ESTRO-ASTRO Oligometastatic statement

[Chartreuse Wombat]

https://www.astro.org/ASTRO/media/ASTRO/Patient%20Care%20and%20Research/PDFs/OMDManuscriptPC.pdf?utm_source=MagnetMail&utm_medium=email&[email protected]&utm_content=ASTROgram_121119&utm_campaign=LBAs%20deadline%20for%20H&N%20Symposium,%20Skin%20cancer%20guideline%20released,%202020%20HOPPS%20comments%20letter

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[lhl]

Interesting how liberal they are with the definition of oligometastatic disease...more than for which we have solid data at this point in time...there's no doubt this is the direction the field is heading though...it may be difficult to get referring physician buy-in.

Where to draw the upper limit of oligometastatic disease will be the most significant challenge for our field in the next few years (in terms of initial # lesions, number of active lesions, duration of time between oligometastatic RT directed treatment, likelihood of toxicity predictors, etc.)

 

[Palex80]

No numbers? I was getting used to this...

Other than that, I have serious concerns about some of the statements in the paper, like...

"Patients with prior polymetastatic disease can become OM based on response to systemic therapy (Statement 12)."

Right... We all know those SCLC extensive disease patients that present with countless liver mets and a primary with bulky mediastinal nodes. They get first line Carbo/Eto, respond incredibly well and maybe one or two liver mets are residual. You wanna tell me, that these patients are now considered to be Oligometastatic???


After all...
"The concept of OMD is independent of primary tumour type and histology (Statement 1) and of the metastatic site(s) (Statement 2). "

Yeah! SBRT for residual mets in SCLC extensive disease. A true chance to prolong PFS for 2-3 weeks!

 

[PhotonBomb]

No numbers? I was getting used to this...

Other than that, I have serious concerns about some of the statements in the paper, like...

"Patients with prior polymetastatic disease can become OM based on response to systemic therapy (Statement 12)."

Right... We all know those SCLC extensive disease patients that present with countless liver mets and a primary with bulky mediastinal nodes. They get first line Carbo/Eto, respond incredibly well and maybe one or two liver mets are residual. You wanna tell me, that these patients are now considered to be Oligometastatic???


After all...
"The concept of OMD is independent of primary tumour type and histology (Statement 1) and of the metastatic site(s) (Statement 2). "

Yeah! SBRT for residual mets in SCLC extensive disease. A true chance to prolong PFS for 2-3 weeks!

I mean I don't know why you are picking extensive stage small cell? Probably every single person on that forum would probably agree with you?

seems like you're looking for a reason to criticize, not sure what your angle is.

 

[medgator]

I mean I don't know why you are picking extensive stage small cell? Probably every single person on that forum would probably agree with you?

seems like you're looking for a reason to criticize, not sure what your angle is.

I don't know, maybe because of what @Palex80 quoted regarding the statement? Doesn't seem like there has been any exception made, and I would agree with palex that it is ridiculous to consider something like sclc to be similar to breast or renal

"The concept of OMD is independent of primary tumour type and histology (Statement 1) and of the metastatic site(s) (Statement 2). "

Starting off the trolling early today, aren't we?

 

[PhotonBomb]

I don't know, maybe because of what @Palex80 quoted regarding the statement? Doesn't seem like there has been any exception made, and I would agree with palex that it is ridiculous to consider something like sclc to be similar to breast or renal



Starting off the trolling early today, aren't we?

