2020
JAK inhibition synergistically potentiates BCL2, BET, HDAC, and proteasome inhibition in advanced CTCL
Yumeen S, Mirza FN, Lewis JM, King ALO, Kim SR, Carlson KR, Umlauf SR, Surovtseva YV, Foss FM, Girardi M. JAK inhibition synergistically potentiates BCL2, BET, HDAC, and proteasome inhibition in advanced CTCL. Blood Advances 2020, 4: 2213-2226. PMID: 32437546, PMCID: PMC7252559, DOI: 10.1182/bloodadvances.2020001756.Peer-Reviewed Original ResearchConceptsCutaneous T-cell lymphomaJAK inhibitionCTCL cellsMalignant cutaneous T-cell lymphomasAdvanced cutaneous T-cell lymphomaTreatment of CTCLAvailable systemic treatment optionsSkin-homing T lymphocytesSystemic treatment optionsT-cell lymphomaCTCL cell linesHistone deacetylase inhibitionGeneralized cytotoxic effectExpression of Bcl2Advanced diseaseSuch patientsPeripheral bloodTreatment optionsJAK/STAT pathwayT lymphocytesPreclinical assessmentTherapeutic targetStrong potentiationExtrinsic apoptosis pathwayDeacetylase inhibition
2018
BET inhibition in advanced cutaneous T cell lymphoma is synergistically potentiated by BCL2 inhibition or HDAC inhibition
Kim R, Lewis JM, Cyrenne BM, Monico PF, Mirza FN, Carlson KR, Foss FM, Girardi M. BET inhibition in advanced cutaneous T cell lymphoma is synergistically potentiated by BCL2 inhibition or HDAC inhibition. Oncotarget 2018, 9: 29193-29207. PMID: 30018745, PMCID: PMC6044378, DOI: 10.18632/oncotarget.25670.Peer-Reviewed Original ResearchCutaneous T-cell lymphomaT-cell lymphomaCTCL cellsBCL2 inhibitionCell lymphomaAdvanced cutaneous T-cell lymphomaHDAC inhibitionSkin-homing T cellsPromising novel therapeutic strategyBET inhibitionNon-Hodgkin lymphomaPotential novel therapyCTCL cell linesDose-dependent decreaseNovel therapeutic strategiesHistone deacetylase inhibitionExtraterminal protein inhibitorSystemic therapyLymph nodesPeripheral bloodNovel therapiesT cellsTherapeutic strategiesCaspase-3/7 activationAdvanced stage
2017
Synergy of BCL2 and histone deacetylase inhibition against leukemic cells from cutaneous T-cell lymphoma patients
Cyrenne BM, Lewis JM, Weed JG, Carlson KR, Mirza FN, Foss FM, Girardi M. Synergy of BCL2 and histone deacetylase inhibition against leukemic cells from cutaneous T-cell lymphoma patients. Blood 2017, 130: 2073-2083. PMID: 28972015, PMCID: PMC5680613, DOI: 10.1182/blood-2017-06-792150.Peer-Reviewed Original ResearchConceptsCutaneous T-cell lymphomaB-cell lymphoma 2Advanced cutaneous T-cell lymphomaCutaneous T-cell lymphoma patientsHDAC inhibitionT-cell lymphoma patientsNovel BCL2 inhibitorPeripheral blood involvementAvailable systemic therapiesWorse clinical outcomesTreatment of patientsNon-Hodgkin lymphomaT-cell lymphomaCTCL cell linesPotential therapeutic targetHistone deacetylase inhibitionQuality of lifeHistone deacetylase inhibitorsBlood involvementSystemic therapyClinical outcomesTumor burdenLymphoma patientsCombination therapyBCL2 inhibitors
2011
Characterization of the DNA Copy-Number Genome in the Blood of Cutaneous T-Cell Lymphoma Patients
Lin WM, Lewis JM, Filler RB, Modi BG, Carlson KR, Reddy S, Thornberg A, Saksena G, Umlauf S, Oberholzer PA, Karpova M, Getz G, Mane S, Garraway LA, Dummer R, Berger CL, Edelson RL, Girardi M. Characterization of the DNA Copy-Number Genome in the Blood of Cutaneous T-Cell Lymphoma Patients. Journal Of Investigative Dermatology 2011, 132: 188-197. PMID: 21881587, PMCID: PMC3841973, DOI: 10.1038/jid.2011.254.Peer-Reviewed Original ResearchConceptsCutaneous T-cell lymphomaBlood involvementLeukemic cutaneous T-cell lymphomaCutaneous T-cell lymphoma patientsT-cell lymphoma patientsNormal CD4 countPeripheral blood isolatesT-cell lymphomaCTCL cell linesPotential future therapeutic developmentsT-cell malignanciesFuture therapeutic developmentSignificant copy number alterationsCD4 countSpectrum of stagesCTCL patientsSézary syndromeLymph nodesLymphoma patientsHodgkin's lymphomaPeripheral bloodBlood isolatesCutaneous patchCTCL samplesPatientsHigh-throughput mutation profiling of CTCL samples reveals KRAS and NRAS mutations sensitizing tumors toward inhibition of the RAS/RAF/MEK signaling cascade
Kießling M, Oberholzer PA, Mondal C, Karpova MB, Zipser MC, Lin WM, Girardi M, MacConaill LE, Kehoe SM, Hatton C, French LE, Garraway LA, Polier G, Süss D, Klemke CD, Krammer PH, Gülow K, Dummer R. High-throughput mutation profiling of CTCL samples reveals KRAS and NRAS mutations sensitizing tumors toward inhibition of the RAS/RAF/MEK signaling cascade. Blood 2011, 117: 2433-2440. PMID: 21209378, PMCID: PMC3952811, DOI: 10.1182/blood-2010-09-305128.Peer-Reviewed Original ResearchMeSH KeywordsBiopsyHigh-Throughput Screening AssaysHumansLymphoma, T-Cell, CutaneousMitogen-Activated Protein Kinase KinasesMutationMycosis FungoidesNeoplasm StagingProtein Kinase InhibitorsProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)Raf KinasesRas ProteinsSezary SyndromeSignal TransductionConceptsCutaneous T-cell lymphomaStage IV patientsHUT78 cellsIV patientsPleomorphic cutaneous T-cell lymphomaHigh-throughput mutation profilingMEK inhibitorsCTCL cell line Hut78T-cell lymphomaRAS/RAF/MEKCTCL cell linesOncogenic mutationsCommon oncogenic mutationsCTCL patientsOverall survivalSézary syndromeMycosis fungoidesBiopsy specimensPatients profitPreclinical resultsMEK inhibitor U0126NRAS mutationsLymphoid cellsCTCL samplesRAS mutations