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Human Molecular Genetics Advance Access originally published online on April 21, 2008
Human Molecular Genetics 2008 17(14):2144-2149; doi:10.1093/hmg/ddn113
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© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

DNA instability in low-risk myelodysplastic syndromes: refractory anemia with or without ring sideroblasts

Bozena Novotna1,*, Radana Neuwirtova2, Magda Siskova2 and Yana Bagryantseva1

1 Department of Genetic Ecotoxicology, Institute of Experimental Medicine, v.v.i., Academy of Sciences of the Czech Republic, Prague 4 142 20, Czech Republic 2 Hematooncology, 1st Medical Clinic, General University Hospital, Prague 2 128 08, Czech Republic

* To whom correspondence should be addressed at: Department of Genetic Ecotoxicology, Institute of Experimental Medicine, v.v.i., Academy of Sciences of the Czech Republic, Videnska 1083, Prague 4 142 20, Czech Republic. Tel: +420 241062209; Fax: +420 241062785; Email: novotna{at}biomed.cas.cz

Received January 17, 2008; Revised March 20, 2008; Accepted April 8, 2008

We tested genomic instability in patients with myelodysplastic syndrome (MDS) by the comet assay and verified the suitability of this approach as a tool for analysis of ineffective hematopoiesis in refractory anemia (RA) and RA with ring sideroblasts (RARS). Erythroid and myeloid cell populations from bone marrow aspirates of 20 RA, 14 RARS and 15 control subjects were separated by differential expression of glycophorin A and subjected to comet assay. The extent of DNA migration was measured in single cells (200 cells/bone marrow fraction/subject). The results were in agreement with the concept of increased apoptosis in low-risk MDS subtypes. The RA samples had a significantly higher DNA instability than controls in glycophorin A positive cells, and the extent of DNA breakage correlated with the degree of cytopenia. Although RARS had an even higher rate of genomic instability in bone marrow cells than RA, there was no clear relationship to peripheral cytopenia. This suggests an additional DNA instability of non-apoptotic origin. Whether this increase is associated with an increased repair of oxidative damage in DNA arising due to iron deposits in ring sideroblasts remains to be formally proven. Comet assay provides a promising tool for the investigation of difference between RA and RARS pathobiology.


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