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• W1760760259 abstract "Large granular lymphocyte (LGL) leukemia is a rare clonal disease characterized by a persistent increase in the number of CD8+ cytotoxic T cells or CD16/56+ natural killer (NK) cells.1 Patients are prone to recurrent infections and often suffer from severe cytopenias and autoimmune diseases that are thought to be mediated by cytotoxic LGL lymphocytes. LGL leukemia is believed to begin as an antigen-driven immune response followed by the constitutive activation of cytotoxic T lymphocytes or NK cells. Overall, studies have highlighted the dysregulation of different apoptotic pathways (for example, sphingolipid and FAS/FAS ligand) and the activation of survival signaling pathways (for example, PI3K/AKT and RAS).1" @default.
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• W1760760259 date "2015-09-30" @default.
• W1760760259 modified "2023-10-14" @default.
• W1760760259 title "Activating somatic mutations outside the SH2-domain of STAT3 in LGL leukemia" @default.
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• W1760760259 doi "https://doi.org/10.1038/leu.2015.263" @default.
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