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 ResearchConceptsPancreatic adenocarcinomaPreclinical modelsObesity-cancer connectionObesity-associated cancersMicrobial dysbiosisHormone dysregulationEarly progressionRisk factorsWorldwide prevalencePancreatic tumorigenesisObesityPreclinical modelingCancer typesCancer developmentTumor cellsAdenocarcinomaTumor initiationCancerMetabolic stateCellular metabolismNovel strategyDysbiosisInflammationTherapyPrevalence
2018
iRGD-guided tumor-penetrating nanocomplexes for therapeutic siRNA delivery to pancreatic cancer
Lo JH, Hao L, Muzumdar MD, Raghavan S, Kwon EJ, Pulver EM, Hsu F, Aguirre AJ, Wolpin BM, Fuchs CS, Hahn WC, Jacks T, Bhatia SN. iRGD-guided tumor-penetrating nanocomplexes for therapeutic siRNA delivery to pancreatic cancer. Molecular Cancer Therapeutics 2018, 17: molcanther.1090.2017. PMID: 30097486, PMCID: PMC6298224, DOI: 10.1158/1535-7163.mct-17-1090.Peer-Reviewed Original ResearchConceptsPancreatic ductal adenocarcinomaPancreatic cancerCancer-related deathReceptor expression patternsSite of diseasePDAC cell linesMol Cancer TherTherapeutic trialsAutochthonous tumorsDuctal adenocarcinomaMouse modelStromal barrierTumor growthSystemic deliveryNeuropilin-1Peptide iRGDTumor-penetrating abilityThree-dimensional organoidsSiRNATumor targetingCell linesTherapyCancerStromaIRGD
2016
Clonal dynamics following p53 loss of heterozygosity in Kras-driven cancers
Muzumdar MD, Dorans KJ, Chung KM, Robbins R, Tammela T, Gocheva V, Li CM, Jacks T. Clonal dynamics following p53 loss of heterozygosity in Kras-driven cancers. Nature Communications 2016, 7: 12685. PMID: 27585860, PMCID: PMC5025814, DOI: 10.1038/ncomms12685.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaAnimalsCarcinogenesisCarcinoma, Pancreatic DuctalCell ProliferationCyclin-Dependent Kinase Inhibitor p16Disease ProgressionGene Expression Regulation, NeoplasticLung NeoplasmsMiceMice, TransgenicPancreatic NeoplasmsProto-Oncogene Proteins p21(ras)Tumor Cells, CulturedTumor Suppressor Protein p53ConceptsLung adenomasLow-grade pancreatic intraepithelial neoplasiaP53 lossEarly tumor progressionPancreatic intraepithelial neoplasiaAdvanced adenocarcinomaIntraepithelial neoplasiaPancreatic tumorsP53 knockoutSolid tumorsOncogenic KrasTumor progressionSuppressive roleTumor developmentExtensive cellular heterogeneityLineage-related cellsP53AdenomasTumorsCancerContiguous growthDouble markersProgressionDistinct clonesDifferential expression
2007
Modeling sporadic loss of heterozygosity in mice by using mosaic analysis with double markers (MADM)
Muzumdar MD, Luo L, Zong H. Modeling sporadic loss of heterozygosity in mice by using mosaic analysis with double markers (MADM). Proceedings Of The National Academy Of Sciences Of The United States Of America 2007, 104: 4495-4500. PMID: 17360552, PMCID: PMC1810340, DOI: 10.1073/pnas.0606491104.Peer-Reviewed Original ResearchConceptsTumor suppressor geneHuman cancersDouble markersCyclin-dependent kinase inhibitorLoss of heterozygositySporadic lossKinase inhibitorsMiceSporadic cellsSimilar degreeSomatic activationCancerCell-autonomous controlConcurrent labelingTSG lossCell expansionMarkersCellsProof of principleProtooncogeneMosaic analysisTSG function