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• W2112577492 abstract "Summary Pre‐B cells within the bone marrow represent the normal counterpart for most acute lymphoblastic leukemia ( ALL ). During normal early B‐cell development, survival and proliferation signals are dominated by cytokines, particularly interleukin‐7 ( IL ‐7) for murine developing B cells. With expression of a functional pre‐B‐cell receptor ( BCR ), cytokine signaling is attenuated and the tonic/autonomous pre‐ BCR signaling pathway provides proliferation as well as differentiation signals. In this review, we first describe checkpoint mechanisms during normal B‐cell development and then discuss how genetic lesions in these pathways function as oncogenic mimicries and allow transformed pre‐B cells to bypass checkpoint control. We focus on cytokine receptor signaling that is mimicked by activating lesions in receptor subunits or downstream mediators as well as aberrant activation of non‐B lymphoid cytokine receptors. Furthermore, we describe the molecular switch from cytokine receptor to pre‐ BCR signaling, how this pathway is of particular importance for certain ALL subtypes, and how pre‐ BCR signaling is engaged by genetic lesions, such as BCR ‐ ABL 1. We discuss the transcriptional control mechanisms downstream of both cytokine‐ and pre‐ BCR signaling and how normal checkpoint control mechanisms are circumvented in pre‐B ALL . Finally, we highlight new therapeutic concepts for targeted inhibition of oncogenic cytokine or pre‐ BCR signaling pathways." @default.
• W2112577492 created "2016-06-24" @default.
• W2112577492 creator A5049679155 @default.
• W2112577492 creator A5050087793 @default.
• W2112577492 creator A5074664283 @default.
• W2112577492 creator A5081605030 @default.
• W2112577492 date "2014-12-15" @default.
• W2112577492 modified "2023-10-17" @default.
• W2112577492 title "Mechanisms of pre-B-cell receptor checkpoint control and its oncogenic subversion in acute lymphoblastic leukemia" @default.
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