I mean, yes, they could have specifically excluded things like ES-SCLC and pancreatic cancer as examples, but they probably wanted to be as broad as possible to account for rare scenarios.

for example, the ES-SCLC patient that palex mentioned as an example would surely not be considered to have an oligometastatic biology, by any definition of the word, by anyone. But Palex also specifically picked that example, in order to be difficult, not sure why.

one can imagine an ES-SCLC patient with one contralateral thoracic metastasis at diagnosis who then has a CR in the primary after chemo/IO (a year or more, say, whether following CASPIAN or IMPOWER paradigm, whatever you like) where it may be worth treating the lung oligomet if still there and nothing else. If they had specifically excluded small cell histology, then the official guidelines would say you shouldn't consider even talking about consolidation in this patient.


that's the histology point.

then you have the poly-metastatic point, which certainly has a role for consolidating 1-2 areas of disease after up-front wide-spread metastasis in specific histologies, especially in ALK or EGFR mutated lung cancer.

what Palex did is take two different points and try to mix them and apply to polymetastatic SCLC. Perhaps the authors should have accounted that people aren't able to think at all, and should have specifically excluded every scenario that does not make sense.

But Medgator, you are board certified and at some point passed medical school, so one would hope you can think.

I urge you to empower yourself, and think.

 

[OTN]

I've successfully treated oligometastatic neuroendocrine/small cell cancer. Rare, but it can happen. Patient selection of course is paramount.

 

[BobbyHeenan]

It's good that we're starting to try to lay some parameters out here...ultimately though we've GOT to have more data and med onc buy in.

One thing from a practical perspective I can say is that the best way to see and treat these folks is follow your patients long term. If you get a palliative bone met referral then continue to see them at regular intervals. I seem to find a lot of appropriate SBRT cases when patients have a solitary site of progression and I see them in follow up and broach the subject of SBRT to med onc. It's often not on the med onc radar.

 

[Haybrant]

I've successfully treated oligometastatic neuroendocrine/small cell cancer. Rare, but it can happen. Patient selection of course is paramount.

Same here. Not sure what Palex is on about, biology is a funny thing not an absolute thing keep an open mind or your patients will suffer bc you’re gonna tell them their going to die

 

[Palex80]

for example, the ES-SCLC patient that palex mentioned as an example would surely not be considered to have an oligometastatic biology, by any definition of the word, by anyone. But Palex also specifically picked that example, in order to be difficult, not sure why.

I was being provocative. Why?
Because the paper does not refer to "oligometastatic biology" at all. In fact it tell us, that any tumor can potentially be oligometastatic. And even if a tumor was polymetastatic, it can still be turned into oligometastatic (and then be treated as oligometastatic). Which in my opinion is a totally new concept (and one I do not agree with)...

then you have the poly-metastatic point, which certainly has a role for consolidating 1-2 areas of disease after up-front wide-spread metastasis in specific histologies, especially in ALK or EGFR mutated lung cancer.

Precisely! "especially in ALK and EGFR mutated lung cancer", like you said. I totally agree with that. But those patients are about 1% of all metastatic patient I see in practice. The rest are... well the rest...
But this paper does not divide them from the rest. This paper says that location and histology are not relevant, everyone can potentially be oligometastatic (or be turned into oligometastatic!)



Now, don't get me wrong. I find the oligometastatic field fascinating and I do treat quite a few of those patients. I just don't like the way things are being put on paper as solid statement, when the evidence we have to make those statements is non-existant.

"The concept of OMD is independent of primary tumour type and histology (Statement 1) and of the metastatic site(s) (Statement 2)."

In my opinion this is not a correct statement.
I do not consider NSCLC (without any driver mutations) and with liver mets oligometastatic.
The same goes for head & neck cancer with visceral or bone mets (I would potentially exclude lung mets, because often you cannot tell if it's a second primary or a true lung met)
The same goes for any pancreatic adenocarcinoma with any mets
The same goes for urothelial cancer with visceral or bone metastasis
The same goes for soft tissue sarcoma with liver metastasis
The same goes for castration resistant prostate cancer progressing with mets

In all these situations I do not see the evidence yet out there for me to change my practice based on a "concept". And I do not agree that a "concept" should guide treatment decisions. Data from clinical trials (preferably) or at least solid retrospective should. And we do have data for some classic oligometastatic scenarios advocating local ablative treatment of limited numbers of mets, like lung mets from sarcoma, liver mets from colorectal cancer, bone mets from prostate cancer, bone mets from breast cancer, brain mets from pretty much any tumor... Sure. But to say that you apply this concept independent of primary tumor and histology, despite the lack of data, is questionable.

