Impact of growth factors in the regulation of apoptosis in low-risk myelodysplastic syndromes.
Increased apoptosis of hematopoietic progenitors is a hallmark of myelodysplastic syndromes (MDS) and results in ineffective hematopoiesis. Erythroid apoptosis is thought to be the main mechanism underlying the severe anemia observed in the low-risk subgroups, refractory anemia (RA) and RA with ringed sideroblasts (RARS). Treatment with erythropoietin (Epo) alone or in combination with granulocyte colony- stimulating factor (G-CSF) may significantly improve anemia and reduce bone marrow apoptosis. A synergistic effect between Epo and G-CSF has been observed in the clinic, in particular in RARS. However, the molecular mechanisms beyond the anti-apoptotic effect of these growth factors have not been fully understood. This paper outlines the potential mechanisms underlying the augmented apoptosis during the erythroid differentiation in low-risk MDS as well as the anti-apoptotic effect of the growth factors.[1]References
- Impact of growth factors in the regulation of apoptosis in low-risk myelodysplastic syndromes. Tehranchi, R. Med. Oncol. (2006) [Pubmed]
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