Myelofibrosis (MF) is a rare blood cancer that progressively impairs red blood cell production. It is thought to be driven by dysregulation of the JAK-STAT pathway.1
Continual activation of this pathway results in local inflammation and progressive bone marrow fibrosis, reducing the hematopoietic capacity of the marrow (anemia) and triggering extramedullary hematopoiesis in the spleen (splenomegaly).2 The systemic pro-inflammatory cytokine profile (eg IL-6) induces a hyper-metabolic state and constitutional symptoms3 and drives production of hepcidin, the master regulator of iron homeostasis. Elevated hepcidin restricts iron availability for erythropoiesis, further reducing red blood cell.