 

[Mandelin Rain]

Same here. Not sure what Palex is on about, biology is a funny thing not an absolute thing keep an open mind or your patients will suffer bc you’re gonna tell them their going to die

If you tell any E-SCLC patient that they're not going to die of their disease, I'm not sure you're doing them any favors.

 

[Palex80]

Same here. Not sure what Palex is on about, biology is a funny thing not an absolute thing keep an open mind or your patients will suffer bc you’re gonna tell them their going to die

Everyone dies eventually. And patients can also be grateful if you don't give them false hope.

 

[Palex80]

If you tell any E-SCLC patient that they're not going to die of their disease, I'm not sure you're doing them any favors.

Treatment can still kill them, before the tumor does... Ok, now I am trolling.

Or perhaps not? 3 Grade V events due to SBRT out of 66 patients in SABR-COMET...

 

[scarbrtj]

But Medgator, you are board certified and at some point passed medical school, so one would hope you can think.
I urge you to empower yourself, and think.

Gedankenexperiments worked (really well) for Einstein. They won't work in medicine, ever, to determine if a clinical action is superior, inferior, or similar to other clinical actions. The problem with this "oligometastatic statement" is that it seems to be, at outset, almost pure gedankenexperiment. So one can't really argue cogently for or against it IMHO. Especially if it's going to be really broad in its definition. But clinical decision-making via afflatus is something rad onc has been pretty wont to do recently. Which is fine I guess as long as no one uses it as a cudgel.

 

[Haybrant]

If you tell any E-SCLC patient that they're not going to die of their disease, I'm not sure you're doing them any favors.

Ha, the only thing you can tell them is what impower showed and that’s it. But any patient can look that up. Your role is to help stratify them within those studies. Not all ESCLC is equal not even close and that’s what you’re suggesting, it’s a resident mentality thing

 

[evilbooyaa]

I was being provocative. Why?
Because the paper does not refer to "oligometastatic biology" at all. In fact it tell us, that any tumor can potentially be oligometastatic. And even if a tumor was polymetastatic, it can still be turned into oligometastatic (and then be treated as oligometastatic). Which in my opinion is a totally new concept (and one I do not agree with)...



Precisely! "especially in ALK and EGFR mutated lung cancer", like you said. I totally agree with that. But those patients are about 1% of all metastatic patient I see in practice. The rest are... well the rest...
But this paper does not divide them from the rest. This paper says that location and histology are not relevant, everyone can potentially be oligometastatic (or be turned into oligometastatic!)

This is literally what the Gomez trial did and is being evaluated in LU-002. If you don't believe in this then you don't believe in Gomez or LU-002, only SABR-COMET.

Now, don't get me wrong. I find the oligometastatic field fascinating and I do treat quite a few of those patients. I just don't like the way things are being put on paper as solid statement, when the evidence we have to make those statements is non-existant.

"The concept of OMD is independent of primary tumour type and histology (Statement 1) and of the metastatic site(s) (Statement 2)."

In my opinion this is not a correct statement.
1.I do not consider NSCLC (without any driver mutations) and with liver mets oligometastatic.
2. The same goes for head & neck cancer with visceral or bone mets (I would potentially exclude lung mets, because often you cannot tell if it's a second primary or a true lung met)
3. The same goes for any pancreatic adenocarcinoma with any mets
4. The same goes for urothelial cancer with visceral or bone metastasis
5. The same goes for soft tissue sarcoma with liver metastasis
6. The same goes for castration resistant prostate cancer progressing with mets

In all these situations I do not see the evidence yet out there for me to change my practice based on a "concept". And I do not agree that a "concept" should guide treatment decisions. Data from clinical trials (preferably) or at least solid retrospective should. And we do have data for some classic oligometastatic scenarios advocating local ablative treatment of limited numbers of mets, like lung mets from sarcoma, liver mets from colorectal cancer, bone mets from prostate cancer, bone mets from breast cancer, brain mets from pretty much any tumor... Sure. But to say that you apply this concept independent of primary tumor and histology, despite the lack of data, is questionable.

