Abstract
Myeloproliferative neoplasms (MPNs) are characterized by the activation of the JAK-STAT pathway due to driver mutations, including JAK2V617F, but some additional abnormalities may be necessary to maintain an MPN clone and develop a more advanced disease. The HMGA2 proto-oncogene, which regulates the expression of various genes, is often overexpressed due to downregulation of let-7 microRNAs or EZH2 mutations in advanced MPNs such as myelofibrosis. In mice with JAK2V617F, Ezh2 deletion deregulates Hmga2, which plays a crucial role in MPN progression. Correspondingly, Hmga2 overexpression causes massive splenomegaly and severe anemia in mice carrying JAK2V617F, mimicking severe MPN. Herein, we discuss the mechanisms of HMGA2 deregulation and its possible use as a therapeutic target.
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