ASCO 2022 abstracts

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Palex80

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ASCO 2022 abstracts are out. Here are some interesting radonc picks:

SBRT & surgery for oligometastastic breast cancer does not seem to work.

Perhaps new s.o.c. for mucositis prevention in H&N cancer

PSMA-PET-CT changing management in almost half of the patients receiving salvage RT for biochemical recurrent prostate cancer. Raises questions on how to interpret results of recently published RTOG 0534

Addition of early SBRT to M1 EGFR mutated NSCLC beneficial.

Proton-CSI superior to Photon-IFRT for leptomeningeal M1 breast & NSCLC. I have no idea what to make out of this! [Corrected]

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It’s proton csi vs photon involved field

Surprised by the degree of benefit. Maybe should be doing more csi but most of my leptomeningeal disease patients already look like they are near death. Hard to imagine putting them through csi
 
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It’s proton csi vs photon involved field

Surprised by the degree of benefit. Maybe should be doing more csi but most of my leptomeningeal disease patients already look like they are near death. Hard to imagine putting them through csi
Oh, thank you for that, I totally misread it! That makes (more) sense then! Will edit post.
 
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Raises questions on how to interpret results of recently published RTOG 0534
You could replace those 4 numbers with any other set of 4 numbers that pertain to an RTOG prostate trial ever within 2 years of it being published.
 
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ASCO 2022 abstracts are out. Here are some interesting radonc picks:

SBRT & surgery for oligometastastic breast cancer does not seem to work.

Perhaps new s.o.c. for mucositis prevention in H&N cancer

PSMA-PET-CT changing management in almost half of the patients receiving salvage RT for biochemical recurrent prostate cancer. Raises questions on how to interpret results of recently published RTOG 0534

Addition of early SBRT to M1 EGFR mutated NSCLC beneficial.

Proton-CSI superior to Photon-IFRT for leptomeningeal M1 breast & NSCLC. I have no idea what to make out of this! [Corrected]

Wait where are all the omit RT trials?
 
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ASCO 2022 abstracts are out. Here are some interesting radonc picks:

SBRT & surgery for oligometastastic breast cancer does not seem to work.

Perhaps new s.o.c. for mucositis prevention in H&N cancer

PSMA-PET-CT changing management in almost half of the patients receiving salvage RT for biochemical recurrent prostate cancer. Raises questions on how to interpret results of recently published RTOG 0534

Addition of early SBRT to M1 EGFR mutated NSCLC beneficial.

Proton-CSI superior to Photon-IFRT for leptomeningeal M1 breast & NSCLC. I have no idea what to make out of this! [Corrected]
...vis a vis EGFR+ NSCLC, this has been my anecdotal experience as well. Development of resistance to Osi is stochastic... so it makes sense to give the cancer fewer opportunities to happen upon on a favorable mutation.

I suspect that we will see a trend across all disease sites: the better the sytemic therapy, the more helpful SBRT to oligoprogressive/oligometastatic disease.
 
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...vis a vis EGFR+ NSCLC, this has been my anecdotal experience as well. Development of resistance to Osi is stochastic... so it makes sense to give the cancer fewer opportunities to happen upon on a favorable mutation.

I suspect that we will see a trend across all disease sites: the better the sytemic therapy, the more helpful SBRT to oligoprogressive/oligometastatic disease.
Systemic therapy is pretty good for breast cancer. I am so surprised that it seems to not help.
Unlike @OTN experience - I always felt that the breast cancer patient with 1-2 mets was potentially "curable"
But, probably did not follow up long enough.
 
Systemic therapy is pretty good for breast cancer. I am so surprised that it seems to not help.
Unlike @OTN experience - I always felt that the breast cancer patient with 1-2 mets was potentially "curable"
But, probably did not follow up long enough.
I haven't treated breast cancer in a bit...

My (uneducated) sense is that many patients who are depending on cytotoxic therapy (not Her2) for systemic control with only a few mets will still have ongoing distant progression. This is what I have seen with other types of cancer. Remind me, is hormone therapy tumorocidal for breast... or just tumorostatic?
 