I've numbered your statements above:
1 - Literally was included on every single oligomet trial that allowed NSCLC primary regardless of driver mutation status (Gomez, SABR-Comet, Allowed on LU-002)
2 - Rare clinical scenario to have H&N with an oligomet to NOT the lung. However, have seen a patient with a synchronous solitary bone met with a year+ PFS off systemic therapy when the met was treated with SBRT after definitive management of the primary. Agree that there is not sufficient evidence to be routinely recommending this.
3 - I agree with you on this one.... most of the time.
4 - Don't see enough of this to have an opinion.
5 - Disagree. Why does location of the met matter in your mind? If it was a lung metastasis the patient would get surgery or SBRT without a second thought.
6 - Resistant to just ADT? What about Abi? Enzalutamide? Chemo?


I think the term oligometastatic disease should be 1-3 sites outside of regional disease. Some may argue 5 or higher and until we have data from SABR-COMET 10 I would be wary. The only trial I'm familiar with that even allowed more than 3 was the original SABR-COMET, and there was maybe 1 patient that 4 or 5 mets.

I think defining oligometastatic disease should be easy. But, the decision on whether to TREAT oligometastatic aggressively is what we should really be discussing here. I agree not to treat oligometastatic pancreatic cancer..... most of the time. Same with SCLC..... most of the time. There are unique clinical situations.

I personally favor a 'testing' of biology for all oligometastatic patients with upfront systemic therapy, especially in patients who have synchronous metastatic disease at initial presentation. I know people like Iyengar are doing upfront SBRT followed by systemic therapy and that could work in very select scenarios with excellent systemic control rates to initial therapy (like mutation driven NSCLC) but I'm not a fan of that.

I'm not sure how I feel about metachronous metastatic disease in regards to sequencing. This was one of my biggest questions about SABR-COMET (which was for this population), and I think this is one of the best areas for additional research and evaluation.

As an aside - another area with no published data that really needs some form of evaluation is 'oligoprogressive' disease where disease is controlled on systemic therapy, and one or two lesions 'escape' the function of the systemic therapy. In this scenario the thought process is that if you zap the 'escaped' lesions then that patient can continue on the systemic therapy that is working for 95%+ of his/her disease. This was evaluated in the ASTRO update to the Gomez trial but it's very low numbers.

 

[PhotonBomb]

not to treat oligometastatic pancreatic cancer..... most of the time. Same with SCLC..... most of the time. There are unique clinical situations.

I personally favor a 'testing' of biology for all oligometastatic patients with upfront systemic therapy, especially in patients who have synchronous metastatic disease at initial presentation. I know people like Iyengar are doing upfront SBRT followed by systemic therapy and that could work in very select scenarios with excellent systemic control rates to initial therapy (like mutation driven NSCLC) but I'm not a fan of that.

I don't see the point of doing it together really for mutation driven lung cancer, but I DO see a point to SBRT up-front concurrently with immunotherapy, given the potential for synergistic effect. some prospective data will be coming out soon regarding this is my understanding.

 

[Palex80]

Ha, the only thing you can tell them is what impower showed and that’s it. But any patient can look that up. Your role is to help stratify them within those studies. Not all ESCLC is equal not even close and that’s what you’re suggesting, it’s a resident mentality thing

They all have one in common, though.

 

[Palex80]

This is literally what the Gomez trial did and is being evaluated in LU-002. If you don't believe in this then you don't believe in Gomez or LU-002, only SABR-COMET.



I've numbered your statements above:
1 - Literally was included on every single oligomet trial that allowed NSCLC primary regardless of driver mutation status (Gomez, SABR-Comet, Allowed on LU-002)
2 - Rare clinical scenario to have H&N with an oligomet to NOT the lung. However, have seen a patient with a synchronous solitary bone met with a year+ PFS off systemic therapy when the met was treated with SBRT after definitive management of the primary. Agree that there is not sufficient evidence to be routinely recommending this.
3 - I agree with you on this one.... most of the time.
4 - Don't see enough of this to have an opinion.
5 - Disagree. Why does location of the met matter in your mind? If it was a lung metastasis the patient would get surgery or SBRT without a second thought.
6 - Resistant to just ADT? What about Abi? Enzalutamide? Chemo?

