The case for extracellular Nm23-H1 as a driver of acute myeloid leukaemia (AML) progression

Studies in the 1990s identified a link between extracellular Nm23 proteins and acute myeloid leukaemia (AML). Confidence in the importance of these observations was undermined by a lack of appreciation that extracellular Nm23 proteins were relevant to either normal or pathophysiology coupled with th...

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Bibliographic Details
Published in:Naunyn-Schmiedeberg's archives of pharmacology 2015-02, Vol.388 (2), p.225-233
Main Authors: Lilly, A. Joshua, Khanim, Farhat L., Bunce, Christopher M.
Format: Article
Language:English
Subjects:
Animals
Biomedical and Life Sciences
Biomedicine
Disease Progression
Humans
Leukemia, Myeloid, Acute - metabolism
Mucin-1 - metabolism
Neurosciences
NM23 Nucleoside Diphosphate Kinases - metabolism
Pharmacology/Toxicology
Receptors, Cell Surface - metabolism
Review
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Summary:Studies in the 1990s identified a link between extracellular Nm23 proteins and acute myeloid leukaemia (AML). Confidence in the importance of these observations was undermined by a lack of appreciation that extracellular Nm23 proteins were relevant to either normal or pathophysiology coupled with the lack of demonstrable activity of Nm23 proteins against human AML cell lines. However, independent studies have highlighted the importance of Nm23-H1 in AML and have identified an elaborate Nm23-H1-mediated cross talk between cells within the AML clone. In other studies, roles for Nm23-H1 have now also been implicated in the maintenance of the stem cell state of embryonic stem (ES) cells and induced pluripotent stem (IPS) cells. In this review, we have generated a unifying model of the action of Nm23-H1 in AML, including previously unpublished data from our laboratory, and provide arguments as to why we consider this role to be distinct from that in ES and IPS cells.
ISSN:0028-1298
1432-1912
DOI:10.1007/s00210-014-1027-8