The oligomet trials (and leptomeningeal trial) are small, small, small. Leptomeningeal trial with uneven arms (WHYYYYYYY!!!!) and a roughly 20 person control arm within which anything could have happened. At least they attempted a CSI vs WBRT trial.

I am curious about the breast patient makeup. Breast CA is roughly 3 different diseases and really many more. No way to get survival signal out of this trial given the risk of death over their f/u period was roughly 30% with 60 pts per arm. Just not powered for that sort of thing.

That being said, if we were giving TKIs or CDK4 /6 inhibitors, our internal equipoise in reviewing these trials would be quite different.

I never liked the RW concept of oligometastatic disease as "curable". I suspect this is vanishingly rare. This doesn't mean that focal therapy doesn't have a clinical benefit or even a survival benefit in selected patients.
 
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I’m surprised at the results of the mucositis trial. We had a bunch of people on the trial and it seemed night and day. Obviously we were blinded but I had 4 people never have a symptom, they must have been getting the drug because I think prior to that I maybe had one patient get through 70 Gy to oropharynx without a complaint.
 
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I am curious about the breast patient makeup. Breast CA is roughly 3 different diseases and really many more. No way to get survival signal out of this trial given the risk of death over their f/u period was roughly 30% with 60 pts per arm. Just not powered for that sort of thing.

That being said, if we were giving TKIs or CDK4 /6 inhibitors, our internal equipoise in reviewing these trials would be quite different.

I never liked the RW concept of oligometastatic disease as "curable". I suspect this is vanishingly rare. This doesn't mean that focal therapy doesn't have a clinical benefit or even a survival benefit in selected patients.
Breast appears to behave different than other diseases.
You will recall that the ECOG-ACRIN trial on locoregional treatment for M1 breast patients also came back negative (despite all the shortcomings of the trial).
 
Breast appears to behave different than other diseases.
I agree.

The thing that gets me is the remarkable survival benefit of post-mastectomy RT in locally advanced breast CA trials, where benefit was relatively delayed but really quite remarkable (10% on up) and regional burden of disease relatively high. I'm guessing if we had an equivalent to a PSMA scan for breast or performed a high sensitivity bone marrow, a significant number of these patients would demonstrate low burden metastatic disease.

I would not expect a survival benefit, even if it was real, for most breast within a time frame of 3-5 years for any sort of oligometastatic treatment.

Maybe @TheWallnerus and you can do the whole CD8 positive thing for oligometastatic disease? 10 year f/u?
 
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I’m surprised at the results of the mucositis trial. We had a bunch of people on the trial and it seemed night and day. Obviously we were blinded but I had 4 people never have a symptom, they must have been getting the drug because I think prior to that I maybe had one patient get through 70 Gy to oropharynx without a complaint.
Us too. I would have expected a bigger difference in the incidence of SOM. That said, I think the data are still meaningful. The reduction in duration of SOM is clinically meaningful. Mean 18 vs 8 days. The onset is also delayed. It may not completely prevent a lot of patients from experiencing SOM at any point in treatment, but it does seem to make the overall treatment corse more tolerable. Considering it’s a long and rough course to begin with, I’d still consider it a step forward.
 
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Us too. I would have expected a bigger difference in the incidence of SOM. That said, I think the data are still meaningful. The reduction in duration of SOM is clinically meaningful. Mean 18 vs 8 days. The onset is also delayed. It may not completely prevent a lot of patients from experiencing SOM at any point in treatment, but it does seem to make the overall treatment corse more tolerable. Considering it’s a long and rough course to begin with, I’d still consider it a step forward.
Looks like this is a 60minute infusion before each treatment. What will prevent this from going the way of other IV radiomodulators?
 
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Looks like this is a 60minute infusion before each treatment. What will prevent this from going the way of other IV radiomodulators?
The company is working on an oral version, but logistically it is difficult if the infusion center is not right next to your department. Although maybe a good opportunity to get into the infusion world! Come get your radioprotector and radiopharmaceuticals!
 
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Looks like this is a 60minute infusion before each treatment. What will prevent this from going the way of other IV radiomodulators?
At this point there are a couple big questions. First, is the data good enough to get the NDA through the FDA and make it available? That hurdle still has to be cleared.

