Zoledronic acid at the time of castration prevented castration-induced bone metastasis in mice

Research output: Contribution to journalArticle

Abstract

Androgen deprivation therapy (ADT) is known to cause bone loss in a majority of patients with castration-resistant prostate cancer (CRPC). A study published in this issue of Endocrine-Related Cancer by Ottewell and colleagues shows that ADT increased bone resorption and triggered growth of disseminated prostate cancer (CaP) cells to form bone metastasis using an in vivo model. However, prevention of bone decay by weekly administration of zoledronic acid (ZOL) at the time of castration prevented ADT-induced tumor growth in bone. Recently, two publications from Japan have demonstrated that ZOL combined with ADT improved outcomes for patients with treatment-naïve CaP with bone metastasis. The mechanistic cause for these patients having an improved overall survival compared with those who were treated with ZOL after ADT initiation or before metastasis development was never explained. Ottewell and colleague's study now suggests that it is the bone loss caused by ADT that promoted bone metastasis, and if ZOL is administered at the time of ADT initiation, it would prevent this bone loss and prolong skeletal-related event-free survival.

Original languageEnglish (US)
Pages (from-to)C11-C14
JournalEndocrine-Related Cancer
Volume21
Issue number5
DOIs
StatePublished - Oct 1 2014

Fingerprint

zoledronic acid
Castration
Androgens
Neoplasm Metastasis
Bone and Bones
Therapeutics
Prostatic Neoplasms
Endocrine Gland Neoplasms
Bone Development
Bone Resorption

Keywords

  • Androgen
  • Bone loss
  • Deprivation therapy
  • Prostate cancer
  • Zoledronic acid

ASJC Scopus subject areas

  • Endocrinology
  • Oncology
  • Cancer Research
  • Endocrinology, Diabetes and Metabolism

Cite this

Zoledronic acid at the time of castration prevented castration-induced bone metastasis in mice. / Ghosh, Paramita M; Gao, Allen C.

In: Endocrine-Related Cancer, Vol. 21, No. 5, 01.10.2014, p. C11-C14.

Research output: Contribution to journalArticle

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