Thank you for your post.

Let me reply.

1. Gomez was by all means small and certainly did feature some "restriction" criteria, like number of mets, response to first line treatment and so on.
So it certainly wasn't as "broad" as the "concept" of the position-paper we are discussing about.

2. Yes, we have all seen that one or two patients, that we can recall. This is cognitive bias. I have also seen THAT glioblastoma patients that recurred 6 years after primary treatment and I recall her by name. I do not recall the other dozens that died within a year or two from diagnosis.

5. Soft tissue sarcoma with a liver met is a different deal than soft tissue sarcoma with a lung met. Lung mets are considered as a rather favorable prognostic feature (as much a favorable can apply in a metastatic situation) and there are good papers showing long lasting remissions after aggressive local therapy (mostly surgery so far). The same does not apply for liver mets.

6. Resistant to ADT +/- first line Taxane or new AR-pathway inhibition. mCRPC basically.

I think the term oligometastatic disease should be 1-3 sites outside of regional disease. Some may argue 5 or higher and until we have data from SABR-COMET 10 I would be wary. The only trial I'm familiar with that even allowed more than 3 was the original SABR-COMET, and there was maybe 1 patient that 4 or 5 mets.

Sounds reasonable to me. A lot more reasonable than the position paper we are discussing and which obviously declined to set a limit to the number of mets.

I think defining oligometastatic disease should be easy. But, the decision on whether to TREAT oligometastatic aggressively is what we should really be discussing here. I agree not to treat oligometastatic pancreatic cancer..... most of the time. Same with SCLC..... most of the time. There are unique clinical situations.

Agreed.

I personally favor a 'testing' of biology for all oligometastatic patients with upfront systemic therapy, especially in patients who have synchronous metastatic disease at initial presentation. I know people like Iyengar are doing upfront SBRT followed by systemic therapy and that could work in very select scenarios with excellent systemic control rates to initial therapy (like mutation driven NSCLC) but I'm not a fan of that.

Good point. Sounds good to me too.
One could advocate that you may be missing out any "abscopal" effects if you were delivering first line immunotherapy, but we don't really know what the correct sequence for that effect is, anyhow.

I'm not sure how I feel about metachronous metastatic disease in regards to sequencing. This was one of my biggest questions about SABR-COMET (which was for this population), and I think this is one of the best areas for additional research and evaluation.

Indeed. And that's also an issue with this position. They claimed that you can pretty much adopt the "concept" irrelevant of synchronous or metachronous.

As an aside - another area with no published data that really needs some form of evaluation is 'oligoprogressive' disease where disease is controlled on systemic therapy, and one or two lesions 'escape' the function of the systemic therapy. In this scenario the thought process is that if you zap the 'escaped' lesions then that patient can continue on the systemic therapy that is working for 95%+ of his/her disease. This was evaluated in the ASTRO update to the Gomez trial but it's very low numbers.

A big issue, certainly. There is one trial running for NSCLC, called HALT, testing that.

HALT - The Institute of Cancer Research, London

www.icr.ac.uk

 

[ramsesthenice]

It's good that we're starting to try to lay some parameters out here...ultimately though we've GOT to have more data and med onc buy in.

Ding Ding Ding!

I would argue you can’t really define Oligometastatic without the test of time which invariably includes systemic therapy. It’s one thing to look Oligometastatic on a scan but the term really implies there is a manageable disease course. Indolent diseases like prostate and renal aside, you can’t know that for most other cancers until they declare their biology. You have to convince the surgeons and med oncs you are being thoughtful of how you are defining who warrants consolidative radiation after standard of care therapies and provide a clear and realistic rationale. Small chance of cure with higher chance of durable control with delayed need for second line therapy etc. At this point, I more frequently find myself telling med oncs SBRT would be a stretch more than the other way around.

