The involvement of Galectins in the modulation of the JAK/STAT pathway in myeloproliferative neoplasia

[摘要] In patients with myeloproliferative neoplasia (MPN) the development of fibrosis and increased vessel density correlate with poor prognosis. The JAK2^V617F mutation constitutively activates JAK2, which phosphorylates signal transducer activator of transcription (STAT), up-regulating vascular endothelial growth factor (VEGF), which might be responsible for angiogenesis in MPN. Galectins are involved in the development of fibrosis and angiogenesis and might also be involved in activation of the JAK/STAT pathway in MPN.

[学科分类] 血液学

[关键词] MPN;myeloproliferative neoplasia;galectin;JAK;STAT;angiogenesis;MVD