Abstract |
The purpose of this study was to investigate the in vitro effects of thalidomide on long-term bone marrow cultures from patients with myelodysplastic syndrome. We demonstrated that thalidomide induced an increase in granulocyte-macrophage colony forming unit numbers and in IL-10 expression. Thalidomide also promoted a slight increase in IL-6, IL-1β and TNF-α expression in the stromal layers. The numbers of erythroid burst forming units, the apoptosis rate of hematopoietic cells, and VEGF and TNF-α expression levels in culture supernatants were not modulated. Our results indicate a participation of thalidomide upon the hematopoietic microenvironment of patients with myelodysplastic syndromes, especially in the up regulation of IL-10.
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Authors | Mariana Lazarini, Fabíola Traina, Sheila M Winnischofer, Fernando F Costa, Mary Luci S Queiroz, Sara T Olalla Saad |
Journal | Leukemia research
(Leuk Res)
Vol. 35
Issue 8
Pg. 1102-7
(Aug 2011)
ISSN: 1873-5835 [Electronic] England |
PMID | 21511336
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2011 Elsevier Ltd. All rights reserved. |
Chemical References |
- Angiogenesis Inhibitors
- Interleukin-1beta
- Interleukin-6
- RNA, Messenger
- Tumor Necrosis Factor-alpha
- VEGFA protein, human
- Vascular Endothelial Growth Factor A
- Interleukin-10
- Thalidomide
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Topics |
- Adult
- Aged
- Angiogenesis Inhibitors
(therapeutic use)
- Bone Marrow
(drug effects)
- Coculture Techniques
- Colony-Forming Units Assay
- Enzyme-Linked Immunosorbent Assay
- Female
- Hematopoietic Stem Cells
- Humans
- Interleukin-10
(genetics, metabolism)
- Interleukin-1beta
(genetics, metabolism)
- Interleukin-6
(genetics, metabolism)
- Male
- Middle Aged
- Myelodysplastic Syndromes
(drug therapy, genetics, metabolism)
- RNA, Messenger
(genetics)
- Reverse Transcriptase Polymerase Chain Reaction
- Stromal Cells
(drug effects, metabolism)
- Thalidomide
(therapeutic use)
- Tumor Necrosis Factor-alpha
(genetics, metabolism)
- Vascular Endothelial Growth Factor A
(genetics, metabolism)
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