Pathogenesis of Myeloproliferative Neoplasms: Role and Mechanisms of Chronic Inflammation

Figure 1

Progression from chronic inflammation to solid and blood cancers. A physical, chemical, or infectious injury leads to tissue and cell damage and activation of antiapoptosis signaling pathways in affected cells, which results in the autocrine and paracrine production and consumption of prosurvival, inflammatory cytokines, as well as chemokines, to attract immune cells of the lymphoid and myeloid lineages to the site of injury. Over time, established inflammation (chronic inflammation) constantly overstimulates the production of hematopoietic cells and induces more tissue and cell damage, hereby increasing the rate of DNA duplication and risk of defective DNA reparation and mutation, both in cells from affected tissues (increased risk of solid cancer) and in lymphoid and myeloid cells participating in the immune/inflammatory response (increased risk of hematological malignancy).