Haematopoiesis is controlled by a number of growth factors and cytokines, a number of which act through binding to high-affinity receptor tyrosine kinases (RTKs). Approximately 20 different RTK classes have been identified, all of which share a similar structure that includes a ligand binding extracellular domain, a single transmembrane domain and an intracellular tyrosine kinase domain. Recent studies have linked an increasing number of mutations in the RTKs to the pathogenesis of both acute and chronic leukaemia. For example, the FLT3 receptor, a RTK class III, is the most commonly mutated gene in acute myeloid leukaemia, while c-kit mutations are strongly linked to the development of mast cell malignancy. This review summarizes the RTK classes that are known to be expressed on normal haematopoietic tissue and highlights the many 'gain-of-function' mutations involved in leukaemogenesis. It is to be hoped that this knowledge will provide important new insights for targeted therapy in leukaemia.

中文翻译：

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正常和恶性造血过程中的受体酪氨酸激酶。

造血作用受多种生长因子和细胞因子的控制，其中许多因子通过与高亲和力受体酪氨酸激酶（RTK）结合而起作用。已鉴定出约20种不同的RTK类，所有这些类均具有相似的结构，包括与配体结合的细胞外结构域，单个跨膜结构域和细胞内酪氨酸激酶结构域。最近的研究已将越来越多的RTK突变与急性和慢性白血病的发病机制联系起来。例如，FLT3受体，RTK III类，是急性髓细胞性白血病中最常见的突变基因，而c​​-kit突变与肥大细胞恶性肿瘤的发生密切相关。这篇综述总结了已知在正常造血组织上表达的RTK类，并强调了许多' 白血病发生中涉及的“功能获得”突变。希望这一知识将为白血病的靶向治疗提供重要的新见解。