Salvage prostate XRT

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.

Reaganite

Member
15+ Year Member
Joined
Apr 6, 2006
Messages
816
Reaction score
1,276
Points
4,931
  1. Resident [Any Field]
Advertisement - Members don't see this ad
I have had a recent run of salvage prostate XRT cases whose PSA has continued to rise after treatment (usually checked about 3 months after last treatment). These were all borderline cases from the get-go (e.g. Gleason 9-10 disease, negative margins, detectable postop PSA). Have any of you considered checking PSAs in the latter half of treatment in these high risk cases and stopping xrt if PSA has risen?
 
I have had a recent run of salvage prostate XRT cases whose PSA has continued to rise after treatment (usually checked about 3 months after last treatment). These were all borderline cases from the get-go (e.g. Gleason 9-10 disease, negative margins, detectable postop PSA). Have any of you considered checking PSAs in the latter half of treatment in these high risk cases and stopping xrt if PSA has risen?
No, I counsel them upfront that it's a 50-50 shot overall for all comers, worse in the group you're mentioning.

We don't have the data to do that plus radiobiologically it doesn't make sense to do that imo, sometimes it can take weeks to months after treatment to see the full effect of xrt.

By the time you document a doubling time a month or two apart, they are almost done with their salvage course anyways
 
Last edited:
Kind of brings up another point as to why is there a PSA bounce after definitive RT if there is an initial decrease after treatment? I know I probably could look it up but I'm watching the game.
 
Yes, sometimes I do check midway. Options if PSA still rising include adding ADT to XRT or ADT alone without XRT. Not sure if either of these approaches is supported by good data.

The ADT option is interesting and I think about this a lot. There is no good data either way but my question to everyone is who else adds ADT to RT in salvage patients? Especially for patients who were high risk in the first place who would have gotten ADT if they were treated definitively. Whether you believe that ADT improves outcomes in the definitive setting by improving radiosensitivity or eradicating micro (probably more appropriately to say nano) metastases, one could argue it could also be beneficial in the salvage setting as well. We have started adding ADT to most all of our salvage patients, especially those who now appear to be salvageable at this point (reasonable PSA, reasonable PSA velocity, clincally M0 with appropriate radiographic staging, etc). Just curious, is anyone else is doing likewise?
 
I do 6-12 months of ADT, and try to start 1-2 months before XRT. I do it in high risk pts (LN+, G8+, T3b), still stick to salvage xrt alone in intermediate-risk pts

I don't do the 28-36 months of ADT studied in the definitive setting, curious if anyone does that.
 
I would think checking PSA would not be useful because I have seen PSA rise from radiation alone, then trend down.

These high risk guys certainly may have systemic disease and I have seen up to 2 yr ADT to answer medgator's question.

But that is extrapolation and not based on any data.
 
I would think checking PSA would not be useful because I have seen PSA rise from radiation alone, then trend down.

These high risk guys certainly may have systemic disease and I have seen up to 2 yr ADT to answer medgator's question.

But that is extrapolation and not based on any data.

We don't do two years for any of these guys though I have suggested it and would consider doing it. I think in the right patients two years makes sense. My thinking is pretty simple: in definitive treatment 2 years is better than 6 months in high risk patients. That strongly suggests to me that at least part of the benefit of ADT in these patients is not local but distant (since RT only lasts the first couple months of the 2 years). That being the case patients who are not at a really high risk of already having a high burden of metastases really could benefit from 2 years of ADT in terms of cure and OS.

I wouldn't do two years in patients I suspect have a good chance of already being metastatic though (patients with rapid PSA velocities etc). IF ADT cures micromets the evidence suggests that they likely have to be really small/early/poorly established...whatever descriptor you prefer. Its not going to cure patients who already have established metastatic deposits. In those cases I think its better for them in the long-run if they declare their metastatic status and move on to appropriate systemic therapy.
 
I wasn't aware that people thought that the 2yr ADT was actually improving cure rates. Improvements in OS can be due to delay in progression, altering natural history of disease.
 
Another question for me is if any of you have started considering docetaxel for high risk patients - if so, who?
 
Advertisement - Members don't see this ad
I wasn't aware that people thought that the 2yr ADT was actually improving cure rates. Improvements in OS can be due to delay in progression, altering natural history of disease.

Agree that it is unknown (reason I underlined IF in my post above) but yes some people do interpret the results as long-term ADT likely improves cure rates in high-risk patients. The natural history of PC makes this hard to discern and it's always an important point to consider.
 
Another question for me is if any of you have started considering docetaxel for high risk patients - if so, who?

these patients were included in the STAMPEDE trial
 
Correct, which is why I asked. If I recall correctly, also RTOG data reported. So are people starting this in clinical practice? At my institution, last time I asked this question (June 2015, after ASCO) they said they weren't ready yet. I should probably ask again, I think it's time to at least offer to the appropriate patient (good PS and chemo appropriate, high risk).
 
