Abstract
The myelodysplastic syndrome (MDS), as currently defined, incorporates the clinical states earlier recognised as “chronic refractory anaemia” (RA), “primary acquired sideroblastic anaemia” (PASA) and “smouldering leukaemia”. It is now generally accepted that this disorder results from the proliferation of an abnormal clone of haemopoietic stem cells which gradually predominates over normal haemopoiesis and may undergo clonal evolution [14, 21]. There is a diversity of abnormalities affecting all cell lines, and although it is possible to group certain cases together, as in the FAB classification [3], the biological and functional aberrations vary from case to case, and the mechanisms causing anaemia may not be the same in all patients. While this paper relates only to erythroid abnormalities, it should be remembered that even when only erythropoiesis appears to be involved by the pathological process, apparently normal cells of other lineages may be derived from the abnormal clone [22].
Leukaemia Research Fund, Preleukaemia Unit, University of Wales, College of Medicine, Cardiff, UK
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Jacobs, A. (1992). Pathogenesis of Anaemia in the Myelodysplastic Syndrome. In: Schmalzl, F., Mufti, G.J. (eds) Myelodysplastic Syndromes. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-75952-9_4
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DOI: https://doi.org/10.1007/978-3-642-75952-9_4
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