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Strange that it is not open access.
Increased rates of acute GU toxicity and GU toxicity at one year.
Here we go again. I look forward to the same arguments as in the prostate hypofrac thread(s). I imagine people will tell us to ignore increased acute toxicity (as was done with moderate hypofrac) in the interest of shortening treatment schedules. Can be offered to patients if you want to bill 7fx IMRT.
All people wanna do is justify treating with less fractions. European trials focused on cost-cutting will do this despite increases in toxicity, and scream that fee-for-service is the enemy of the patient.
If it's me I want the treatment that will give me the least toxicity in all phases with the best outcome, duration of treatment be damned.
Why don't we work on increasing that 84% bPFS at 5 years number? Why is that not the focus, rather than inducing more toxicity to get patients done in the interest of patient convenience?
Increased rates of acute GU toxicity and GU toxicity at one year.
Here we go again. I look forward to the same arguments as in the prostate hypofrac thread(s). I imagine people will tell us to ignore increased acute toxicity (as was done with moderate hypofrac) in the interest of shortening treatment schedules. Can be offered to patients if you want to bill 7fx IMRT.
All people wanna do is justify treating with less fractions. European trials focused on cost-cutting will do this despite increases in toxicity, and scream that fee-for-service is the enemy of the patient.
If it's me I want the treatment that will give me the least toxicity in all phases with the best outcome, duration of treatment be damned.
Why don't we work on increasing that 84% bPFS at 5 years number? Why is that not the focus, rather than inducing more toxicity to get patients done in the interest of patient convenience?
When single payer hits the US, we will also be convieniantly ignoring this as well. Naysayers will be silenced accordingly.
I'm sorry, but give me a break - acute urinary toxicity was 6% vs 2% at 1 year. You would need to treat 25 people with conventional fractionation to save a single person from acute toxicity at a single time point. Care to do the math on the cost to save that single toxicity outcome, which ironically balances out in the long-term? We also know once-weekly fractionation decreases acute GU/GI toxicity in 5 fraction SBRT, instead of accelerating the treatment as well.
We aren't rad oncs from the 1980's anymore using conventional sims and treating large areas unnecessarily, and choosing our doses by toxicity. It's ok to move away from 1.8-2 Gy per day, and we now have level 1 evidence to support ultrahypofractionation.
This is why I am a believer in breast hypofrac (I wouldn't even really offer standard breast for WBI alone anymore) and not a mandatory adopter of prostate hypofrac.
But I look forward to people telling me I am just another money-grubbing Rad Onc.
Those pushing for ultra-hypofrac - what would you want as a patient? Do you discuss the increase in toxicity seen with your recommendation?
The least toxic? Care to tell me what your dose is for typical conventional fractionation prostate? You know that 79.2 Gy is more toxic than 70.2 with no difference in OS.Called it.
Why is Radiation Oncology the only specialty that has to self-regulate on cost? Why are we the only specialty to insist on self-flagellation to recommend to our patients a more toxic treatment in the interest of cost savings?
Surgery doesn't do this. Med-onc doesn't do this.
I will continue pushing for the LEAST toxic treatment for my patients regardless of reimbursement schedule. I will certainly offer it to patients if they want to get done super quickly. This is why I am a believer in breast hypofrac (I wouldn't even really offer standard breast for WBI alone anymore) and not a mandatory adopter of prostate hypofrac.
But I look forward to people telling me I am just another money-grubbing Rad Onc.
Those pushing for ultra-hypofrac - what would you want as a patient? Do you discuss the increase in toxicity seen with your recommendation?
what would you want as a patient?
My retired patients hate waking up more at night than the 2-3x they are already than coming in for more fractions. They'd really hate having to get a Foley catheter even more.Easy. To not have to come for 9 weeks. During training especially, cost has nothing to do with it, but I did love to be able to tell a patient they only had to come for 28 or 20 treatments or for those who elected it - only 5.
Foley catheter...hmmm what is the published rate of urinary retention with external beam?My retired patients hate waking up more at night than the 2-3x they are already than coming in for more fractions. They'd really hate having to get a Foley catheter even more.
I've done 28 fx hypofx a few times for the pts I've had that worked through tx. They definitely noticed the GU effects more but were fine with their decision
I actually saw it happen once....Foley catheter...hmmm what is the published rate of urinary retention with external beam?
