Single Cell Phospho-Signaling Analysis in Myeloid Malignancies

نویسنده

  • Ioannis Kotsianidis
چکیده

Abnormal hematopoietic stem/progenitor cell (HSPC) signaling is a hallmark of leukemic hematopoiesis and a common denominator in the pathobiology of all types of myeloid malignancies. The most studied pathways are the JAK/ STAT, MAPK/ERK and PI3K/AKT cascades [1]. Constitutive activation of STAT molecules has been reported in almost all myeloid malignancies. Basal STAT3 and less often STAT5 levels are encountered in acute myeloid leukemia (AML) blasts and have been associated with worse outcome [2], whereas STAT1 is sporadically overexpressed in AML and CML and its role in leukemogenesis is unclear [3]. The central role of the JAK/ STAT network in clonal myelopoiesis is typically illustrated in Phmyeloproliferative neoplasms (MPN). The activating V617F mutation of JAK2 kinase is encountered in all MPN types, whereas it has been recently suggested that the antagonism between STAT1 and STAT5 activation in CD34+ cells determines the final phenotype of a JAK2V617F-positive MPN [4].

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تاریخ انتشار 2014