When we make feeble arguments like, well there are only 3 sites, or focus on unrealistic goals like cure in the absence of data, pessimism is entirely warranted.

Also, I would strongly argue that it is possible to convert metastatic patients to regional disease with systemic therapy. As an example, over the last three years I have personally treated 4 patients who presented with esophageal adenocarcinoma and extensive non-regional nodal and/or bone Mets who had resolution of all non-regional disease after 8-12 cycles of FOLFOX (and herceptin when appropriate) that we decided to treat with conventional preop chemorads for the primary. Two had surgery and two had cCRs and were observed. So far only one (who did have surgery) has progressed. These are pretty rare exceptions and I think it’s hard to argue there is something about their biology that is different we can’t yet define without seeing how they respond to treatment.

 

[ramsesthenice]

Re: conversion of polymetastatic to Oligometastatic: I do think there are important exceptions like pancreatic adenocarcinoma and SCLC that require a much higher bar to convince you it’s worth considering anything outside the box. They just don’t generally behave in a way that is conducive to benefiting from local therapies even in the best circumstances. I have pulled the trigger maybe 3-4 times on patients with pancreatic adenocarcinoma for YEARS and even then I can only recall one of them that ended being in anyway gratifying

 

[medgator]

Re: conversion of polymetastatic to Oligometastatic: I do think there are important exceptions like pancreatic adenocarcinoma and SCLC that require a much higher bar to convince you it’s worth considering anything outside the box. They just don’t generally behave in a way that is conducive to benefiting from local therapies even in the best circumstances. I have pulled the trigger maybe 3-4 times on patients with pancreatic adenocarcinoma for YEARS and even then I can only recall one of them that ended being in anyway gratifying

Exactly. Can't be completely histology agnostic when it comes to oligo-mets

 

[PhotonBomb]

agree that you cannot be histology agnostic. of course.

also don't think that the guidelines needed to come out and exclude histologies from ever being considered to have oligometastatic disease, because that removes the ability to consider other factors.

 

[evilbooyaa]

Good post @Palex80 . I agree that Gomez/LU-002 had some cut-offs, and I do think that there needs to be clinical decision making in certain scenarios, but I still disagree with you - a non-mutated NSCLC with a solitary liver met is getting systemic therapy and LCT.

I suppose I see the guidelines as a 'catch-all' to not exclusively remove certain aspects of the patient population from being eligible. I suppose some folks would prefer it to be more strict (as the question of LCT in say 5 vs 3 metastases is not well defined based on current available data).

I guess I'm not reading the guidelines as a "if patient meets OMD criteria they should be offered LCT" but rather, if a patient meets OMD criteria the physician can potentially consider the rationale and potential risks/benefits for a discussion with the patient about LCT. However, I do see that this may open the flood gates for 'routine' treatment of OMD with 7-10+ lesions by unscurupulous folks treating for profit rather than patient benefit.

In regards to histology, similar concept. A ES-SCLC patient who has been without disease for 2 years who pops up with recurrence at his index lesion is a different scenario than 99% of SCLCs. It's a factor in the decision process but not, IMO, the only factor to consider in a clinical course.

 

[Neuronix]

How do I get on these guidelines? I need some free papers and to pretend like I'm an expert in something. Just kidding, sort of.

I've submitted comments in the past on consensus statements and never gotten a response.

 

[Palex80]

Good post @Palex80 . I agree that Gomez/LU-002 had some cut-offs, and I do think that there needs to be clinical decision making in certain scenarios, but I still disagree with you - a non-mutated NSCLC with a solitary liver met is getting systemic therapy and LCT.

Provided the primary is controlled, as in the context of metachronous metastasis in the liver, right? Or let's say the primary is small, peripheral cT2 cN0, then you could irradiate both.
I wouldn't treat if the primary was a large IIIB untreated NSCLC.