The least toxic? Care to tell me what your dose is for typical conventional fractionation prostate? You know that 79.2 Gy is more toxic than 70.2 with no difference in OS.
I look forward to the 'bPFS isn't a worthwhile endpoint in prostate cancer' argument.
It is a serious statement. BTW you didn't answer the question I asked. From your response I am guessing that you use 79.2 Gy. The absolute difference in toxicity is 10-15% (cf. 4% as described above) with 79.2 versus 70.2.Yes, but there are improvements in bPFS with 79.2 compared to 70.2! Is this a serious statement? We, as oncologists, accept higher toxicity rates when we are curing more people. You are advocating for increasing toxicity rates with the only benefit to the patients being less treatments.
Listen, if you told me that a 5 or 10 fraction regimen had improved bPFS but higher rates of toxicity I'd be all about it. That's what the initial hypofractionation trials were supposed to show anyways. Then the push became cost, cost, and convenience at the expense of patient toxicities.
Again, if YOU want to do offer or recommend it to your patients then fine, do your thing. To each their own.
I look forward to the 'bPFS isn't a worthwhile endpoint in prostate cancer' argument.
They definitely noticed the GU effects more but were fine with their decision
@Lamount and @Chartreuse Wombat
Early results of other prostate trials initially showing just bPFS benefits eventually turned into DM/OS benefits.
Do we have a robust, validated, means of differentiating these two patient populations (whether the PSA is predictive of DMFS or OS or not) from one another? No. (Happy to be educated on this topic btw, if there are nomograms or other evidence evaluating this beyond just 'PSADT matters!!')ok ok... let's clear a few things up.
For individual patients:
Are PSAs important in screening for prostate cancer and monitoring response to therapy? yes
If a patient develops a biochemical failure following radiation therapy, is this a significant event that could lead to additional therapies? yes
For a given individual patient, could a biochemical failure be a harbinger for additional prostate cancer associated morbidity and mortality? yes
is this always the case?...no
For patient populations:
Are there studies where differences in bPFS led to differences in metastasis-free survival or OS? yes
Can we conclude that for, for every population, under every circumstance, bPFS can be a surrogate for MFS or OS (or even correlated with MFS or OS)?... no
Even if bPFS were always correlated with MFS and OS, can we conclude that a statistically significant difference in bPFS translates to a statistically significant and/or clinically meaningful difference in MFS or OS?... no.
Thus, can we assume that bPFS is always a meaningful endpoint when evaluating the efficacy of oncologic treatments for prostate cancer?... nope
Might this change in the future?...yes, but we aren't there yet.
Where to begin?Do we have a robust, validated, means of differentiating these two patient populations (whether the PSA is predictive of DMFS or OS or not) from one another? No. (Happy to be educated on this topic btw, if there are nomograms or other evidence evaluating this beyond just 'PSADT matters!!')
Agree with all of the above.
Does a biochemical recurrence lead to symptomatic local or distant recurrence prior to the patient dying of other causes near 100% of the time? No
Does a biochemical recurrence lead to additional testing, treatment, and/or anxiety near 100% of the time? Yes
Does a biochemical recurrence mean that the patient is not 'cured' of their prostate cancer near 100% of the time? Yes
Similar thought process - do you consider local recurrence as a valid endpoint for breast cancer, or do you only believe in DMFS or OS?
I'll ask it again - what dose do you use for conventionally fractionated prostate radiation? Based off your arguments about the invalidity of bPFS I'm assuming you only treat these to 70Gy.
Slippery slope. Technically if I have the machine time, I shouldn't offer the patient a less toxic treatment if they are willing to come in more often?. One of the tenets of medical professionalism is to use resources wisely. Part of my practice is in a resource constrained environment. If I hypofractionate prostate then the folks with locally advanced head and neck or lung cancer can begin treatment without delay because there are fewer demands on linac time.
I have a hard time reconciling the viewpoint that bPFS is not a "meaningful" endpoint while simultaneously saying that saving a few weeks by doing hypofractionation is "meaningful."
Firstly, there are numerous trials that demonstrate non-inferiority of hypo-fract with respect to biochemical control... and the early results from extreme hypo-fact are encouraging. So you don't have to choose.
