Conflict of interest: The authors declare no conflict of interest.
JAK2 and genomic instability in the myeloproliferative neoplasms: A case of the chicken or the egg?†
Version of Record online: 28 MAY 2012
Copyright © 2012 Wiley Periodicals, Inc.
American Journal of Hematology
Volume 87, Issue 11, pages 1028–1036, November 2012
How to Cite
Scott, L. M. and Rebel, V. I. (2012), JAK2 and genomic instability in the myeloproliferative neoplasms: A case of the chicken or the egg? . Am. J. Hematol., 87: 1028–1036. doi: 10.1002/ajh.23243
- Issue online: 23 OCT 2012
- Version of Record online: 28 MAY 2012
- Accepted manuscript online: 26 APR 2012 07:43AM EST
- Manuscript Accepted: 17 APR 2012
- Manuscript Received: 16 APR 2012
- Congressionally-Directed Medical Research Program Bone Marrow Failure Research Program Exploration-Hypothesis Development Award. Grant Number: W81XWH-10-1-0314
- National Institutes of Aging R21 Award. Grant Number: 5R21AG033339
The myeloproliferative neoplasms (MPNs) are a particularly useful model for studying mutation accumulation in neoplastic cells, and the mechanisms underlying their acquisition. This review summarizes our current understanding of the molecular defects present in patients with an MPN, and the effects of mutations targeting Janus kinase 2 (JAK2)-mediated intracellular signaling on DNA damage and on the elimination of mutation-bearing cells by programmed cell death. Moreover, we discuss findings that suggest that the acquisition of disease-initiating mutations in hematopoietic stem cells of some MPN patients may be the consequence of an inherent genomic instability that was not previously appreciated. Am. J. Hematol. 2012. © 2012 Wiley Periodicals, Inc.