[Mechanisms of resistance to CYP17A1 inhibitors in castrate resistant prostate cancer].

INTRODUCTION

Abiraterone acetate has increased the overall survival of patients with metastatic castration-resistant prostate cancer. However, despite an initial response to treatment, many patients develop resistance to the drug. In this paper we present different hypotheses that may explain the emergence of resistance.

METHOD

This review was conducted from the PubMed database. The most relevant articles were selected and analyzed.

RESULTS

The molecular mechanisms of resistance to abiraterone acetate remain largely elusive. We detailed some of them including the reactivation of the androgen receptor through alternative biosynthesis of androgens, over expression or mutation of the androgen receptor gene, or the action of co-activators. The over expression of CYP17A1 or the alteration of other genes' expression involved in steroidogenesis could also contribute to the resistance.

CONCLUSION

Some of the molecular mechanisms involved in the resistance to abiraterone acetate were detailed. Better understanding of these mechanisms is a key step to allow the emergence of new therapeutic options and personalized treatments of castration resistant prostate cancer.