But hypothetically, just to posit a question... if there were a trial with a sample size large enough to demonstrate that there was a 1.5% improvement in biochemical control with a 9 week course of EBRT vs. a 5 day course of SBRT (NNT to prevent 1 biochemical failure = 67), would you offer SBRT, or would you keep this option from the patient because of the inferior control... or would you discuss the pros and cons of each modality. Convenience may not seem like an important factor to us... but for many patients, it entirely influences their decision to undergo treatment. Some don't have the luxury of being able to put their life on hold for treatment.
I think you completely missed the point of my post.
First of all, I'm not saying that hypofrac has worse biochemical control. I'm referring to those posters who are simultaneously advocating for hypofrac while pooh-poohing BFS as an endpoint. I'm saying those viewpoints are incongruent.
I'm not saying patient convenience is unimportant. I'm saying that the patient experience is important, but the impact on patient experience of a biochemical failure far exceeds that of a longer radiation course, so if you care about one you should definitely care about the other. To hold up hypofrac as a shining boon for patients due to the convenience while passing off a biochemical failure as just a "bad lab test" and state that "people do not suffer from bad lab tests" is nonsensical.
I think you are painting with a rather large brush to suggest that academic departments don't operate in resource constrained environments. There are some that can charge monopolistic rates but not all.Thank you for repeating your arguments from the prostate hypofrac thread once again. Please stop attempting to put words in my mouth about late toxicities because you are unable to remember the discussion of that topic across multiple threads. My issue with prostate moderate hypofrac is primarily on rates of ACUTE GI toxicity being higher, and the hypofrac guidelines AGREE with me, with this statement in their guidelines:
Statement KQ1E: "Men should be counseled about the small increased risk of acute gastrointestinal (GI) toxicity with moderate hypofractionation."
My beef with ultrahypofrac is not only late GU toxicity at 1 year, but acute GU toxicity. We are making patients feel worse as a result of our treatment without an oncological benefit to the individual patient.
I still offer prostate hypofrac to the rare intact patient I see (usually 70/28). I discuss with them the potential for increased acute GI toxicity as a result of treatment.
And come on at your last paragraph, Aren't you in academics or something given your history with RRC? Are we calling academic departments 'resource constrained' like they're in the middle east or Africa, that we need to increase machine throughput for 'societal' good?
I'm guessing a big chunk, if not the majority, carry NCI designation, with the resultant special treatment from CMS in terms of reimbursementI think you are painting with a rather large brush to suggest that academic departments don't operate in resource constrained environments. There are some that can charge monopolistic rates but not all.
Of all the cancers I have treated in my career, I have treated prostate the most. By far. Thousands. I am as intimately acquainted with all the potentialities—good, bad, acute, late, technique, imponderables—of 81/45 as I am my own fingernails. Anything else I’ll try will be a mini-experiment I’m running on the first, second, hundredth patient I try to treat differently. This is from whence I come when I talk about prostate. Have pity on this poor, anachronistic fellow who’s been phenomenally clinically successful and happy with his prostate cancer treatments.
The preferential reimbursement is not nearly as big an issue as the rates that these and similar centers can negotiate with insurance. NCI designation does not carry a benefit, it is the pps exemption for a select group of academic centers.Marvelously imprecise "big chunk". I am not an expert in this particular are to be sure.
I know that there are 11 cancer centers in the US that are exempt from Medicare PPS; recent analysis at link below
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Comparison of PPS-Exempt Hospitals, NCI-Designated Hospitals, and Other Hospitals That Provide Cancer Care
This cohort study compares the characteristics and postoperative outcomes of hospitals affiliated with Prospective Payment System (PPS)-exempt cancer centers, other hospitals affiliated with National Cancer Institute (NCI)-designated cancer centers, and other hospitals that provide cancer care in...jamanetwork.com
I have not seen specifics on reimbursement for these exempt centers to know whether they are recieving more for the same service but the paper above makes clear that the regulatory burden is less.
Please enlighten me as to whether NCI designation, in and of itself, is associated with more favorable reimbursement. Serious question.
There are roughly 40 NCI designated centers and approximately 90 "academic" programs with radiation oncology residency.
