Therapeutic targeting of FLT3 and associated drug resistance in acute myeloid leukemia.
Therapeutic targeting of FLT3 and associated drug resistance in acute myeloid leukemia.
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DOI：
10.1186/s13045-020-00992-1
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发表时间：
2020-11-19
影响因子：
28.5
通讯作者：
Wang HG
中科院分区：
文献类型：
--
作者：
Gebru MT;Wang HG
急性髓系白血病（AML）是一种异质性疾病，由影响髓系细胞分化和增殖的几种基因突变和细胞遗传学异常引起。FLT3是一种受体酪氨酸激酶，通常过表达或突变，其突变与AML预后不良相关。虽然积极的化疗通常随后进行造血干细胞移植是目前的标准治疗，但最近批准的FLT3靶向药物正在彻底改变自20世纪70年代以来一直保持不变的AML治疗。然而，尽管对靶向药物（如FLT3抑制剂）有显著的临床反应，但缓解几乎总是短暂的，并随后出现复发和耐药性。因此，迫切需要了解导致耐药性的分子机制，以防止复发。在这篇综述中，我们讨论了FLT3作为一个目标，并强调目前对FLT3抑制剂耐药性的理解。
Acute myeloid leukemia (AML) is a heterogeneous disease caused by several gene mutations and cytogenetic abnormalities affecting differentiation and proliferation of myeloid lineage cells. FLT3 is a receptor tyrosine kinase commonly overexpressed or mutated, and its mutations are associated with poor prognosis in AML. Although aggressive chemotherapy often followed by hematopoietic stem cell transplant is the current standard of care, the recent approval of FLT3-targeted drugs is revolutionizing AML treatment that had remained unchanged since the 1970s. However, despite the dramatic clinical response to targeted agents, such as FLT3 inhibitors, remission is almost invariably short-lived and ensued by relapse and drug resistance. Hence, there is an urgent need to understand the molecular mechanisms driving drug resistance in order to prevent relapse. In this review, we discuss FLT3 as a target and highlight current understanding of FLT3 inhibitor resistance.
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影响因子：
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作者：
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影响因子：
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DOI：
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发表时间：
2013-10-15
期刊：
Clinical cancer research : an official journal of the American Association for Cancer Research
影响因子：
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作者：
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