Paclitaxel/Taxol® sensitivity in human renal cell carcinoma is not determined by the p53 status

Petra Reinecke, Thomas Kalinski, Csaba Mahotka, Michael Schmitz, Marion Déjosez, Helmut Erich Gabbert, Claus Dieter Gerharz

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


In this study, we analyzed the role of the p53 status for paclitaxel/Taxol® sensitivity in renal cell carcinomas (RCCs) of the clear cell type. Using immunohistochemistry, nuclear p53 accumulation could not be correlated to the paclitaxel/Taxol® 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® 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 from the CD95 system. In conclusion, the p53 status cannot predict paclitaxel/Taxol® sensitivity in RCC cell lines of the clear cell type.

Original languageEnglish
Pages (from-to)165-171
Number of pages7
JournalCancer Letters
Issue number2
StatePublished - 26 May 2005
Externally publishedYes


  • CD95
  • Drug resistance
  • Renal cell carcinoma
  • Taxol®
  • p53


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