The expression of lysyl‐oxidase gene family members in myeloproliferative neoplasms |
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Authors: | T. Tadmor J. Bejar D. Attias E. Mischenko E. Sabo G. Neufeld Z. Vadasz |
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Affiliation: | 1. The Hematology Unit, Bnai‐Zion Medical Center, , Haifa;2. The Rappaport Faculty of Medicine, Technion‐Israel Institute of Technology, , Haifa;3. Department of Pathology, Bnai‐Zion Medical Center, , Haifa;4. Department of Pathology and Oncology, Rambam Health Care Campus;5. The Bruce Rappaport Faculty of Medicine, Cancer and Vascular Biology Research Center, Rappaport Family Institute for Research in the Medical Sciences, Technion, Israel Institute of Haifa, , Israel |
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Abstract: | Myeloproliferative neoplasms (MPNs) are malignant disorders originating from clonal expansion of a single neoplastic stem cell and characteristically show an increase in bone marrow reticulin fibers. Lysyl oxidases (LOXs) are copper‐dependent amine oxidases that play a critical role in the biogenesis of connective tissue by crosslinking extracellular matrix proteins, collagen and elastin. Expression of LOX gene family members is increased in disorders associated with increased fibrosis. To evaluate involvement of LOX gene family in various MPNs. In‐situ hybridization was used to detect Lysyl‐Oxidase family members in bone marrow biopsies from patients with different MPNs. We compared normal bone marrows and those from patients with polycythemia vera, essential thrombocythemia, chronic myeloid leukemia, and primary myelofibrosis (PMF). Serum levels of lysyl‐oxidase from patients with PMF and healthy controls were also examined. LOX gene family was not detected in normal bone marrows. All members of the LOX gene family were over expressed in PMF. In other MPNs a differential pattern of expression was observed. Differences in gene expression were statistically significant (P < 0.010). The medianserum LOX levels in normal controls was 28.4 ± 2.5 ngml and 44.6 ± 9.44 ngml in PMF (P = 0.02). The varying pattern of expression of LOX genes may reflect differences in the pathophysiology of bone marrow fibrosis in these MPNs. These observations could be used as the basis for future targeted therapy directed against bone marrow fibrosis. Am. J. Hematol. 88:355–358, 2013. © 2013 Wiley Periodicals, Inc. |
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