Pathogenesis of myeloproliferative neoplasms

Skoda, Radek C. and Duek, Adrian and Grisouard, Jean. (2015) Pathogenesis of myeloproliferative neoplasms. Experimental Hematology, 43 (8). pp. 599-608.

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Official URL: https://edoc.unibas.ch/62463/

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Major progress has been recently made in understanding the molecular pathogenesis of myeloproliferative neoplasms (MPN). Mutations in one of four genes-JAK2, MPL, CALR, and CSF3R-can be found in the vast majority of patients with MPN and represent driver mutations that can induce the MPN phenotype. Hyperactive JAK/STAT signaling appears to be the common denominator of MPN, even in patients with CALR mutations and the so-called "triple-negative" MPN, where the driver gene mutation is still unknown. Mutations in epigenetic regulators, transcription factors, and signaling components modify the course of the disease and can contribute to disease initiation and/or progression. The central role of JAK2 in MPN allowed development of small molecular inhibitors that are in clinical use and are active in almost all patients with MPN. Advances in understanding the mechanism of JAK2 activation open new perspectives of developing the next generation of inhibitors that will be selective for the mutated forms of JAK2.
Faculties and Departments:03 Faculty of Medicine > Departement Biomedizin > Department of Biomedicine, University Hospital Basel > Experimental Hematology (Skoda)
UniBasel Contributors:Skoda, Radek C.
Item Type:Article, refereed
Article Subtype:Further Journal Contribution
ISSN:1873-2399 (Electronic) 0301-472X (Linking)
Note:Publication type according to Uni Basel Research Database: Journal item
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Last Modified:24 Nov 2018 14:47
Deposited On:24 Nov 2018 14:47

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