Stirewalt Derek L, Meshinchi Soheil
Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA, USA.
Cancer Treat Res. 2010;145:85-108. doi: 10.1007/978-0-387-69259-3_6.
Acute myeloid leukemia (AML) is the most common form of leukemia in adults, and despite some recent progress in understanding the biology of the disease, AML remains the leading cause of leukemia-related deaths in adults and children. AML is a complex and heterogeneous disease, often involving multiple genetic defects that promote leukemic transformation and drug resistance. The cooperativity model suggests that an initial genetic event leads to maturational arrest in a myeloid progenitor cell, and subsequent genetic events induce proliferation and block apoptosis. Together, these genetic abnormalities lead to clonal expansion and frank leukemia. The purpose of this chapter is to review the biology of receptor tyrosine kinases (RTKs) in AML, exploring how RTKs are being used as novel prognostic factors and potential therapeutic targets.
急性髓系白血病（AML）是成人中最常见的白血病形式，尽管在了解该疾病生物学方面最近取得了一些进展，但AML仍然是成人和儿童白血病相关死亡的主要原因。AML是一种复杂的异质性疾病，通常涉及促进白血病转化和耐药性的多种基因缺陷。协同模型表明，初始基因事件导致髓系祖细胞成熟停滞，随后的基因事件诱导增殖并阻止细胞凋亡。这些基因异常共同导致克隆性扩增和明显的白血病。本章的目的是综述AML中受体酪氨酸激酶（RTK）的生物学，探讨RTK如何被用作新的预后因素和潜在的治疗靶点。
