Transcriptional differences between JAK2-V617F and wild-type bone marrow cells in patients with myeloproliferative neoplasm
The JAK2 V617F mutation is a somatic mutation found in most patients with myeloproliferative neoplasms (MPNs) [1]. The mutation causes constitutive JAK –STAT pathway activation in hematopoietic stem and progenitor cells (HSPCs), leading to overproduction of red blood cells, platelets, and white blood cells and/or bone marrow fibrosis. Previous work characterizing JAK2-mutant mouse models [2,3] and MPN patient samples [4] has revealed that JAK2 V6 17F increases the fitness of hematopoietic stem cells (HSCs) and promotes megakaryocyte–erythroid differentiation.
Source: Experimental Hematology - Category: Hematology Authors: Debra Van Egeren, Baransel Kamaz, Shichen Liu, Maximilian Nguyen, Christopher R. Reilly, Maria Kalyva, Daniel J. DeAngelo, Ilene Galinsky, Martha Wadleigh, Eric S. Winer, Marlise R. Luskin, Richard M. Stone, Jacqueline S. Garcia, Gabriela S. Hobbs, Franzi Tags: Brief Communication Source Type: research