Targeting selective autophagy in acute myeloid leukemia (E08 (C05))

与正常造血干细胞相比，原发性急性髓性白血病（AML）样品中的自噬通量显著增加。基于我们以前的数据，我们现在的目标是了解AML中线粒体自噬的分子机制，我们的目标是确定调节线粒体自噬的激酶和激酶抑制剂。此外，我们计划研究MST激酶在调节AML自噬中的作用，并开发高度选择性的MST 1/2和MST 3/4抑制剂（所谓的化学探针），并评估其在AML新治疗策略中的潜力。

Autophagic flux is significantly increased in primary acute myeloid leukemia (AML) samples compared to normal hematopoietic stem cells. Based on our previous data, we now aim to understand the molecular mechanisms governing mitophagy in AML, and we aim to identify kinases and kinase inhibitors regulating mitophagy. Furthermore, we plan to study the role of MST kinases in regulating autophagy in AML and to develop highly selective MST1/2 and MST3/4 inhibitors (so called chemical probes), and to assess their potential for new treatment strategies in AML.