慢性淋巴细胞白血病中SLAMF1与自噬和治疗敏感性的联系。

Molecular & cellular oncology Pub Date : 2018-04-10 eCollection Date: 2018-01-01 DOI:10.1080/23723556.2016.1143077
Cinzia Bologna, Silvia Deaglio
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引用次数: 6

摘要

我们最近报道了共刺激分子和微生物传感器SLAMF1(信号淋巴细胞激活分子家族1,也称为CD150)的表达在慢性淋巴细胞白血病(CLL)患者中丢失,其特征是总生存期较短。SLAMF1调节CLL对趋化因子的反应并调节自噬。SLAMF1的缺失使得CLL细胞对自噬诱导药物(包括b细胞CLL/淋巴瘤2 (BCL2)抑制剂)相对无反应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Linking SLAMF1 to autophagy and sensitivity to therapy in chronic lymphocytic leukemia.

Linking SLAMF1 to autophagy and sensitivity to therapy in chronic lymphocytic leukemia.

We recently reported that expression of the costimulatory molecule and microbial sensor SLAMF1 (signaling lymphocytic activation molecule family 1, also known as CD150) is lost in chronic lymphocytic leukemia (CLL) patients characterized by a shorter overall survival. SLAMF1 modulates CLL responses to chemokines and regulates autophagy. Loss of SLAMF1 renders CLL cells relatively unresponsive to autophagy-inducing drugs, including B-cell CLL/lymphoma 2 (BCL2) inhibitors.

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