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CATEGORIES:Cambridge Oncology Seminar Series
SUMMARY:Steroid Hormone Receptors in Prostate Cancer: A Ha
 rd Habit to Break? - Dr Gerhardt Attard\, The Inst
 itute of Cancer Research and the Royal Marsden Hos
 pital
DTSTART;TZID=Europe/London:20091027T120000
DTEND;TZID=Europe/London:20091027T130000
UID:TALK19418AThttp://talks.cam.ac.uk
URL:http://talks.cam.ac.uk/talk/index/19418
DESCRIPTION:The clinical data from abiraterone acetate and MDV
 -3100 confirm continued androgen receptor (AR) add
 iction in a significant proportion of castration-r
 esistant prostate cancers (CRPC). Abiraterone acet
 ate is a highly specific inhibitor of CYP17 and re
 sults in significant suppression of serum androgen
 ic steroids and oestrogens1. Declines in PSA by ≥5
 0% and ≥90% with abiraterone acetate have been rep
 orted in 50-60% and 20-30% of CRPC patients respec
 tively\, despite prior progression while castrate 
 on several hormonal agents2. Importantly\, decline
 s in PSA were associated with radiological tumour 
 regression\, declines in circulating tumour cell (
 CTC) count and symptomatic benefit2. Moreover\, pr
 ior treatment with docetaxel chemotherapy did not 
 significantly alter sensitivity to abiraterone ace
 tate3. MDV-3100 is a potent AR antagonist which al
 so induces tumour responses in CRPC patients4. Bot
 h these agents are now undergoing evaluation in la
 rge\, randomized\, global\, phase III studies desi
 gned to identify a survival benefit and obtain reg
 ulatory approval to treat CRPC. However\, resistan
 ce to these agents commonly develops within 18 mon
 ths and is nearly invariably characterized by a ri
 sing PSA\, suggesting resumption of transcription 
 of hormone-regulated genes. In fact\, although ETS
  gene fusions appear to be an early event in prost
 ate carcinogenesis\, hormone-regulated over-expres
 sion of ERG persists in end-stage CRPC5. Also\, CR
 PC patients with a hormone-dependent ERG gene fusi
 on are significantly more likely to have a ≥90% PS
 A decline with abiraterone acetate5. The future de
 velopment of therapeutics for CRPC should be infor
 med by the molecular classification of CRPC using 
 analytically validated predictive biomarkers in a 
 combination of tumour tissue and CTC and by a bett
 er understanding of the mechanisms underlying dise
 ase progression following treatment with these nov
 el\, hormonal agents.\n\nReferences:\n\n1.	Attard 
 G et al\, J Clin Oncol 26:4563-71\, 2008\n\n2.	Att
 ard G et al\, J Clin Oncol\, 2009 XXX\n\n3.	Attard
  G et al\, Cancer Res 69:4937-40\, 2009\n\n4.	Tran
  C et al\, Science\, 2009 XXX\n\n5.	Attard G et al
 \, Cancer Res 69:2912-8\, 2009\n\n\n\n\n\n
LOCATION:CRI Lecture Theatre
CONTACT:Mala Jayasundera
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