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
2008
To kill a tumor cell: the potential of proapoptotic receptor agonists
Ashkenazi A, Herbst RS. To kill a tumor cell: the potential of proapoptotic receptor agonists. Journal Of Clinical Investigation 2008, 118: 1979-1990. PMID: 18523647, PMCID: PMC2396896, DOI: 10.1172/jci34359.Peer-Reviewed Original ResearchConceptsProapoptotic receptor agonistsApo2L/TRAILReceptor agonistRecombinant human Apo2L/TRAILExtrinsic apoptosis pathwayPotential therapeutic interventionsNovel molecular biomarkersApoptosis pathwayAgonistic mAbConventional therapyPreclinical dataTherapeutic interventionsTumor cellsMolecular biomarkersAbnormal cellsLogical targetTherapyAgonistsCellsExciting opportunitiesTumorigenesisPatientsApoptosisPathway
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