Managing Prostate CA in the community

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medgator

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Just wanted to get a sense of what everyone else has noticed in their transition from residency to practice, particularly with regards to Prostate CA.

I'm sure it may have been common for some of you to give hormones/ADT and place fiducials for IGRT, but I did neither where I trained. It's interesting to find out that it's pretty common in the community for both of those things to fall to the rad onc.

I'm guessing the ADT trend happened within the last few years, probably along with this trend :laugh:
 
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I only insist on ADT for high-intermediate and high risk. Very rare for our urologists to put in fiducials, we do daily CBCT. I like to use Cleveland Clinic hypofrac for low and low-intermediate risk.

Gfunk,

Have you had any experience using the newer GnRH antagonists (like Firmagon)? Some of the GUs in my area swear by it.

NCCN recommends using either an agonist or an antagonist for localized high-risk disease when treating with XRT.

There is however some recent data presented at ASCO regarding a possible benefit for the antagonist over the agonist: http://www.asco.org/ascov2/Meetings/Abstracts?&vmview=abst_detail_view&confID=104&abstractID=72251
 
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Interesting data, I'd never even heard of a GnRH antagonist until I read that abstract.

Where I practice, all of the urologists I know still use GnRH agonists with a couple of weeks of anti-androgens in the beginning to mitigate testosterone flare.
 
Interesting data, I'd never even heard of a GnRH antagonist until I read that abstract.

Where I practice, all of the urologists I know still use GnRH agonists with a couple of weeks of anti-androgens in the beginning to mitigate testosterone flare.

Being an antagonist, there is theoretically no flare. Another benefit of it supposedly
 
Being an antagonist, there is theoretically no flare. Another benefit of it supposedly

Where I practice, we use firmagon for patients treated off trial without anti-androgen. PSA response rates in the neoadjuvant setting appear superior to GnRH agonists, and time to castrate testosterone is shorter (as has been demonstrated in clinical trials). Downside is monthly administration. Since there is no theoretical benefit of antagonist vs agonist after castrate levels of testosterone have been acheived, we have been giving two months of firmagon followed by GnRH agonist.
 
Where I practice, we use firmagon for patients treated off trial without anti-androgen. PSA response rates in the neoadjuvant setting appear superior to GnRH agonists, and time to castrate testosterone is shorter (as has been demonstrated in clinical trials). Downside is monthly administration. Since there is no theoretical benefit of antagonist vs agonist after castrate levels of testosterone have been acheived, we have been giving two months of firmagon followed by GnRH agonist.

I also hear the local site reaction/discomfort is worse with firmagon. interesting idea with the crossover back to the agonist
 
I also hear the local site reaction/discomfort is worse with firmagon. interesting idea with the crossover back to the agonist

The early reports of this trial (2008 and 2010) suggest that the superiority of firmagon is primarily related to more rapid achievement of castrate levels of testosterone and lower day 14 and day 28 PSA values. After re-reading this abstract, with long term follow-up and cross-over data, it suggests that firmagon is superior to lupron even after castrate levels of testosterone are acheived (hence lower PSA nadirs and prolonged time to PSA >20ng/mL among patients who crossed-over from lupron to firmagon after 1 year compared to those who remained on lupron). In light of this data, I plan to adjust my practice for patients treated off trial and continue firmagon for the entire duration of hormonal Tx (rather than crossing over to GnRH agonist). We treat a lot of patients on RTOG trials as well... of course, these patients are treated with GnRH agonist and anti-androgen per protocol.

Thanks for posting this abstract!
 
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