• Media type: E-Article
  • Title: Mutations in BRCA2 and taxane resistance in prostate cancer
  • Contributor: Nientiedt, Cathleen [Author]; Heller, Martina [Author]; Endris, Volker [Author]; Volckmar, Anna-Lena [Author]; Zschäbitz, Stefanie [Author]; Tapia-Laliena, María Angeles [Author]; Jäger, Dirk [Author]; Schirmacher, Peter [Author]; Sültmann, Holger [Author]; Stenzinger, Albrecht [Author]; Hohenfellner, Markus [Author]; Grüllich, Carsten [Author]; Duensing, Stefan [Author]
  • Published: 4 July 2017
  • Published in: Scientific reports ; 7(2017), Artikel-ID 4574
  • Language: English
  • DOI: 10.1038/s41598-017-04897-x
  • Identifier:
  • Origination:
  • Footnote: Im Titel ist "BRCA2" kursiv geschrieben
  • Description: Mutations in BRCA1 or BRCA2 define a subset of prostate cancer patients. Herein, we address the question whether BRCA1/2 mutations have a predictive impact on chemotherapy with docetaxel, a widely used drug in patients with metastatic castration resistant prostate cancer (mCRPC). Fifty-three men treated with docetaxel for mCRPC were tested for somatic BRCA1/2 mutations of the primary tumor. In a subgroup of patients, BRCA1/2 protein expression was tested as a potential surrogate marker for BRCA1/2 inactivation. Eight of 53 patients (15.1%) harbored a deleterious BRCA2 mutation. No BRCA1 mutation was found. Patients with a BRCA2 mutation showed a response rate of 25% to docetaxel in comparison to 71.1% in men with wildtype BRCA2 (p = 0.019). While the time to develop castration resistance was similar in both subgroups, the overall survival was significantly shorter in patients harboring a BRCA2 mutation. No correlation between the BRCA1/2 protein expression and the response to docetaxel was found. While the presence of a BRCA2 mutation does not preclude a response to docetaxel, there is overall a significant correlation between BRCA2 inactivation and a poor response rate. Our results suggest that a close oncological monitoring of patients with BRCA2 mutations for taxane resistance is warranted.
  • Access State: Open Access