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Blood, 15 April 2004, Vol. 103, No. 8, pp. 3230-3232. Prepublished online as a Blood First Edition Paper on December 30, 2003; DOI 10.1182/blood-2003-06-1985. This Article Full Text (PDF) All Versions of this Article: 2003-06-1985v1 103/8/3230    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Jakupovic, I. Articles by Khwaja, A. Search for Related Content PubMed PubMed Citation Articles by Jakupovic, I. Articles by Khwaja, A. Social Bookmarking                   What's this? Submitted June 19, 2003 Accepted December 19, 2003 Lack of effect of the human GM-CSF analogue E21R on the survival of primary human acute myeloid leukaemia cells Ira Jakupovic, Victoria L Grandage, David C Linch, and Asim Khwaja* Haematology, Royal Free & University College Medical School, London, United Kingdom * Corresponding author; email: a.khwaja{at}ucl.ac.uk. The GM-CSF analogue E21R binds to the GM-CSF receptor complex with low affinity and acts as a competitive antagonist. In addition, it has been reported to be a potent direct activator of apoptosis in primary human acute myeloid leukaemia (AML) cells. We have confirmed the ability of E21R to neutralise the biological effects of GM-CSF and investigated its activity on primary AML blasts. We find that it failed to induce cell death in blast cells from 23 separate AML cases treated in vitro at concentrations of E21R up to 30µg/ml. Significant cell death resulted in all cases after incubation with cytosine arabinoside. The lack of effect of E21R on AML blasts was unlikely to be due to an absence of functional GM-CSF receptors as 13 cases demonstrated an increase in cell number with the addition of exogenous GM-CSF. These results do not support the use of E21R for the treatment of AML. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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