Acute myeloid leukemia (AML) is a type of leukemia with a poor prognosis and survival characterized by abnormal cell proliferation and differentiation. Despite advances in treatment, AML still has a low complete remission rate, particularly in elderly patients, and recurrences are frequently seen even after complete remissions. The major challenge in treating AML is the resistance of leukemia cells to chemotherapy drugs. Thus, to overcome this issue, it can be crucial to conduct new investigations to explore the mechanisms of chemo-resistance in AML and target them. In this review, the potential role of autophagy induced by FLT3-ITD and acid ceramidase in chemo-resistance in AML patients are analyzed. With regard to the high prevalence of FLT3-ITD mutation (about 25% of AML cases) and high level of acid ceramidase in these patients, we hypothesized that both of these factors could lead to chemo-resistance by inducing autophagy. Therefore, pharmacological targeting of autophagy, FLT3-ITD, and acid ceramidase production could be a promising therapeutic approach for such AML patients to overcome chemo-resistance.

中文翻译：

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FLT3-ITD 和酸性神经酰胺酶诱导的自噬在急性髓性白血病化疗耐药中的潜在作用：新见解

急性髓性白血病(acute myeloid leukemia, AML)是一类以细胞增殖和分化异常为特征的预后和生存较差的白血病。尽管治疗取得了进展，但 AML 的完全缓解率仍然很低，尤其是在老年患者中，而且即使在完全缓解后也经常会复发。治疗 AML 的主要挑战是白血病细胞对化疗药物的耐药性。因此，为了克服这个问题，进行新的研究以探索 AML 中的化学抗性机制并针对它们可能是至关重要的。在这篇综述中，分析了 FLT3-ITD 和酸性神经酰胺酶诱导的自噬在 AML 患者化疗耐药中的潜在作用。关于这些患者中 FLT3-ITD 突变的高患病率（约占 AML 病例的 25%）和高水平的酸性神经酰胺酶，我们假设这两个因素都可能通过诱导自噬而导致化学抗性。因此，针对自噬、FLT3-ITD 和酸性神经酰胺酶产生的药理学靶向可能是此类 AML 患者克服化疗耐药性的一种有前途的治疗方法。