Sounds promising. These patients had a PSADT of 3.2 months before RT. After RT, it took 15.6 months for the PSA to increase from nadir to nadir+2. Looking forward to the prospective study.
Conclusions: A relevant subset of patients with 68Ga PSMA-PET-detected oligometastatic low volume CRPC had a meaningful PSA-response with aRT. They were reverted into an earlier stage of their disease again. A prospective clinical trial on this clinically highly relevant question is being prepared.
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tango65
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Unfounded conclusion. Here's why (let's put aside the fact that it was only noted in 15 patients):
1) In metastatic disease, the larger mets put out most of the PSA. That's because metastases create their own (leaky) blood supply, and that is the only way their PSA can leach out into the serum.
2) There is no question that radiation ablates cancer cells. By destroying the largest source of PSA, PSA will go down (after an initial increase).
3) Metastases are always some mixture of hormone sensitive and resistant clones. Older mets, the larger ones that become visible on scans, have a higher percentage of hormone-resistant clones.
4) By ablating the metastases with more hormone-resistant clones, one is left with only micrometastases that do not put out as much PSA. There is no "reversion." The cancer responds to ADT just as it always did, but it wasn't apparent, because hormone-resistance was judged by rising PSA.
In short, all the authors accomplished is "treating PSA" rather than treating the underlying cancer (which would require systemic therapy). They would have to look at the effect on survival to reach a conclusion that it was beneficial.
Addendum:
The lead author wrote to me that he largely agrees with me. He speculates that PSMA-based imaging can preferentially detect the androgen independent clones. He says that only large randomized clinical trials can ascertain whether there is a benefit to metastasis-directed therapy. He apologized for the provocative headline (journal editors often supply the headline).
I agree, reversion is the wrong descriptive term to use to describe the response to ablative SBRT. After reading the paper, I concluded that the intergenetic variability of metastases would result in some being more resistant than others to hormone therapy, and that it was a more probabilistic process that some men were able to continue to be hormone sensitive. The visible metastases that got zapped happened to be more resistant. I like the size issue that you mention. Cheers, Phil
TA is correct. We will all be dead of old age before this goes anywhere..Depending of course on how much money you are willing to spend someplace outside the U.S.
I think debulking the tumor is beneficial. Both in the hormone-sensitive and castration resistent situation. Patients with a low volume disease have a better prognosis than patients with a high-volume disease. Debulking reduces the tumor volume.
Gravis G, et al., Eur Urol (2018), 10.1016/j.eururo.2018.02.001
Patient summary: Patients with a higher burden of metastatic prostate cancer starting androgen deprivation therapy (ADT) have a poorer prognosis and are more likely to benefit from early docetaxel. Low-volume patients have longer overall survival with ADT alone, and the toxicity of docetaxel may outweigh its benefits.
Parker et al., The Lancet, Oct 21, 2018, 10.1016/S0140-6736(18)32486-3
From table 2: survival at 3 years in the control group: Low metastatic burden 62%, High metastatic burden 37%
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Any Curative Treatments after RT as Sole Primary Treatment?
Is it useful to get a PSMA-PET scan with low volume cancer, newly castration resistant and PSA below 1?
PSA teating or wait it out?
Castration resistant prostate cancer - Starting Jevtana with Prednisone in a few days
Low PSA levels are associated with greater prostate cancer-specific mortality among men with a Gleason score of 8 to 10
