Pharmacological doses of all-trans retinoic acid promote G0/G1 transition and G1 arrest of normal human marrow CD34+ cells

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In myelodysplasia (MDS), a clone from defective pluripotential stem cells tends to dominate the marrow.¹ Progenitors from the abnormal clone exhibit ineffective haematopoiesis in vitro and in vivo,² and fail to generate fully functional neutrophils or sufficient mature red cells. This has prompted an intensive search for ways to circumvent the differentiation block in this condition. All trans-retinoic acid (ATRA) has attracted much interest as a potential enhancer of neutrophilic differentiation in MDS, since the demonstration that it is an effective inducer of differentiation in HL60 cells.³ Retinoid therapy (13-cis and all-trans) has been attempted in MDS, but the effectiveness was limited when used alone.^{4, 5, 6} This could be explained in part by the effects of pharmacological doses of retinoids on progenitors from normal resting haematopoiesis.

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