hepatocellular carcinomaHepatocellular carcinomaRational clinical trial designC-MetHGF/c-Met pathwayTyrosine kinase inhibitor sorafenibLimited survival benefitMajority of patientsCancer-related morbidityPathogenesis of HCCLatest clinical trialsKinase inhibitor sorafenibC-Met pathwayClinical trial designAdvanced diseaseLiver transplantationSurgical resectionSurvival benefitSystemic therapyLocal therapyTransarterial embolizationPreclinical dataClinical trialsInhibitor sorafenibTrial design