In regards to histology, similar concept. A ES-SCLC patient who has been without disease for 2 years who pops up with recurrence at his index lesion is a different scenario than 99% of SCLCs. It's a factor in the decision process but not, IMO, the only factor to consider in a clinical course.

Well said!

 

[evilbooyaa]

Provided the primary is controlled, as in the context of metachronous metastasis in the liver, right? Or let's say the primary is small, peripheral cT2 cN0, then you could irradiate both.
I wouldn't treat if the primary was a large IIIB untreated NSCLC.

For the bolded scenario, I would treat the primary with 45/15 and SBRT the liver met. I would personally favor doing this AFTER patient completes a few months of systemic therapy (again, just personal preference to 'test the biology') but we've been asked to radiate in the upfront setting as time from diagnosis to identification of potential driving mutation can be on the order of weeks from the initial diagnosis, and IMO while it's not ideal it's better than just sitting around for 2-3 weeks with no therapy initiated.

 

[Burt Radnolds]

For the bolded scenario, I would treat the primary with 45/15 and SBRT the liver met. I would personally favor doing this AFTER patient completes a few months of systemic therapy (again, just personal preference to 'test the biology') but we've been asked to radiate in the upfront setting as time from diagnosis to identification of potential driving mutation can be on the order of weeks from the initial diagnosis, and IMO while it's not ideal it's better than just sitting around for 2-3 weeks with no therapy initiated.

Would it bother you that you were giving wildly different BEDs to the primary versus the met?

 

[medgator]

Would it bother you that you were giving wildly different BEDs to the primary versus the met?

Do you normally give stereotactic doses when you treat primary nsclc in the mediastinum?

 

[Burt Radnolds]

Do you normally give stereotactic doses when you treat primary nsclc in the mediastinum?

No, do you? Was asking a genuine philosophical question.

 

[StIGMA]

Would it bother you that you were giving wildly different BEDs to the primary versus the met?

We treat to different BEDs all the time depending on the site- consider brain metastases (generally with lower BED to the brain lesion vs. the primary)- to treat to a dose that is reasonably safe and balances toxicity. Bone metastases are another example. We don't have great data to predict what dose a particular met needs based on its metastatic site (new microenvironment), but we regularly treat to an acceptable toxicity level. In that case, 45/15 to the lung is a reasonable dose (one could argue to be more or less aggressive in this case, even definitive intent chemo RT vs. no RT based on patient factors)- and it makes sense to choose a reasonable treatment scheme that balances toxicity risk. This would make more sense than say, 20/5 to the lung with 40/5 to the liver. I think most of us here consider these things and try to make reasonable choices.

 

[Palex80]

We treat to different BEDs all the time depending on the site- consider brain metastases (generally with lower BED to the brain lesion vs. the primary)- to treat to a dose that is reasonably safe and balances toxicity.

A III primary in the lung will cause more trouble than a liver met is it's not well controlled.
I do not see a reason in "ablating" the liver met, when you are not killing off the primary in the mediastinum.

 

[medgator]

A III primary in the lung will cause more trouble than a liver met is it's not well controlled.
I do not see a reason in "ablating" the liver met, when you are not killing off the primary in the mediastinum.

So you would do chemo rt?

 

[medgator]

No, do you? Was asking a genuine philosophical question.

No. Not sure the point of that question, better to do no harm first and foremost, correct?

 

[StIGMA]

A III primary in the lung will cause more trouble than a liver met is it's not well controlled.
I do not see a reason in "ablating" the liver met, when you are not killing off the primary in the mediastinum.

I would want at least a reasonable attempt at controlling the primary if the liver met were to be addressed (for instance, I would not address the liver if 20/5 were used to the lung in my example).

 

[Palex80]

No, I wouldn't do Chemo-RT.

I think that the patient should get systemic treatment first and perhaps "consolidative" RT to the primary & metastasis.
However I would deliver a "non-ablative" dose to both.

 

[PhotonBomb]

interesting. what would you give liver - 45/15?

