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Downregulation of neuropilin‐1 in patients with acute myeloid leukemia treated with thalidomide
Author(s) -
Kreuter Michael,
Steins Martin,
Woelke Katja,
Buechner Thomas,
Berdel Wolfgang E.,
Mesters Rolf M.
Publication year - 2007
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1111/j.1600-0609.2007.00954.x
Subject(s) - thalidomide , neuropilin 1 , medicine , myeloid leukemia , downregulation and upregulation , cd34 , angiogenesis , refractory (planetary science) , bone marrow , immunohistochemistry , oncology , vascular endothelial growth factor , cancer research , vegf receptors , multiple myeloma , biology , stem cell , biochemistry , genetics , astrobiology , gene
Objective: Neuropilin‐1 (NRP‐1), a non‐tyrosine kinase receptor functioning as a mediator of angiogenesis and neuronal guidance, was recently found to be significantly overexpressed in newly diagnosed acute myeloid leukemia (AML) patients with significant correlation to survival. The role of NRP‐1 in refractory or relapsed AML patients and its regulation during anti‐angiogenic treatment remain to be elucidated. Methods: Bone marrow biopsies of 10 patients with refractory or relapsed AML were evaluated for NRP‐1 expression by immunohistochemical analysis, and NRP‐1 expression level was determined before and after start of thalidomide therapy and correlated to response and growth factor expression. Results: NRP‐1 expression was significantly increased in AML patients [median 7 arbitrary units (AU)] when compared with controls ( n = 38, median 2.75 AU). Under thalidomide treatment, a marked difference in the course of NRP‐1 expression between responders and non‐responders was observed, however, without a statistical significance ( P = 0.071) being reached. Additionally, a significant correlation of the NRP‐1 expression level to microvessel density could be detected under treatment with thalidomide ( P = 0.018). Conclusion: Our data provide evidence of increased NRP‐1 expression in relapsed or refractory AML. Additionally, our results suggest that thalidomide‐induced antileukemic properties might at least in part be mediated by NRP‐1 downregulation.