Canonical Wnt/β-Catenin Signaling Pathway Is Dysregulated in Patients With Primary and Secondary Myelofibrosis.

摘要: Abstract Introduction β-Catenin is a central effector molecule of the canonical wingless-related integration site (Wnt) signaling pathway. It important for maintenance stem cell homeostasis and its aberrant activation has been implicated in wide array malignant hematological disorders. There are few reports suggesting dysregulation Philadelphia chromosome-negative (Ph−) myeloproliferative neoplasms (MPNs). Patients Methods We analyzed β-catenin mRNA expression bone marrow (BM) aspirates 29 patients with primary (PMF) 4 secondary, post Ph− MPN, myelofibrosis (SMF) using quantitative real-time polymerase chain reaction (qRT PCR). The control group consisted 16 BM from limited-stage aggressive non-Hodgkin lymphoma without involvement. compared relative gene clinical parameters. Results Relative differed significantly among groups ( P  = .0002), it was higher PMF SMF than group, but did not differ between SMF. A negative correlation found regarding hemoglobin level .017). No association according to Janus kinase 2 (JAK2) V617F mutational status or JAK2 allele burden detected. Conclusion Our results show first time that increased upregulation might potentiate anemia. number inflammatory cytokines associated capable mediating their effects through expression. Accordingly, can induce genes processes cycle control, fibrosis, angiogenesis, which pathogenesis. Therefore, represent an interesting new therapeutic target these diseases.