Fig 2.

Various pathways to transformation. The defining feature of myelodysplastic syndromes is clonal and inefficient hematopoiesis that causes peripheral cytopenias. A heterogeneous set of genetic and epigenetic abnormalities drive the cellular events that give rise to clinical phenotypes. Individual lesions may be responsible for one transformative step alone (eg, enhanced self-renewal or altered apoptosis) and therefore be clinically silent in isolation, or they could result in several abnormalities (eg, acquired self-renewal and impaired differentiation). Cooperation between two or more lesions is likely needed for the full expression of disease.