Smoking as a contributing factor for development of polycythemia vera and related neoplasms.

Smoking may be associated with accelerated erythropoiesis, leukocytosis and thrombocytosis, which are also hallmarks in patients with polycythemia vera, essential thrombocythemia and early stages of myelofibrosis (MPNs). The JAK-STAT and NF-κB signaling pathways are activated in both smokers and in patients with MPNs. Additionally, both share elevated levels of several proinflammatory cytokines, in vivo activation of leukocytes and platelets, endothelial dysfunction and increased systemic oxidative stress. Based upon experimental, epidemiological and clinical data it is herein argued and discussed, if smoking may be involved in MPN pathogenesis, considering most recent studies and reviews which are supportive of the concept that chronic inflammation with NF-κB activation and oxidative stress may have a major role - both as triggers but also as the driving force for clonal expansion in MPNs.