Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Correspondence
  • Published:

Immunophenotypic normalization of aberrant mast cells accompanies histological remission in imatinib-treated patients with eosinophilia-associated mastocytosis

Leukemia volume 18, pages 1027–1029 (2004)Cite this article

TO THE EDITOR

Imatinib mesylate produces complete hematologic and cytogenetic remissions in chronic myeloid leukemia (CML) by effectively inhibiting the resident BCR/ABL oncoprotein.1 More recently, the drug was also shown to be active in eosinophilic and mast cell disorders in the absence of the bcr/abl mutation.2,3 The drug target in the latter disorders was subsequently discovered to be an activating mutation of the platelet-derived growth factor receptor-α gene (FIP1L1-PDGFRA).4,5 In the current case report, we demonstrate a morphologic as well as immunophenotypic normalization of bone marrow mast cells in a patient with eosinophilia-associated systemic mastocytosis treated with imatinib mesylate.

This is a preview of subscription content, access via your institution

Access options

Buy this article

  • Purchase on Springer Link
  • Instant access to full article PDF
Buy now

Prices may be subject to local taxes which are calculated during checkout

Figure 1

References

  1. Druker BJ, Talpaz M, Resta DJ, Peng B, Buchdunger E, Ford JM et al. Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. N Engl J Med 2001; 344: 1031–1037.

    Article  CAS  Google Scholar 

  2. Gleich GJ, Leiferman KM, Pardanani A, Tefferi A, Butterfield JH . Treatment of hypereosinophilic syndrome with imatinib mesilate. Lancet 2002; 359: 1577–1578.

    Article  CAS  Google Scholar 

  3. Pardanani A, Elliott M, Reeder T, Li C-Y, Baxter EJ, Cross NCP et al. Imatinib for systemic mast-cell disease. Lancet 2003; 362: 535–536.

    Article  CAS  Google Scholar 

  4. Cools J, DeAngelo DJ, Gotlib J, Stover EH, Legare RD, Cortes J et al. A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome. N Engl J Med 2003; 348: 1201–1214.

    Article  CAS  Google Scholar 

  5. Pardanani A, Ketterling RP, Brockman SR, Flynn HC, Paternoster SF, Shearer BM et al. CHIC2 deletion, a surrogate for FIP1L1-PDGFRA fusion, occurs in systemic mastocytosis associated with eosinophilia and predicts response to imatinib therapy. Blood 2003; 102: 3093–3096.

    Article  CAS  Google Scholar 

  6. Pardanani A, Kimlinger TK, Reeder TL, Li CY, Tefferi A . Differential expression of CD2 on neoplastic mast cells in patients with systemic mast cell disease with and without an associated clonal haematological disorder. Br J Haematol 2003; 120: 691–694.

    Article  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Mayo Clinic, Rochester, MN, USA

    M A Elliott, A Pardanani, C Y Li & A Tefferi

Authors
  1. M A Elliott
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. A Pardanani
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. C Y Li
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. A Tefferi
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to A Tefferi.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Elliott, M., Pardanani, A., Li, C. et al. Immunophenotypic normalization of aberrant mast cells accompanies histological remission in imatinib-treated patients with eosinophilia-associated mastocytosis. Leukemia 18, 1027–1029 (2004). https://doi.org/10.1038/sj.leu.2403329

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/sj.leu.2403329

This article is cited by

Search

Advanced search

Quick links