2017
Human Pancreatic Cancer Cells Induce a MyD88-Dependent Stromal Response to Promote a Tumor-Tolerant Immune Microenvironment
Delitto D, Delitto AE, DiVita BB, Pham K, Han S, Hartlage ER, Newby BN, Gerber MH, Behrns KE, Moldawer LL, Thomas RM, George TJ, Brusko TM, Mathews CE, Liu C, Trevino JG, Hughes SJ, Wallet SM. Human Pancreatic Cancer Cells Induce a MyD88-Dependent Stromal Response to Promote a Tumor-Tolerant Immune Microenvironment. Cancer Research 2017, 77: 672-683. PMID: 27864347, PMCID: PMC5290036, DOI: 10.1158/0008-5472.can-16-1765.Peer-Reviewed Original ResearchConceptsTumor-associated stromaPancreatic cancerTumor microenvironmentT cell-mediated cytotoxicityCancer cell-conditioned mediumImmunosuppressive tumor microenvironmentT cell proliferationCell-conditioned mediumHuman cell culture modelsTh1 ratioProtective immunityCancer differsHealthy controlsMemory Th17Pancreatic lysatesCell culture modelPrimary human cell culture modelsRobust secretionCancer cellsCD8TA responsesPatientsImmunomodulatory characterCancerCulture model
2015
Patient-Derived Xenograft Models for Pancreatic Adenocarcinoma Demonstrate Retention of Tumor Morphology through Incorporation of Murine Stromal Elements
Delitto D, Pham K, Vlada AC, Sarosi GA, Thomas RM, Behrns KE, Liu C, Hughes SJ, Wallet SM, Trevino JG. Patient-Derived Xenograft Models for Pancreatic Adenocarcinoma Demonstrate Retention of Tumor Morphology through Incorporation of Murine Stromal Elements. American Journal Of Pathology 2015, 185: 1297-1303. PMID: 25770474, PMCID: PMC4419203, DOI: 10.1016/j.ajpath.2015.01.016.Peer-Reviewed Original ResearchConceptsPancreatic adenocarcinoma specimensStromal elementsTumor morphologyAdenocarcinoma specimensSuccessful engraftmentXenograft modelPatient-derived xenograft modelsCancer cellsPatient-derived xenograftsPancreatic adenocarcinoma xenograftsAdenocarcinoma xenograft modelTumor-stromal interactionsPatient demographicsClinicopathologic factorsPatient survivalNonobese diabeticPancreatic adenocarcinomaSurgical specimensImmunodeficiency miceInitial implantationPathological analysisPreclinical platformAdenocarcinoma xenograftsXenograft microenvironmentTumor growth
2012
An in vivo model of epithelial to mesenchymal transition reveals a mitogenic switch
Jahn SC, Law ME, Corsino PE, Parker NN, Pham K, Davis BJ, Lu J, Law BK. An in vivo model of epithelial to mesenchymal transition reveals a mitogenic switch. Cancer Letters 2012, 326: 183-190. PMID: 22906417, PMCID: PMC3705571, DOI: 10.1016/j.canlet.2012.08.013.Peer-Reviewed Original ResearchConceptsCancer cellsPre-EMT cellsNumber of genesMesenchymal transitionDNA microarray analysisEpithelial cell transitionPost-EMT cellsMitogenic signalingMicroarray analysisCell transitionMesenchymal phenotypeBreast cancer cellsERK phosphorylationLPA receptorsVivo modelMEK inhibitorsTissue architectureGrowth inhibitory effectsEpithelial cellsC-MetInhibitors/antagonistsPDGFCellsPhenotypeEMTGlucocorticoids and histone deacetylase inhibitors cooperate to block the invasiveness of basal-like breast cancer cells through novel mechanisms
Law ME, Corsino PE, Jahn SC, Davis BJ, Chen S, Patel B, Pham K, Lu J, Sheppard B, Nørgaard P, Hong J, Higgins P, Kim JS, Luesch H, Law BK. Glucocorticoids and histone deacetylase inhibitors cooperate to block the invasiveness of basal-like breast cancer cells through novel mechanisms. Oncogene 2012, 32: 1316-1329. PMID: 22543582, PMCID: PMC3773700, DOI: 10.1038/onc.2012.138.Peer-Reviewed Original ResearchConceptsE-cadherin localizationE-cadherinPlasma membraneCytoplasmic vesiclesWild-type E-cadherinBreast cancer cellsSerine protease inhibitor plasminogen activator inhibitor-1HDAC inhibitorsCancer cellsBasal-like breast cancer cellsPro-invasive activityGreen fluorescent proteinFull-length formCDCP1 cleavageAnti-invasive functionInhibitor plasminogen activator inhibitor-1MDA-MB-231 cellsHistone deacetylase inhibitorsTriple-negative breast cancerE-cadherin levelsCellular invasionE-cadherin expressionFluorescent proteinCDCP1 proteinOrthotopic xenograft tumors