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Cross-Resistance to Docetaxel and Cabazitazel in CRPC Mediated by ABCB1 Gene

Ariela Katz
Published: Thursday, Jun 22, 2017

Alan P. Lombard, PhD

Alan P. Lombard, PhD

Results of an investigation presented at the 2017 American Urological Association Annual Meeting indicate that resistance to docetaxel and cabazitaxel (Jevtana) in patients with castration-resistant prostate cancer (CRPC) is mediated by a common mechanism, overexpression of the ABCB1 gene.1 The study authors further concluded that inhibiting this gene with antiandrogen therapy, such as enzalutamide (Xtandi) and bicalutamide (Casodex), could increase the effectivity of taxane-based therapies in patients with CRPC.

This research provides a better understanding of the mechanism of resistance for a large and underserved population of patients with CRPC. It could even indicate not only that there is potential for combination therapies with antiandrogen agents to enhance the effectiveness of cabazitaxel in the docetaxel-resistant setting, but also that cabazitaxel may be a better drug in the pre-docetaxel setting for these patients. “Our work indicates that it may be more beneficial to move cabazitaxel into the docetaxel treatment space,” Lombard et al concluded.


  1. Lombard AP, Liu C, Armstrong C, et al. Elucidating cross-resistance between docetaxel and cabazitaxel in castration resistant prostate cancer. Presented at: 2017 American Urological Association Annual Meeting; May 12-16, 2017; Boston, MA. Abstract MP83-09.
  2. Genetics Home Reference. ABCB1 gene. NIH US National Library of Medicine website. Updated May 16, 2017. Accessed May 16, 2017.

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