The Role of β-Catenin in Bcr/Abl Negative Myeloproliferative Neoplasms: An Immunohistochemical Study

The dysregulation of the Wnt/beta-catenin signaling pathway causes various diseases. In this study we aimed to reveal the role of beta-catenin in bcr/abl-negative myeloproliferative neoplasms. The expression of beta-catenin was examined in bone marrow with immunohistochemical method in 66 patients and in 30 control participants. The results suggest that beta-catenin has a role in the angiogenesis of primary myelofibrosis and in the thrombopoiesis of policythemia vera and essential thrombocytemia. Introduction: beta-Catenin is a multifunctional protein that acts as a central effector molecule in the Wnt signaling pathway. Aberrant activation of the Wnt/beta-catenin signaling pathway causes various diseases including cancer. In this study we evaluated beta-catenin expression in bcr/abl-negative myeloproliferative neoplasms (MPNs). Materials and Methods: The expression of beta-catenin was evaluated in bone marrow using immunohistochemical methods in 66 patients with bcr/abl-negative myeloproliferative neoplasms (MPNs) and in 30 healthy control subjects. Immunreactive score (IRS; staining intensity x percentage of positive stained cells) was used for the evaluation of the cell staining reaction. Results: IRS of megakaryocytes (IRSmega) was higher in essential thrombocytemia (ET) compared with the control group (P = .022) and primary myelofibrosis (PMF; P = .001). IRS of vascular endothelial cells (IRSvas) was higher in the bcr/abl negative MPN compared with the control group (P = .024). Also, IRSvas was higher in the PMF compared with the control group (P = .001), policythemia vera (PV; P = .005), and ET (P = .006). A positive correlation was detected between IRSmega and platelet counts (P = .019). Conclusion: Results of this study suggest that the Wnt/beta-catenin signaling pathway has a role in the angiogenesis of PMF and in the thrombopoiesis of PV and ET. Hence, targeting the Wnt/beta-catenin signaling pathway could open new avenues for novel therapeutic approaches in bcr/abl-negative MPNs. (C) 2015 Elsevier Inc. All rights reserved.