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Izbicka, E. et al.

Molecular determinants of differential sensitivity to docetaxel and paclitaxel in human pediatric cancer models.

BACKGROUND: The differential sensitivity of some tumors to paclitaxel and docetaxel raises questions regarding the specific mechanisms responsible for the discrepant sensitivity to these taxanes. MATERIALS AND METHODS: Docetaxel and paclitaxel were evaluated and compared at maximum tolerated doses (MTD) and 0.5 MTDs against the human pediatric tumor xenograft models SK-N-MC and IMR32 (neuroblastoma), RH1 and RH30 (rhabdomyosarcoma) and KHOS/ NP (osteosarcoma), with 8-10 animals per group. The drug effects on the expression of the beta-tubulin isotypes, Bcl-2, Bax, Bcl-XL and proteomic profiles were evaluated by immunobloting and SELDI mass spectrometry in tumor xenografts dosed at 0.5 MTDs. RESULTS: At MTDs, docetaxel was superior in neuroblastoma and osteosarcoma, while paclitaxel was more active in the rhabdomyosarcoma models. Docetaxel showed remarkable efficacy in KHOS/ NP even at 0.5 MTD. The drugs had significantly different, yet highly heterogeneous effects on the tumor levels of betaI-tubulin (RH30), betaIII-tubulin (IMR32, KHOS/ NP, RH]), Bax (IMR32, SK-N-MC) and Bcl-XL (KHOS/ NP). In contrast, six protein species identified by proteomic profiling were consistently and differentially regulated by docetaxel and paclitaxel in all KHOS/ NP xenografts. CONCLUSION: Anticancer activity showed no apparent correlation with drug effects on beta-tubulin isotypes and apoptotic markers. The mass spectrometry approach has potential for the discovery of proteomic biomarkers for drug sensitivity.[1]

References

Molecular determinants of differential sensitivity to docetaxel and paclitaxel in human pediatric cancer models. Izbicka, E., Campos, D., Marty, J., Carrizales, G., Mangold, G., Tolcher, A. Anticancer Res. (2006) [Pubmed]

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