No telomere shortening in marrow stroma from patients with MDS.
Telomere shortening with age may lead to genomic instability and an increased risk of cancer. Given the role of the microenvironment in the pathophysiology of the myelodysplastic syndrome (MDS), primarily a disease of older age, we determined telomere length in primary cultured marrow stroma cells using quantitative fluorescent in situ hybridization (qFISH) and quantitative polymerase chain reaction (qPCR). qFISH showed comparable rates of decrease in telomere length with age in MDS patients and age-matched healthy controls. Telomere length assessment by qPCR showed similar results. These findings suggest a lack of significant differences between MDS patients and healthy controls in terms of telomere stability in marrow stroma in contrast to that observed in hematopoietic cells. In conclusion, this demonstrates that, although MDS stroma cells and hematopoietic cells share the same microenvironment, the stromal cells do not share the processes that contribute to accelerated telomere attrition, suggesting that stromal cell proliferative potential is not limiting in MDS.
Marcondes
A Mario
AM
Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. mmarcond@fhcrc.org
Bair
Steven
S
Rabinovitch
Peter S
PS
Gooley
Ted
T
Deeg
H Joachim
HJ
Risques
Rosana
R
D000328:Adult; D000367:Age Factors; D000368:Aged; D000369:Aged, 80 and over; D001853:Bone Marrow / Q000473:pathology; D016022:Case-Control Studies; D002478:Cells, Cultured; D005260:Female; D006412:Hematopoietic Stem Cells; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D008297:Male; D008875:Middle Aged; D009190:Myelodysplastic Syndromes / Q000473:pathology*; D016133:Polymerase Chain Reaction; D017154:Stromal Cells / Q000473:pathology*; D016615:Telomere / Q000378:metabolism* / Q000648:ultrastructure