8/1 is my go to and it was easy to incorporate into practice because there was a clinical reason to use it. One, as a radiobiologist it’s easy to predict 8/1 would have less side effects than 30/10 and two, the clinical data backed that up with statistically significant side effect differences. (And the data showed it had less tumor effect; acceptable in palliation.) For prostate hypofx the data has offered no compelling clinical reason for me to change practice. On the contrary, it at times whispers worries in my ear with occasionally statistically significant side effect disimprovement. Radiobiology led us to this state in prostate. It’s predicated on uniformly low alpha/betas for CaP. If you google the recent single shot data for CaP, there are increased failures that shouldn’t happen. I think because CaP is alpha/beta heterogenous; ie biology. Incidentally high dose conventional fractionation is a wonderful hedge against low alpha/beta tumor heterogeneity.For those of you who support long-course, 8 or 9 week regimens for prostate intact due to increased acute toxicity with shorter regimens- I hope you also mostly use 8/1 over 30/10 for bone met palliation.
8/1 - more convenient, less acute toxicity. Higher chance of having to come back in later for another treatment, but hey, these retired patients don't mind a 1 in 5 chance of having to come back (vs 1 in 10).
(for the record, I think 8/1 is great. I suspect some of you don't though. I wonder what the difference is here.....)
8/1 is my go to and it was easy to incorporate into practice because there was a clinical reason to use it. One, as a radiobiologist it’s easy to predict 8/1 would have less side effects than 30/10 and two, the clinical data backed that up with statistically significant side effect differences. (And the data showed it had less tumor effect; acceptable in palliation.) For prostate hypofx the data has offered no compelling clinical reason for me to change practice. On the contrary, it at times whispers worries in my ear with occasionally statistically significant side effect disimprovement. Radiobiology led us to this state in prostate. It’s predicated on uniformly low alpha/betas for CaP. If you google the recent single shot data for CaP, there are increased failures that shouldn’t happen. I think because CaP is alpha/beta heterogenous; ie biology. Incidentally high dose conventional fractionation is a wonderful hedge against low alpha/beta tumor heterogeneity.
Why? If it stays the same, okay. If it goes down, great. If it goes up, you said it doesn't matter as an outcome.ok ok... let's clear a few things up.
For individual patients:
Are PSAs important in screening for prostate cancer and monitoring response to therapy? yes
Well you are on the right track with dose escalation for "palliative SBRT" as now, I guess, in terms of tx effectiveness for bone mets:In the metastatic setting there is something to the alpha beta argument. I use 38/4 for prostate oligomets extrapolating from previous definitive SBRT doses. I am not sure I have ever seen an in field failure with these doses. Granted, they are almost all nodal and bone Mets which biologically seem to be easier to control across the board. But still, does anyone else use those doses for lung, breast, or colon Mets? I don’t. The only other disease I will use this for is RCC...also a low alpha/beta tumor.
But your point is valid. The extreme hypofrac regimens have vastly higher BEDs and theoretically should be better...but are not. Of course, there is a pretty good explanation. There are not that many isolated local failures after prostate RT using any fractionation. It was never realistic to expect hypofractionation (or Brachy boost for that matter) were likely to significantly change outcomes. It would be nice to be wrong on this one, but I doubt I am.
I thought they went hand in hand, guess not. I know the data/links have been posted on SDN before showing the increased reimbursement for those centers.The preferential reimbursement is not nearly as big an issue as the rates that these and similar centers can negotiate with insurance. NCI designation does not carry a benefit, it is the pps exemption for a select group of academic centers.
Why? If it stays the same, okay. If it goes down, great. If it goes up, you said it doesn't matter as an outcome.
I'd posit that if DMFS and OS are the outcomes that actually matter, you'd be best served by checking to make sure the patient is alive and ordering a bone scan periodically.
So... why are you measuring an outcome you find meaningless and has the potential to cause further harm? Unless, of course, you don't actually believe it's meaningless.
Sophists will always show up on the scene and say, "It's tough to make predictions, especially about the future."So biochemical progression doesn't matter in patients actively dying of an unrelated issue. I will agree and raise you, that progression of any type of cancer doesn't matter if the patient is actively dying from an unrelated issue.
Yet, we all still continue to order PSA post treatment on EVERY man who is well enough to make it into clinic.