A Novel Mechanism to Drive Castration-Resistant Prostate Cancer

Salma Kaochar; Nicholas Mitsiades

doi:10.1016/j.tem.2018.03.006

A Novel Mechanism to Drive Castration-Resistant Prostate Cancer

Trends Endocrinol Metab. 2018 Jun;29(6):366-368. doi: 10.1016/j.tem.2018.03.006. Epub 2018 Mar 28.

Authors

Salma Kaochar¹, Nicholas Mitsiades²

Affiliations

¹ Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA; Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA.
² Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA; Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA. Electronic address: [email protected].

Abstract

Androgen receptor signaling is critical for prostate adenocarcinoma, even after androgen deprivation therapy. Persistence of intratumoral androgens has been found in castration-resistant prostate cancer and attributed to increased in situ synthesis. Recently, Sharifi and colleagues reported an additional mechanism that can enhance local androgenic exposure: downregulation of an androgen-inactivating enzyme.

Keywords: DHT; HSD17B4 variant 2; androgen receptor (AR) signaling; castration-resistant prostate cancer; testosterone.

Publication types

Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Comment

MeSH terms

Androgens*
Down-Regulation / drug effects
Humans
Male
Peroxisomal Multifunctional Protein-2
Prostatic Neoplasms
Prostatic Neoplasms, Castration-Resistant
Protein Isoforms
Receptors, Androgen / genetics*

Substances

Androgens
Protein Isoforms
Receptors, Androgen
Peroxisomal Multifunctional Protein-2
HSD17B4 protein, human

Abstract

Publication types

MeSH terms

Substances

Grants and funding