 

[Burt Radnolds]

No. Not sure the point of that question, better to do no harm first and foremost, correct?

The point was to generate thoughtful discourse, which it did.

 

[evilbooyaa]

Would it bother you that you were giving wildly different BEDs to the primary versus the met?

Short answer, no.
If it was safely amenable to 50/5 (say it was a T2N0 primary) I would do that.

Every treatment we do is a balance of toxicity and efficacy. While I would shoot for 50/5 in the liver as well, I would accept lower (as low as 30-35/5 prescription dose) if location of the liver met was unfavorable (say in left lateral lobe right next to duodenum).

My main priority in oligomet patients is to radiate them to above 'standard palliation' doses while ensuring their risk of severe RT related toxicity is almost zero. I use stricter dose constraints and will under dose PTV as necessary to meet those constraints in a metastatic patient than I would in a standard curative situation.

This is also why I don't like 60/30 with chemo for the primary. I want the treatment to be faster than 6 weeks because despite what we do, I feel that systemic therapy is still the most important aspect of their therapy and I don't want to delay that further by keeping the patient under my care for double the time that (I feel) is necessary.

 

[scarbrtj]

Would it bother you that you were giving wildly different BEDs to the primary versus the met?

We treat to different BEDs all the time depending on the site- consider brain metastases (generally with lower BED to the brain lesion vs. the primary)- to treat to a dose that is reasonably safe and balances toxicity. Bone metastases are another example. We don't have great data to predict what dose a particular met needs based on its metastatic site (new microenvironment), but we regularly treat to an acceptable toxicity level. In that case, 45/15 to the lung is a reasonable dose (one could argue to be more or less aggressive in this case, even definitive intent chemo RT vs. no RT based on patient factors)- and it makes sense to choose a reasonable treatment scheme that balances toxicity risk. This would make more sense than say, 20/5 to the lung with 40/5 to the liver. I think most of us here consider these things and try to make reasonable choices.

The simple answer to why we give different BEDs in these scenarios can be found here.

 

[Palex80]

interesting. what would you give liver - 45/15?

For instance. I wouldn't push BED to the liver over 100 Gy when I would be delivering something like 50-60 Gy BED to the mediastinum.

 

[Burt Radnolds]

Everyone: "You do your best to balance the risks versus benefits, dummy!"

Yes, this is one of the core missions of being a physician, and one I do not take lightly. It appears I am preaching to the choir on this one, but I do not think that everyone out there practices with this level of nuance. Just looks at some of the other concurrent threads out there bashing shoddy community care. Some (community and academics alike) are very formulaic and dogmatic with their SBRT dosing. SBRT is not entirely benign, as some people like to point out the handful of grade 5 toxicities on the recent trials. Also, despite what some seem to think, toxicities happen even when exercising the utmost caution, if you practice long enough. Finding that elusive middle ground is the goal, and is one of the areas of rad onc where the true art of medicine lies.

I think some people have offered some very thoughtful answers that I enjoyed reading and reflect my own practice patterns. Don't be afraid to dial down the dose to meet your goals of aggressive palliation without harm, if needed. Was merely pointing out the potential dissonance of spraying 45/15 at the disease that will probably kill them versus the atomic bomb full dose SBRT to the met itself. While that dissonance may be justified, and I have done similar things, it gives me some pause as I ask myself "what exactly am I doing here?".

 

[medgator]

While that dissonance may be justified, and I have done similar things, it gives me some pause as I ask myself "what exactly am I doing here?".

Respecting normal tissues and addressing possible toxicity risk?

 

[Burt Radnolds]

Respecting normal tissues and addressing possible toxicity risk?

Every day of my life bro.

 

[scarbrtj]

"what exactly am I doing here?"

The answer to that is 42. But here's a video of a community radiation oncologist wondering how BEDs work...

 

[evilbooyaa]

My goal in liver SBRT is:
1a) Don't put a hole in the duodenum
1b) Don't send the patient into liver failure
2) Treat the disease as much as possible.