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Response to Dr SD Mundle

Leukemia volume 16, page 961 (2002)Cite this article

This is a reply to the letter of Dr S Mundle ‘The role of bone marrow stroma in myelodysplastic syndromes continues to be nebulous’ in this issue of Leukemia 2002; 16: 960–961.

We agree with Dr Mundle that the precise role of the stroma in the pathophysiology of myelodysplasia remains uncertain. However, we think that our data on the effect of normal and MDS stroma on model haemopoietic stem/progenitor cells (HPC), although open to different interpretations, show more than ‘marginal’ effects. We have used a model that can demonstrate interactions between stromal cells and haemopoietic cells over a relatively short time, unlike previous studies using more prolonged 2-stage Dexter co-cultures,1,2,3 where precise effects on proliferation and survival are difficult to separate. Our central finding is that after 72 h co-culture, F-36P cell numbers increase by a similar amount (approximately 60%) with normal and MDS stromal layers, whereas standardized apoptotic ratios were significantly increased on MDS compared with normal stroma (mean 1.4 ± 0.5). This leads us to suggest that while the ability of MDS stroma to support HPC proliferation appears intact, stromal regulation of HPC survival may be deficient in MDS. Indeed, given the similar increases in F-36P numbers at 72 h, one could argue that the proliferative drive on MDS stroma may be greater than on normal stroma: increased apoptosis on MDS adherent layers might be accompanied by a compensatory increase in the proliferation of sub-populations of F-36P cells that are resistant to the ‘apoptotic stimuli’.

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  1. Department of Molecular and Cellular Pathology, Ninewells Hospital and Medical School, Dundee, UK

    S Tauro, M Hepburn, C Peddie, D Bowen & M Pippard

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  1. S Tauro
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  2. M Hepburn
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  3. C Peddie
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  4. D Bowen
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  5. M Pippard
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Tauro, S., Hepburn, M., Peddie, C. et al. Response to Dr SD Mundle. Leukemia 16, 961 (2002). https://doi.org/10.1038/sj.leu.2402430

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