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Response to thalidomide in progressive multiple myeloma is not mediated by inhibition of angiogenic cytokine secretion.

British Journal of Haematology

Vascular Endothelial Growth Factors, Aged, Angiogenesis Inhibitors, therapeutic use, Cytokines, blood, secretion, Endothelial Growth Factors, Female, Fibroblast Growth Factors, Hepatocyte Growth Factor, Humans, Adult, Interleukin-6, Lymphokines, Male, Middle Aged, Multiple Myeloma, drug therapy, physiopathology, Thalidomide, Tumor Necrosis Factor-alpha, analysis, Vascular Endothelial Growth Factor A

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      Abstract

      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-alpha 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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