1. Yes, I have often performed in-between PSA-measurements. I don't think there is much of a trouble with the PSA-bounce, since you see the bounce usually after treatment and not during it.
I usually perform a PSA-measurement immediately at the beginning of RT and then 5 weeks later. It's not helpful in all patients and in some, the test results will rather confuse you. There are patients who may benefit from this approach, because you will spare them from aggressive treatment.
I've had a patient starting RT with a PSA of 0.4 ng/ml and who at week 5 had a PSA of 0.7 ng/ml. He was tolerating treatment bad, so we decided to stop at week 5. Follow up showed further progression and he was metastatic, as suspected.
I normally do this in-between testing only in patients I know of having a high PSA-velocity. If the PSA was rising at a rate of 0.1-0.2 ng/ml over 3 monthly intervalls before RT, then the test won't help you guide treatment. Patients with a doubling time which is considerably less than 6 months are better candidates for the approach.
Wiegel has studied this:
http://www.ncbi.nlm.nih.gov/pubmed/12240547
He has shown that patients who don't fall off with their PSA by week 6 can almost never be cured with RT.


2. I do not give concurrent ADT for node-negative patients. RTOG 9601 has now reported long-term results with a potential survival benefit of 4% with the concurrent use of 24 months of bicalutamid with RT (after 10 years!), but:
a) this is a 90s trial, meaning that patients recurring after salvage-RT had very little chance of getting any other treatment. Docetaxel was the option in the 2000s, no enzalutamide, no abiraterone. It's thus questionable, if the OS-survival would still happen, if the trial was run again today, especially if we speculate that ADT is not curing patients but rather "pushing" progression "down the road".
b) the patients in the trial, that benefited were mainly those with high PSA-values (>0.7 ng/ml, especially >1.5ng/ml). Patients with PSA-values <0.7ng/ml didn't seem to benefit. Nowadays you shouldn't be getting salvage RT patients referred to you with PSA-values that high and should ideally treat them at PSA-levels <0.5 ng/ml.
c) staging before RT in the trial was done with a CT-pelvis. I presume that since lots of patients in the trial had high PSA-levels, that some of these patients actually had macroscopic recurrences at the time of RT. Nowadays modern MRI would have picked up these patients and you would have good reasons to perform dose escalation or give hormones to RT in those selected cases.
For these reasons I am not convinced, that giving ADT should become standard of care for all patients with salvage RT. One could consider it however for patients with high psa-levels. I would give it for pN1-patients as well.


3. I would be cautious about Docetaxel in non-metastatic patients.
The Stampede data are good, but more than half of the patients randomized has systemic metastasis. We do not know if the locally-advanced & pelvic-node-positive patients will benefit that much from Docetaxel as well. Looking at the CHARTEED data, we know that mostly "high-volume" systemic metastatic patients benefit from Docetaxel, not the "low-volume" disease patients. A patient with a locally advanced N0 M0 tumor is not a patients with "high-volume" disease. The GETUG-12 trial
( http://www.thelancet.com/journals/lanonc/article/PIIS1470-2045(15)00011-X/abstract ) for locally advanced disease did not show an OS-benefit, but only a PFS-benefit. I would await long-term results from this trial, as well as subgroup analysis from the Stampede trial and results from the currently recruiting RTOG-trial before going for Docetaxel in the non-metastatic patients together with RT.
 
"This trial was designed with a short OS assessment period and additional follow-up is warranted to determine the long-term benefit of CT to the current standard of care of long-term AS+RT."

It's still a trial run 10 years ago. No abi, no enza...

 
1. Yes, I have often performed in-between PSA-measurements. I don't think there is much of a trouble with the PSA-bounce, since you see the bounce usually after treatment and not during it.
I usually perform a PSA-measurement immediately at the beginning of RT and then 5 weeks later. It's not helpful in all patients and in some, the test results will rather confuse you. There are patients who may benefit from this approach, because you will spare them from aggressive treatment.
I've had a patient starting RT with a PSA of 0.4 ng/ml and who at week 5 had a PSA of 0.7 ng/ml. He was tolerating treatment bad, so we decided to stop at week 5. Follow up showed further progression and he was metastatic, as suspected.
I normally do this in-between testing only in patients I know of having a high PSA-velocity. If the PSA was rising at a rate of 0.1-0.2 ng/ml over 3 monthly intervalls before RT, then the test won't help you guide treatment. Patients with a doubling time which is considerably less than 6 months are better candidates for the approach.
Wiegel has studied this:
http://www.ncbi.nlm.nih.gov/pubmed/12240547
.

Like the Wiegel data there are other smaller observational studies that have looked at in-treatment PSA and like you may expect - a rising PSA during XRT at a week ~5 check is a very bad sign:

http://www.sciedu.ca/journal/index.php/jst/article/viewFile/2883/1912

https://www.researchgate.net/public...h_an_analysis_of_intra-treatment_PSA_kinetics

I don't usually check an in treatment PSA, but I would support a trial that prospectively looked into stopping local treatment (or adding ADT) if PSA is rising during XRT.
 
Top Bottom