Oncology Medical News about Anemia, Sideroblastic

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Hereditary Sideroblastic Anemias: Pathophysiology, Diagnosis, and Treatment
Seminars in Hematology, 10/05/09

Camaschella C – The most common X–linked sideroblastic anemia (XLSA), due to mutations of the first enzyme of the heme synthetic pathway, delta–aminolevulinic acid synthase 2 (ALAS2), has linked heme deficiency to mitochondrial iron accumulation. The identification of other genes, such as adenosine triphosphate (ATP) binding cassette B7 (ABCB7) and glutaredoxin 5 (GLRX5), has strengthened the role of iron sulfur cluster biogenesis in sideroblast formation and revealed a complex interplay between pathways of mitochondrial iron utilization and cytosolic iron sensing by the iron–regulatory proteins (IRPs). As recently occurred with the discovery of the SLC25A38–related sideroblastic anemia, the identification of the genes responsible for as yet uncharacterized forms will provide further insights into mitochondrial iron metabolism of erythroid cells and the pathophysiology of sideroblastic anemia.

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