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Thalidomide selectively inhibits tumor necrosis factor alpha production by stimulated human monocytes.
Open accessAbstract
Thalidomide selectively inhibits the production of human monocyte tumor necrosis factor alpha (TNF-alpha) when these cells are triggered with lipopolysaccharide and other agonists in culture. 40% inhibition occurs at the clinically achievable dose of the drug of 1 micrograms/ml. In contrast, the amount of total protein and individual proteins labeled with [35S]methionine and expressed on SDS-PAGE are not influenced. The amounts of interleukin 1 beta (IL-1 beta), IL-6, and granulocyte/macrophage colony-stimulating factor produced by monocytes remain unaltered. The selectivity of this drug may be useful in determining the role of TNF-alpha in vivo and modulating its toxic effects in a clinical setting.
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Cited by
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Singhal, S., Mehta, J., Desikan, R., Ayers, D., Roberson, P., Eddlemon, P., Munshi, N., Anaissie, E., Wilson, C., Dhodapkar, M., et al. (1999) · New England Journal of Medicine · doi:10.1056/nejm199911183412102 · Cited by 2,575
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Lenalidomide Causes Selective Degradation of IKZF1 and IKZF3 in Multiple Myeloma Cells
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Metadata
- Authors
- Sampaio, E. P., Sarno, E. N., Galilly, R., Cohn, Z. A., & Kaplan, G.
- Venue
- The Journal of experimental medicine
- Publisher
- Rockefeller University Press
- Published
- 1991-03-01
- Volume
- 173
- Issue
- 3
- Pages
- 699-703
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2162559503
- Cited by
- 1,192
- References
- 0
- FWCI
- 9.34
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Sampaio, E. P., Sarno, E. N., Galilly, R., Cohn, Z. A., & Kaplan, G. (1991). Thalidomide selectively inhibits tumor necrosis factor alpha production by stimulated human monocytes. The Journal of experimental medicine. https://doi.org/10.1084/jem.173.3.699
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.