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Notch and T cell malignancy.

机译:切口和T细胞恶性肿瘤。

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摘要

Notch signaling is required for normal T cell development. However, Notch expression must be precisely regulated as constitutive Notch signaling leads to T cell lymphomas. Recent evidence has provided insights into potential mechanisms of Notch-mediated lymphomagenesis and its relationship to T cell development. The evidence suggests that Notch likely interacts with several important cellular pathways and can cooperate with other oncogenes during lymphomagenesis. In particular, Notch appears to modulate pre-TCR signaling, inhibit the E2A pathway, and in murine leukemia models, frequently cooperates with Myc, E2A-PBX and dominant negative Ikaros dysregulation. This review will present current knowledge in these areas and explore theories on Notch-mediated T cell lymphomagenesis.
机译:正常的T细胞发育需要Notch信号传导。但是,Notch表达必须被精确调节,因为组成性Notch信号传导会导致T细胞淋巴瘤。最近的证据提供了对Notch介导的淋巴瘤发生的潜在机制及其与T细胞发育的关系的见解。有证据表明,Notch可能与几种重要的细胞途径相互作用,并且可以在淋巴瘤发生过程中与其他癌基因协同作用。尤其是,Notch似乎可以调节TCR之前的信号传导,抑制E2A途径,在鼠白血病模型中,经常与Myc,E2A-PBX和显性负Ikaros失调协同作用。本文将介绍这些领域的最新知识,并探讨Notch介导的T细胞淋巴瘤发生的理论。

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