ABSTRACT
Myelodysplastic syndrome (MDS) is a group of heterogeneous clonal hematopoietic stem cell disorders characterized clinically and morphologically by ineffective hematopoiesis and dyspoiesis leading to cytopenia(s) (which often result in transfusion-dependent anemia and/or increased infections or hemorrhage) and risk of progression to acute leukemia [1–11]. The incidence of MDS varies from 2.1 to 12.6 cases per 100,000 population per year but approaches 50 cases per 100,000 per year in persons over age 70 [12–14]. Ineffective hematopoiesis in MDS has been attributed in part to a complex interaction between progenitor cells and the microenvironment that results in the premature apoptotic death of blood cell precursors, which is counterbalanced by increased proliferation of hematopoietic elements [15–17].
