If you are interested in BAT you could just join one of the studies currently being done. Here is another article about
the early findings from one on-going study which were presented at a symposium on Molecular Targets and Cancer Therapeutics in Munich, Germany: How highs and lows in testosterone levels 'shock' prostate cancer cells to death
They are still recruiting participants.
P.S. Finally managed to fix the link to the article above.
P.S. I am citing
here the abstract of the presentation:
Denmeade at http://www.ecco-org.eu/Events/ENA2016/Searchable-Programme#anchorScpr said...
Background: Prostate cancer (PC) becomes resistant to chronic castration via an adaptive increase in androgen receptor (AR) axis activity through overexpression, gene amplification, and expression of ligand independent AR variants. AR overexpression, however, is a liability that can be exploited therapeutically. Mechanistically, supraphysiologic T induces PC death through disruption of DNA relicensing due to persistence of AR at origins of replication during the cell cycle. Ligand bound AR can also induce DNA double strand breaks in androgen starved cells re-exposed to androgen.
Methods: In an ongoing study, asymptomatic men (n = 60) with CRPC and progression on A and/or E (30/cohort) receive T cypionate 400 mg IM every 28 days along with ongoing castration to rapidly cycle between polar extremes of supraphysiologic and near-castrate levels of serum T (bipolar androgen therapy, BAT). Men with declining PSA and/or stable radiographic disease can continue BAT after 3 cycles and are rechallenged with A or E at progression. Co-primary endpoints include ≥50% PSA response after 3 cycles of BAT and after re-treatment of E or A after progression to BAT. The study is designed to reject a treatment with <5% PSA response based on prior data with sequential AR targeted treatments. Secondary endpoints include objective response, safety, quality of life, and effect on CTC-based AR-V7 expression.
Results: The study remains open for patient enrollment; 37 have completed at least 3 cycles of BAT and 31/37 (83%) continued on treatment beyond the initial 3 months; 11/37 (30%) had ≥50% PSA decline and 20/37 (54%) had PSAs decline <50%. 4/17 (23%) with measurable disease had RECIST responses and 11/17 (65%) had stable disease after 3 months of BAT. Of 25 men evaluable in the post BAT phase, 8 (32%) and 15 (60%) had ≥50% and <50% PSA declines after 3 months of retreatment with the same pre-study AR targeted treatment (A or E). 21/34 men tested in this group had detectable CTCs with 6/21 testing AR-V7 +. All AR-V7 + men became AR-V7 negative after BAT, and 2/6 of these AR-V7 + men had a ≥50% PSA decline. BAT has generally been well tolerated and no DLT’s have been seen thus far. 1 patient had a self-limited increase in pain and 1 had urinary retention, otherwise there were no bone/soft tissue AE’s with BAT to suggest disease flare.
Conclusions: This preliminary data demonstrates the safety and activity of BAT in patients with CRPC post-A and/or E with PSA and objective responses, including responses in AR-V7 + men. An ongoing multi-center randomized trial is testing BAT vs E in the post-A CRPC population.
Post Edited (George_) : 12/5/2016 10:28:03 AM (GMT-7)