Moving toward individualized target-based therapies in acute myeloid leukemia

被引:31
作者
Bazinet, A. [1 ]
Kantarjian, H. M. [1 ,2 ]
机构
[1] Univ Texas MD Anderson Canc Ctr, Dept Leukemia, Houston, TX USA
[2] Univ Texas MD Anderson Canc Ctr, Dept Leukemia, 1515 Holcombe Blvd,Unit 428, Houston, TX 77030 USA
关键词
acute myeloid leukemia; targeted therapy; low-intensity therapy; personalized therapy; measurable residual disease; CORE-BINDING-FACTOR; ACUTE PROMYELOCYTIC LEUKEMIA; CONVENTIONAL CARE REGIMENS; ACUTE MYELOGENOUS LEUKEMIA; GENE-EXPRESSION PROFILE; HIGH-DOSE CYTARABINE; GEMTUZUMAB OZOGAMICIN; INDUCTION CHEMOTHERAPY; OLDER PATIENTS; ARSENIC TRIOXIDE;
D O I
10.1016/j.annonc.2022.11.004
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Acute myeloid leukemia (AML) is a heterogeneous disease at the genetic level. The field of AML therapy is increasingly shifting away from uniform approaches based solely on intensive chemotherapy (such as '7 + 3') toward personalized therapy. The treatment of AML can now be individualized based on patient characteristics and cytogenetic/molecular disease features. In this review, we provide a comprehensive updated summary of personalized, target-directed therapy in AML. We first discuss the selection of intensive versus low-intensity treatment approaches based on the patient's age and/or comorbidities. We follow with a detailed review of specific molecularly defined AML subtypes that benefit from the addition of targeted agents. In this context, we highlight the urgent need for novel therapies in tumor protein p53 (TP53)-mutated AML. We then propose approaches to optimize AML therapy in patients without directly actionable mutations. We conclude with a discussion on the emerging role of using measurable residual disease to modify therapy based on the quality of response.
引用
收藏
页码:141 / 151
页数:11
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