Browse by author
Lookup NU author(s): Professor Christine Harrison FRCPath FMedSci
Full text for this publication is not currently held within this repository. Alternative links are provided below where available.
© 2017 ISEH - International Society for Experimental Hematology. 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 <15 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.
Author(s): Laing AA, Harrison CJ, Gibson BES, Keeshan K
Publication type: Article
Publication status: Published
Journal: Experimental Hematology
Print publication date: 01/10/2017
Online publication date: 28/06/2017
Acceptance date: 23/06/2017
ISSN (print): 0301-472X
ISSN (electronic): 1873-2399
Publisher: Elsevier Inc.
Altmetrics provided by Altmetric