FLT3-ITD. Clinical (Sorafenib/AC220)
作者： Naveen Pemmaraju , Jorge Eduardo Cortes
DOI: 10.1007/978-1-4939-1393-0_12
关键词:
摘要: A plethora of new molecular abnormalities has been identified to be associated with acute myelogenous leukemia (AML). These markers have contributed a more accurate prognostic stratification these patients, and nurtured hopes for effective targeted therapies. One such abnormality is the FMS-like tyrosine kinase 3, or FLT3 gene mutation, present in approximately 30 % AML patients. The presence internal tandem duplication (FLT3-ITD) confers poorer prognosis higher risk relapse this subset Rapid development large number inhibitors (TKIs) enabled an exciting era research treatment patients abnormalities. expectation that inhibition may offer improvements outcomes poor group Early data suggest promise materializing This chapter will focus on two inhibitors, sorafenib (Nexavar®) AC220 (quizartinib).
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