Steroid hormone receptors in prostate cancer: a hard habit to break?

Gerhardt Attard; Colin S Cooper; Johann S de Bono

doi:10.1016/j.ccr.2009.11.006

Steroid hormone receptors in prostate cancer: a hard habit to break?

Gerhardt Attard, Colin S Cooper, Johann S de Bono

Research output: Contribution to journal › Article › peer-review

205 Citations (Scopus)

Abstract

The clinical data from abiraterone acetate and MDV-3100 confirm continued androgen receptor (AR) addiction in a significant proportion of castration-resistant prostate cancers (CRPC). However, patients nearly invariably progress with a rise in prostate-specific antigen, suggesting resumption of transcription of hormone-regulated genes. If CRPC remains addicted to steroid receptor signaling, including, but not exclusive, to AR, how does reactivation occur? Or if cancers lose this addiction, do they remain driven by the same oncogenic mechanisms? The future development of therapeutics for CRPC should be informed by an understanding of the mechanisms underlying disease progression following treatment with these novel agents.

Original language	English
Pages (from-to)	458-62
Number of pages	5
Journal	Cancer Cell
Volume	16
Issue number	6
DOIs	https://doi.org/10.1016/j.ccr.2009.11.006
Publication status	Published - 8 Dec 2009

Keywords

Androgens
Androstenols
Disease Progression
Humans
Male
Phenylthiohydantoin
Prostatic Neoplasms
Receptors, Androgen
Receptors, Estrogen
Signal Transduction

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1016/j.ccr.2009.11.006

Cite this

@article{845b6f31a42440ab9a29d45a97e0aa32,

title = "Steroid hormone receptors in prostate cancer: a hard habit to break?",

abstract = "The clinical data from abiraterone acetate and MDV-3100 confirm continued androgen receptor (AR) addiction in a significant proportion of castration-resistant prostate cancers (CRPC). However, patients nearly invariably progress with a rise in prostate-specific antigen, suggesting resumption of transcription of hormone-regulated genes. If CRPC remains addicted to steroid receptor signaling, including, but not exclusive, to AR, how does reactivation occur? Or if cancers lose this addiction, do they remain driven by the same oncogenic mechanisms? The future development of therapeutics for CRPC should be informed by an understanding of the mechanisms underlying disease progression following treatment with these novel agents.",

keywords = "Androgens, Androstenols, Disease Progression, Humans, Male, Phenylthiohydantoin, Prostatic Neoplasms, Receptors, Androgen, Receptors, Estrogen, Signal Transduction",

author = "Gerhardt Attard and Cooper, {Colin S} and {de Bono}, {Johann S}",

year = "2009",

month = dec,

day = "8",

doi = "10.1016/j.ccr.2009.11.006",

language = "English",

volume = "16",

pages = "458--62",

journal = "Cancer Cell",

issn = "1535-6108",

publisher = "Cell Press",

number = "6",

}

TY - JOUR

T1 - Steroid hormone receptors in prostate cancer

T2 - a hard habit to break?

AU - Attard, Gerhardt

AU - Cooper, Colin S

AU - de Bono, Johann S

PY - 2009/12/8

Y1 - 2009/12/8

N2 - The clinical data from abiraterone acetate and MDV-3100 confirm continued androgen receptor (AR) addiction in a significant proportion of castration-resistant prostate cancers (CRPC). However, patients nearly invariably progress with a rise in prostate-specific antigen, suggesting resumption of transcription of hormone-regulated genes. If CRPC remains addicted to steroid receptor signaling, including, but not exclusive, to AR, how does reactivation occur? Or if cancers lose this addiction, do they remain driven by the same oncogenic mechanisms? The future development of therapeutics for CRPC should be informed by an understanding of the mechanisms underlying disease progression following treatment with these novel agents.

AB - The clinical data from abiraterone acetate and MDV-3100 confirm continued androgen receptor (AR) addiction in a significant proportion of castration-resistant prostate cancers (CRPC). However, patients nearly invariably progress with a rise in prostate-specific antigen, suggesting resumption of transcription of hormone-regulated genes. If CRPC remains addicted to steroid receptor signaling, including, but not exclusive, to AR, how does reactivation occur? Or if cancers lose this addiction, do they remain driven by the same oncogenic mechanisms? The future development of therapeutics for CRPC should be informed by an understanding of the mechanisms underlying disease progression following treatment with these novel agents.

KW - Androgens

KW - Androstenols

KW - Disease Progression

KW - Humans

KW - Male

KW - Phenylthiohydantoin

KW - Prostatic Neoplasms

KW - Receptors, Androgen

KW - Receptors, Estrogen

KW - Signal Transduction

U2 - 10.1016/j.ccr.2009.11.006

DO - 10.1016/j.ccr.2009.11.006

M3 - Article

C2 - 19962664

VL - 16

SP - 458

EP - 462

JO - Cancer Cell

JF - Cancer Cell

SN - 1535-6108

IS - 6

ER -