Acute myeloid leukemia (AML) is a heterogeneous disease with limited therapeutic options. A new study identifies leukocyte immunoglobulin-like receptor 3 (LILRB3) as a marker of monocytic AML, with the ability to modulate NF-κB signaling and to promote survival and immune evasion. Blockade of LILRB3 signaling could provide a novel therapeutic strategy in monocytic AML.
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CLPs-miR-103a-2-5p inhibits proliferation and promotes cell apoptosis in AML cells by targeting LILRB3 and Nrf2/HO-1 axis, regulating CD8 + T cell response
Journal of Translational Medicine Open Access 14 March 2024
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Lasry, A., Aifantis, I. LILRB3 as a regulator of AML survival. Nat Cancer 2, 1122–1123 (2021). https://doi.org/10.1038/s43018-021-00285-7
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DOI: https://doi.org/10.1038/s43018-021-00285-7
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CLPs-miR-103a-2-5p inhibits proliferation and promotes cell apoptosis in AML cells by targeting LILRB3 and Nrf2/HO-1 axis, regulating CD8 + T cell response
Journal of Translational Medicine (2024)