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Blood, 1 May 2004, Vol. 103, No. 9, pp. 3549-3551.
Prepublished online as a Blood First Edition Paper on January 15, 2004; DOI 10.1182/blood-2003-08-2734.
Submitted August 8, 2003
Accepted December 30, 2003
Reversal of bone marrow angiogenesis in chronic myeloid leukemia following imatinib mesylate (STI571) therapy
Hans Michael Kvasnicka*, Juergen Thiele, Peter Staib, Annette Schmitt-Graeff, Martin Griesshammer, Jens Klose, Knut Engels, and Susanne Kriener
Institute of Pathology, University of Cologne, Cologne, Germany
First Clinic of Medicine, University of Cologne, Cologne, Germany
Institute of Pathology, University of Freiburg, Freiburg, Germany
Third Clinic of Medicine, University of Ulm, Ulm, Germany
Institute of Pathology, University of Frankfurt, Frankfurt, Germany
* Corresponding author; email: hm.kvasnicka{at}uni-koeln.de.
The effect of imatinib mesylate therapy on angiogenesis and myelofibrosis was investigated and compared with interferon (IFN) and hydroxyurea (HU) in 98 patients with newly diagnosed Ph+/BCR-ABL+ chronic myeloid leukemia in first chronic phase and no other pretreatment. By applying immunostaining (CD34) and morphometry a relationship between microvessel frequency and fiber density was detectable in initial bone marrow (BM) biopsies and sequential examinations after at least 8 months of therapy. First-line monotherapy with imatinib induced a significant reduction (normalization in comparison to controls) of microvessels and reticulin fibers. In most patients decrease in BM vascularity was associated with a complete cytogenetic response. A significant angiogenic effect was also observed after HU treatment, contrasting IFN administration or combination regimens (IFN+HU). In conclusion, our data support the angiogenic capacity of imatinib by normalization of vascularity. In contrast, hematological response following IFN treatment is independent from BM angiogenesis.
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