Childhood acute myeloid leukaemia

被引:68
作者
Rubnitz, Jeffrey E. [1 ,2 ]
Inaba, Hiroto [1 ,2 ]
机构
[1] St Jude Childrens Res Hosp, Dept Oncol, Memphis, TN 38105 USA
[2] Univ Tennessee, Ctr Hlth Sci, Coll Med, Dept Paediat, Memphis, TN 38163 USA
基金
美国国家卫生研究院;
关键词
acute myeloid leukaemia; AML; childhood leukaemia; ACUTE MYELOGENOUS LEUKEMIA; STEM-CELL TRANSPLANTATION; MINIMAL RESIDUAL DISEASE; HIGH-DOSE CYTARABINE; BONE-MARROW-TRANSPLANTATION; COLONY-STIMULATING FACTOR; AGENT ARSENIC TRIOXIDE; NATURAL-KILLER-CELLS; ACUTE MYELOBLASTIC-LEUKEMIA; CHILDRENS-ONCOLOGY-GROUP;
D O I
10.1111/bjh.12040
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Although acute myeloid leukaemia (AML) has long been recognized for its morphological and cytogenetic heterogeneity, recent high-resolution genomic profiling has demonstrated a complexity even greater than previously imagined. This complexity can be seen in the number and diversity of genetic alterations, epigenetic modifications, and characteristics of the leukaemic stem cells. The broad range of abnormalities across different AML subtypes suggests that improvements in clinical outcome will require the development of targeted therapies for each subtype of disease and the design of novel clinical trials to test these strategies. It is highly unlikely that further gains in long-term survival rates will be possible by mere intensification of conventional chemotherapy. In this review, we summarize recent studies that provide new insight into the genetics and biology of AML, discuss risk stratification and therapy for this disease, and profile some of the therapeutic agents currently under investigation.
引用
收藏
页码:259 / 276
页数:18
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