Abstract
Many cases of hypereosinophilia, formerly classified as hypereosinophilic syndrome, can now be characterized as chronic eosinophilic leukemia (CEL) based on the demonstration of characteristic genetic markers indicating clonality of hematopoiesis. Here we report on a 33-year-old male patient with central nervous system manifestations of CEL and an excellent response to low-dose imatinib (Glivec). Molecular analysis demonstrated a constitutive activation of the platelet-derived growth factor receptor-alpha (PDGFR-A) as the mechanism of responsiveness to imatinib.
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Abbreviations
- BM:
-
Bone marrow
- CEL:
-
Chronic eosinophilic leukemia
- CML:
-
Chronic myeloid leukemia
- CNS:
-
Central nervous system
- HES:
-
Hypereosinophilic syndrome
- FIP1L1:
-
FIP1-like gene
- PB:
-
Peripheral blood
- PDGFR-A/B:
-
Platelet-derived growth factor receptor-alpha/beta
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Acknowledgements
We would like to thank PD Dr. Claudia Schoch, Munich and Dr. Schwab, Wiesbaden for performing cytogenetics, FISH, and PCR analysis to exclude classic CML.
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Frickhofen, N., Märker-Hermann, E., Reiter, A. et al. Complete molecular remission of chronic eosinophilic leukemia complicated by CNS disease after targeted therapy with imatinib. Ann Hematol 83, 477–480 (2004). https://doi.org/10.1007/s00277-004-0845-z
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DOI: https://doi.org/10.1007/s00277-004-0845-z