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Response to thalidomide in progressive multiple myeloma is not mediated by inhibition of angiogenic cytokine secretion
Author(s) -
Neben Kai,
Moehler Thomas,
Kraemer Alwin,
Benner Axel,
Egerer Gerlinde,
Ho Anthony D.,
Goldschmidt Hartmut
Publication year - 2001
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.2001.03142.x
Subject(s) - thalidomide , hepatocyte growth factor , angiogenesis , cytokine , medicine , multiple myeloma , basic fibroblast growth factor , vascular endothelial growth factor , interleukin 6 , endocrinology , tumor necrosis factor alpha , secretion , growth factor , cancer research , vegf receptors , receptor
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.