Journal
CANCER LETTERS
Volume 222, Issue 2, Pages 165-171Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2004.09.045
Keywords
p53; CD95; renal cell carcinoma; Taxol((R)); drug resistance
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In this study, we analyzed the role of the p53 status for paclitaxel/Taxol (R) sensitivity in renal cell carcinomas (RCCs) of the clear cell type. Using immunohistochemistry, nuclear p53 accumulation could not be correlated to the paclitaxel/Taxol (R) sensitivity. DNA sequencing detected a p53 gene mutation in two out of eight RCC cell lines, i.e. in exon 8 (cell line clearCa-6), and in exon 9 (cell line clearCa-5). No correlation, however, was found between the p53 status of our RCC cell lines and their paclitaxel/Taxol (R) sensitivity as indicated by the IC50 values. However, paclitaxel-induced growth inhibition in paclitaxel-sensitive RCC cell lines was accompanied by an increase in apoptosis, irrespective of their p53 status. Although CD95 up-regulation was observed in renal cell carcinoma with wild-type p53 upon paclitaxel treatment, paclitaxel-induced apoptosis itself is triggered independently front the CD95 system. In conclusion, the p53 status cannot predict paclitaxel/Taxol (R) sensitivity in RCC cell lines of the clear cell type. (c) 2004 Elsevier Ireland Ltd. All rights reserved.
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