Abstract
Myeloid dysplastic syndrome (MDS) reflects a preleukemic bone marrow (BM) disorder with limited treatment options and poor disease survival. As only a minority of MDS patients are eligible for curative hematopoietic stem cell transplantation, there is an urgent need to develop alternative treatment options. Chronic activation of Wnt/β-catenin has been implicated to underlie MDS formation and recently assigned to drive MDS transformation to acute myeloid leukemia. Wnt/β-catenin signaling therefore may harbor a pharmaceutical target to treat MDS and/or prevent leukemia formation. However, targeting the Wnt/β-catenin pathway will also affect healthy hematopoiesis in MDS patients. The control of Wnt/β-catenin in healthy hematopoiesis is poorly understood. Whereas Wnt/β-catenin is dispensable for steady-state erythropoiesis, its activity is essential for stress erythropoiesis in response to BM injury and anemia. Manipulation of Wnt/β-catenin signaling in MDS may therefore deregulate stress erythropoiesis and even increase anemia severity. Here, we provide a comprehensive overview of the most recent and established insights in the field to acquire more insight into the control of Wnt/β-catenin signaling in healthy and inefficient erythropoiesis as seen in MDS.
Original language | English |
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Pages (from-to) | 3726-3735 |
Number of pages | 10 |
Journal | Blood advances |
Volume | 5 |
Issue number | 18 |
DOIs | |
Publication status | Published - 28 Sept 2021 |
Keywords
- Erythropoiesis
- Humans
- Leukemia, Myeloid, Acute
- Myelodysplastic Syndromes
- Wnt Signaling Pathway