gms | German Medical Science

77th Annual Meeting of the German Society of Oto-Rhino-Laryngology, Head and Neck Surgery

German Society of Oto-Rhino-Laryngology, Head and Neck Surgery

24.05. - 28.05.2006, Mannheim

Thalidomide enhances effectiveness of cisplatin in HNSCC in vitro

Meeting Abstract

German Society of Otorhinolaryngology, Head and Neck Surgery. 77th Annual Meeting of the German Society of Otorhinolaryngology, Head and Neck Surgery. Mannheim, 24.-28.05.2006. Düsseldorf, Köln: German Medical Science; 2006. Doc06hno065

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Published: September 7, 2006

© 2006 Dyckhoff et al.
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Introduction: In contrast to multiple myeloma thalidomide as monotherapy has been proved ineffective in HNSCC. In an animal model we have demonstrated a significant enhancement of effectiveness of metronomic cisplatin (low dose over a prolonged period of time) when combined with thalidomide. In order to elucidate its mechanism of action the following in vitro studies were performed.

Materials and methods: The dose-dependent effectiveness of cisplatin and thalidomide as single-agents and in combination on a highly malignant HNSCC cell line and on a human dermal microvascular endothelial cell line was determined as to proliferation (BrDU assay), migration (scratch assay) und tubule formation (Matrigel tubule formation assay).

Results: Cisplatin inhibits proliferation of tumor cells as well as of endothelial cells in a dose-dependent manner. In contrast, thalidomide alone has no antiproliferative effect. In combination with thalidomide cisplatin in low concentrations up to 1 µM exhibits a 50-fold higher antiproliferative action on endothelial cells than on HNSCC. Migration is inhibited dose-dependently by cisplatin as well as by thalidomide. Tubule formation is reduced by thalidomide in a dose-dependent manner, by cisplatin only in cytotoxic concentrations. In combination with thalidomide, however, cisplatin shows a significantly higher inhibition of tubule formation than both drugs as single-agents.

Conclusion: The inhibition of tumor growth in vivo is basically caused by an enhancement of the antiproliferative action of cisplatin by thalidomide and an enhancement of the inhibition of tubule formation of thalidomide by metronomic cisplatin. Our results encourage clinical trials of thalidomide as enhancer of the antineoplastic action of cisplatin.