Response to thalidomide in progressive multiple myeloma is not mediated by inhibition of angiogenic cytokine secretion
Thalidomide (Thal) is a drug with anti-angiogenic properties. To explore whether the effect of Thal on angiogenesis is associated with a reduction of angiogenic cytokine levels in progressive multiple myeloma (MM), plasma levels of basic fibroblast growth factor, vascular endothelial growth factor,...
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| Main Authors: | , , , , , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
20 December 2001
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| In: |
British journal of haematology
Year: 2001, Volume: 115, Issue: 3, Pages: 605-608 |
| ISSN: | 1365-2141 |
| DOI: | 10.1046/j.1365-2141.2001.03142.x |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1046/j.1365-2141.2001.03142.x Verlag, lizenzpflichtig, Volltext: https://onlinelibrary.wiley.com/doi/abs/10.1046/j.1365-2141.2001.03142.x |
| Author Notes: | Kai Neben, Thomas Moehler, Alwin Kraemer, Axel Benner, Gerlinde Egerer, Anthony D. Ho and Hartmut Goldschmidt |
| Summary: | Thalidomide (Thal) is a drug with anti-angiogenic properties. To explore whether the effect of Thal on angiogenesis is associated with a reduction of angiogenic cytokine levels in progressive multiple myeloma (MM), plasma levels of basic fibroblast growth factor, vascular endothelial growth factor, interleukin 6, tumour necrosis factor-α and hepatocyte growth factor (HGF) were measured in 51 patients at 0, 3 and 6 months of Thal therapy. After 6 months of treatment, 26 patients were considered to be responsive to Thal therapy, including 17 minimal responses, eight partial responses and one complete response. Only HGF (decreasing, P = 0·02) in the group of responsive patients showed a statistically significant change over a period of 6 months. Because HGF levels are known to correlate to MM tumour burden, we conclude that the mechanism of action of Thal in MM is not caused by a specific inhibition of angiogenic cytokine secretion. |
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| Item Description: | Gesehen am 14.12.2021 |
| Physical Description: | Online Resource |
| ISSN: | 1365-2141 |
| DOI: | 10.1046/j.1365-2141.2001.03142.x |