کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5527483 | 1547725 | 2017 | 11 صفحه PDF | دانلود رایگان |
- This review provides a summary of the genetic, biological, and cellular differences between adult and childhood acute myeloid leukemia (AML).
- The role of leukemic stem cells in AML is reviewed.
- The rationale for anti-CD33 therapy in adult and childhood AML is discussed.
Acute myeloid leukemia (AML) develops when there is a block in differentiation and uncontrolled proliferation of myeloid precursors, resulting in bone marrow failure. AML is a clinically, morphologically, and genetically heterogeneous disease, and biological differences between adult and childhood AML have been identified. AML comprises 15%-20% of all children <15Â years of age diagnosed with acute leukemia. Relapse occurs in up to 40% of children with AML and is the most common cause of death. Relapse arises from leukemic stem cells (LSCs) that persist after conventional chemotherapy. The treatment of AML is challenging, and new strategies to target LSCs are required. The cell surface marker CD33 has been identified as a therapeutic target, and novel anti-CD33 immunotherapies are promising new agents in the treatment of AML. This review summarizes recent developments emphasizing the genetic differences in adult and childhood AML and highlights the rationale for CD33 as a target for therapy in all age groups.
Journal: Experimental Hematology - Volume 54, October 2017, Pages 40-50