Access through your institution Buy or subscribe As the fusion gene _FIP1L1-PDGFRA_ was identified as being responsible for clonal evolution in some patients clinically diagnosed with

hypereosinophilic syndrome (HES), effective treatment with imatinib became available.1 The inhibitory effect of imatinib on the fusion tyrosine kinase leads to molecular remission in a

subset of patients after several months of therapy.2 The first report of effective imatinib treatment in HES was published in 2001, but the mechanism of action was not known at that time.3

Here, we describe a patient transplanted for HES in 2001 in whom the _FIP1L1-PDGFRA_ transcript was retrospectively shown to be eradicated after transplantation. Attempts of allogeneic stem

the course of the disease.5 Papers describing allogeneic transplantation in HES published are mostly case reports or deal with small series of patients. It is therefore difficult to

establish a transplantation standard for HES patients, particularly given the heterogeneity of the syndrome.6, 7 Recently, _FIP1L1-PDGFRA_ fusion gene was identified as a detrimental factor

causing disease evolution in a subset of patients. Accumulating data confirm imatinib efficacy in those patients. Unfortunately, less than 20% of HES patients carry the mutation.6, 8 Only

those patients have a sustained response to imatinib, whereas others mostly show a transient improvement. It is not known whether molecular remissions will be sustained if therapy is

interrupted, how long the treatment should be continued or if resistance to imatinib will emerge at some point of treatment. Also, it is not well established whether or not prolonged

imatinib administration will result in resolution of organ involvement.2 As in many myeloproliferative disorders, allogeneic stem cell transplantation is the only confirmed curative option

in HES. In case of imatinib failure in _FIP1L1-PDGFRA_-positive patients undergoing transplantation, the fusion transcript may serve as a highly sensitive tool for the evaluation of

molecular remission after grafting. This is a preview of subscription content, access via your institution ACCESS OPTIONS Access through your institution Subscribe to this journal Receive 12

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eosinophilia. _Blood_ 2004; 104: 3038–3045. Article  CAS  Google Scholar  Download references AUTHOR INFORMATION AUTHORS AND AFFILIATIONS * Department of Haematology, Medical University of

Gdańsk, Gdańsk, Poland K Halaburda, W Prejzner, D Szatkowski & A Hellmann * Department of Biology and Genetics, Medical University of Gdańsk, Gdańsk, Poland J Limon Authors * K Halaburda

View author publications You can also search for this author inPubMed Google Scholar * W Prejzner View author publications You can also search for this author inPubMed Google Scholar * D

Szatkowski View author publications You can also search for this author inPubMed Google Scholar * J Limon View author publications You can also search for this author inPubMed Google Scholar

* A Hellmann View author publications You can also search for this author inPubMed Google Scholar CORRESPONDING AUTHOR Correspondence to K Halaburda. RIGHTS AND PERMISSIONS Reprints and

permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Halaburda, K., Prejzner, W., Szatkowski, D. _et al._ Allogeneic bone marrow transplantation for hypereosinophilic syndrome: long-term

follow-up with eradication of _FIP1L1-PDGFRA_ fusion transcript. _Bone Marrow Transplant_ 38, 319–320 (2006). https://doi.org/10.1038/sj.bmt.1705437 Download citation * Published: 03 July

2006 * Issue Date: 01 August 2006 * DOI: https://doi.org/10.1038/sj.bmt.1705437 SHARE THIS ARTICLE Anyone you share the following link with will be able to read this content: Get shareable

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