2020
The role of survivin in the progression of pancreatic ductal adenocarcinoma (PDAC) and a novel survivin-targeted therapeutic for PDAC
Brown M, Zhang W, Yan D, Kenath R, Le L, Wang H, Delitto D, Ostrov D, Robertson K, Liu C, Pham K. The role of survivin in the progression of pancreatic ductal adenocarcinoma (PDAC) and a novel survivin-targeted therapeutic for PDAC. PLOS ONE 2020, 15: e0226917. PMID: 31929540, PMCID: PMC6957139, DOI: 10.1371/journal.pone.0226917.Peer-Reviewed Original ResearchConceptsPancreatic ductal adenocarcinomaTypes of cancerDuctal adenocarcinomaSurvivin expressionSurvivin inhibitorClinical response rateNovel survivin inhibitorHalf of patientsElevated survivin expressionLower patient survivalPancreatic tumor microenvironmentPotential therapeutic targetExpression of survivinRole of survivinField of oncologyPancreatic cancer linesImmunotherapeutic approachesPatient survivalUntreated cohortTherapeutic responseInhibitor of survivinTreatment resistancePDAC progressionEffective treatmentTumor cell migration
2018
RET rearrangements are actionable alterations in breast cancer
Paratala BS, Chung JH, Williams CB, Yilmazel B, Petrosky W, Williams K, Schrock AB, Gay LM, Lee E, Dolfi SC, Pham K, Lin S, Yao M, Kulkarni A, DiClemente F, Liu C, Rodriguez-Rodriguez L, Ganesan S, Ross JS, Ali SM, Leyland-Jones B, Hirshfield KM. RET rearrangements are actionable alterations in breast cancer. Nature Communications 2018, 9: 4821. PMID: 30446652, PMCID: PMC6240119, DOI: 10.1038/s41467-018-07341-4.Peer-Reviewed Original ResearchMeSH KeywordsAnilidesAnimalsAntineoplastic AgentsBreast NeoplasmsCell Line, TumorCell Transformation, NeoplasticFemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsMiceMice, NudeMitogen-Activated Protein KinasesNIH 3T3 CellsNuclear Receptor CoactivatorsOncogene Proteins, FusionPhosphatidylinositol 3-KinasesPiperidinesProto-Oncogene Proteins c-retPyridinesQuinazolinesRas Guanine Nucleotide Exchange FactorsReceptor, ErbB-2Signal TransductionXenograft Model Antitumor AssaysConceptsBreast cancerRET amplificationRET gene alterationsMetastatic breast cancerNCOA4-RET fusionXenograft tumor formationPI3K pathwayRadiographic responseActionable alterationsLung cancerRET fusionsRET alterationsRET inhibitionIndex caseTherapeutic targetRET rearrangementsCancerGenomic profilingGene alterationsK pathwayTumor formationGene RETNon-tumorigenic cellsSubsequent treatmentOncogenic potential
2015
Downstream mediators of the intratumoral interferon response suppress antitumor immunity, induce gemcitabine resistance and associate with poor survival in human pancreatic cancer
Delitto D, Perez C, Han S, Gonzalo DH, Pham K, Knowlton AE, Graves CL, Behrns KE, Moldawer LL, Thomas RM, Liu C, George TJ, Trevino JG, Wallet SM, Hughes SJ. Downstream mediators of the intratumoral interferon response suppress antitumor immunity, induce gemcitabine resistance and associate with poor survival in human pancreatic cancer. Cancer Immunology, Immunotherapy 2015, 64: 1553-1563. PMID: 26423423, PMCID: PMC5129167, DOI: 10.1007/s00262-015-1760-y.Peer-Reviewed Original ResearchMeSH KeywordsAdaptive ImmunityCell Line, TumorChemokine CXCL10DeoxycytidineDrug Resistance, NeoplasmEnzyme-Linked Immunosorbent AssayFlow CytometryGemcitabineGene Expression Regulation, NeoplasticHLA AntigensHumansInterferon-gammaInterferonsPancreatic NeoplasmsReceptors, CXCR3Tumor Cells, CulturedTumor MicroenvironmentConceptsPC cell linesPancreatic cancerAntitumor immunityPoor survivalPC microenvironmentHuman leukocyte antigen (HLA) class IMinimal inflammatory cell infiltrationEffective antitumor immunityImmune checkpoint ligandsUpregulation of PDL1Inflammatory cell infiltrationAntigen class IHuman pancreatic cancerAbsence of CD80Tumor-associated stromaCell linesCancer epithelial cellsCheckpoint ligandsCXCL10 concentrationsCell typesIFNγ responsesIndependent predictorsCD86 expressionChronic pancreatitisCell infiltration
2013
Expression and Functional Heterogeneity of Chemokine Receptors CXCR4 and CXCR7 in Primary Patient-Derived Glioblastoma Cells
Liu C, Pham K, Luo D, Reynolds BA, Hothi P, Foltz G, Harrison JK. Expression and Functional Heterogeneity of Chemokine Receptors CXCR4 and CXCR7 in Primary Patient-Derived Glioblastoma Cells. PLOS ONE 2013, 8: e59750. PMID: 23555768, PMCID: PMC3605406, DOI: 10.1371/journal.pone.0059750.Peer-Reviewed Original ResearchConceptsFunction of CXCR4Chemokine receptor CXCR4CXCR4-CXCR7Receptor CXCR4Common primary brain tumorPrimary human GBM cellsPrimary brain tumorsPersonalized treatment approachesTube formationSurface expressionPatient-derived GBM cell linesNew therapeutic targetsCell linesHuman GBM cellsPatient-derived glioblastoma cellsGBM cell linesClinical benefitPoor prognosisSuccessful treatmentCell surface expressionCXCR7 axisCXCL12-CXCR4Intracranial tumorsGBM patientsBrain tumors