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Blood, 1 April 2002, Vol. 99, No. 7, pp. 2615-2616
BRIEF REPORT
Transient hematologic and clinical effect of E21R in a child with
end-stage juvenile myelomonocytic leukemia
Frédéric Bernard,
Caroline Thomas,
Jean
François Emile,
Timothy Hercus,
Bruno Cassinat,
Christine Chomienne, and
Jean Donadieu
From the Pediatric Department, Hemato-Oncology Unit,
CHU Montpellier, France; Pathology Department, Hôpital P Brousse,
Villejuif, France; Pediatric Hémato-Oncology Department, CHU,
Nantes, France; Cytokine Receptor Laboratory, Hanson Institute,
Adelaide, Australia; Laboratory of Biology of Hematopoietic cells,
Hôpital Saint Louis, Paris, France; and the Pediatric
Hemato-Oncology Department, Hôpital Trousseau, Paris, France.
E21R is a modified granulocyte macrophage-colony-stimulating
factor (GM-CSF) protein which results in antagonism of GM-CSF function
via selective binding to the GM-CSF receptor complex. Juvenile chronic
myelomonocytic leukemia (JMML) is a rare leukemia where spontaneous
proliferation of myeloid and monocytic precursors in patients' bone
marrow cultures is dependent on GM-CSF. For patients who progress after
systemic chemotherapy, there are no effective therapies. In vitro and
in vivo studies in an animal model demonstrating that E21R exerts an
antileukemic action prompted us to consider its potential utility in a
child with end-stage JMML. E21R was well-tolerated during the 3 courses
of subcutaneous treatment. A clear in vivo efficacy was observed after
2 courses of E21R but the disease appeared completely refractory during the third course. This novel therapeutic approach clearly deserves further evaluation in JMML.
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