Does angiogenesis matter in primary myelofibrosis?☆

PMF. Although the number of patients was small, one of rimary myelofibrosis (PMF) is a clonal hematopoietic disorder haracterized by an initial prefibrotic proliferative phase that ver time progresses to bone marrow fibrosis, extramedullary ematopoiesis, peripheral blood cytopenias and an increased isk of developing acute myeloid leukemia (AML). In recent ears, the molecular mechanisms that cause PMF have been xtensively studied and the genomic changes that cause the isease have been widely elucidated.1 A unique feature of PMF is a systemic inflammatory eaction that manifests, among other things, through high erum levels of inflammatory cytokines and chemokines, nd a stromal bone marrow reaction involving collagen eposition and increased vascular proliferation.2,3 There s now convincing evidence that megakaryocytes play a ajor role in this stromal reaction.4,5 More specifically, egakaryocytes from patients with PMF produce high levels f inflammatory cytokines including transforming growth actor-beta 1 (TGF 1).6 Recently, PMF systemic inflammatory eaction has taken center stage after a suggestion that possible mechanism by which ruxolitinib, a JAK1 and AK2 inhibitor, increases overall survival, is through its