The genetics of myelodysplastic syndrome: from clonal hematopoiesis to secondary leukemia
Identifieur interne : 000A12 ( Main/Exploration ); précédent : 000A11; suivant : 000A13The genetics of myelodysplastic syndrome: from clonal hematopoiesis to secondary leukemia
Auteurs : Adam S. Sperling [États-Unis] ; Christopher J. Gibson [États-Unis] ; Benjamin L. Ebert [États-Unis]Source :
- Nature reviews. Cancer [ 1474-175X ] ; 2016.
Abstract
Myelodysplastic syndrome (MDS) is a clonal disease that arises from the expansion of mutated hematopoietic stem cells. In a spectrum of myeloid disorders ranging from clonal hematopoiesis of indeterminate potential (CHIP) to secondary acute myeloid leukemia (sAML), MDS is distinguished by the presence of peripheral blood cytopenias, dysplastic hematopoietic differentiation, and the absence of features that define acute leukemia. Over 50 recurrently mutated genes are involved in the pathogenesis of MDS, including genes that encode proteins involved in pre-mRNA splicing, epigenetic regulation, and transcription. In this review we discuss the molecular processes that lead to CHIP and further clonal evolution to MDS and sAML. We also highlight the ways in which these insights are shaping the clinical management of MDS, including classification schemata, prognostic scoring systems, and therapeutic approaches.
Url:
DOI: 10.1038/nrc.2016.112
PubMed: 27834397
PubMed Central: 5470392
Affiliations:
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