Then the question is will people use it and that remains to be seen. Like xrt123, we had really good experiences with it. Since we have an infusion suite and the staff to easily do this, it was not a problem. About 80% of eligible patients signed up for a randomized trial not even knowing if the drug works or were even getting it so it doesn’t seem like it’s going to be a hard sell for patients.

But the infusion could be a problem. It’s not practical in a lot of community centers and that’s a problem. Hopefully the oral compound pans out.

I’m personally very optimistic some of the classes of redox modulators may actually turn out to be useful normal tissue protectors.
 
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Some centers try to avoid G tubes at all cost. Personally I discuss pros and cons and let patient decide but I probably place more G tubes than average rad onc. I think the trial/drug was an easy sell if it is reducing the chance they need a G tube. It was easy to accrue to the trial because they were getting saline/drug/placebo daily and we felt a whole lot more comfortable waiting to the last possible moment to see if someone needed a G tube. I think I had 1-2 people refuse trial and over 20 enrolled.
 
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At this point there are a couple big questions. First, is the data good enough to get the NDA through the FDA and make it available? That hurdle still has to be cleared.

Then the question is will people use it and that remains to be seen. Like xrt123, we had really good experiences with it. Since we have an infusion suite and the staff to easily do this, it was not a problem. About 80% of eligible patients signed up for a randomized trial not even knowing if the drug works or were even getting it so it doesn’t seem like it’s going to be a hard sell for patients.

But the infusion could be a problem. It’s not practical in a lot of community centers and that’s a problem. Hopefully the oral compound pans out.

I’m personally very optimistic some of the classes of redox modulators may actually turn out to be useful normal tissue protectors.
What mechanism stops it from protecting tumor?
 
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What mechanism stops it from protecting tumor?
That I can explain. It’s an SOD mimetic which converts superoxide to hydrogen peroxide. In normal tissues there is very little superoxide present in the absence of an oxidative stressor. Most tumors have elevated basal oxide levels because they have an excess of unpaired electrons secondary to metabolic abnormalities. These compounds are actually fairly potent radiosensitizers in tumors when given with higher fraction sizes because they stimulate lethal hydrogen peroxide fluxes. The ongoing panc SBRT trial with a similar compound (trial name is Greco2) is banking on tumor sensitization with tumor control endpoints. The preclinical literature on these things is pretty intriguing.

SOD mimics are not the only class, but that’s what’s so exciting about redox modulating drugs. They typically have opposite effects in tumors and normal tissues when given with radiation. That’s one thing that (potentially) makes them different from a lot of other radiation modulators.
 
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It’s proton csi vs photon involved field

Surprised by the degree of benefit. Maybe should be doing more csi but most of my leptomeningeal disease patients already look like they are near death. Hard to imagine putting them through csi

I was already doing this based on the phase 1 data. We have maybe 5 a year at our fairly large center who have early LMD and good performance status. Results have been mixed, and response from other docs in my department has been skeptical. I'm glad to see some positive results. The 20-50 year old beast cancer patient with LMD and no viable systemic options break your heart, and I throw the book at then.
 
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Yeah those are people I would refer to proton centers now. Very cool trial. Not doing photon CSI but will send for proton
 
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Yeah those are people I would refer to proton centers now. Very cool trial. Not doing photon CSI but will send for proton
I’ve been doing VMAT for CSI and it’s worked really well
 
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I’ve been doing VMAT for CSI and it’s worked really well
The investigators deserve congratulations but the issue is that the trial changed two things in the experimental arm: treatment volume and technique.
The argument is, that IFRT with photons was the only possibility, since CSI with photons is too toxic, but CSI with photons is also posssible too.
So, ghe technique was a necessary change to facilitate the volume choice,
It probably comes down to patient selection too, many of these patients will die of extracerebral tumor progression and any treatment escalation to the CSI will not matter.

We had a similar discussion a few months back in an other context. You recall the trial that showed less acute toxicity with MRI linac treatment vs. CBCT based treatment? Then we found out that the MRI linac group also had smaller margins? So what led to less toxicity? MRI based treatment or smaller margins? The authors pointed out that the smaller margins were only possible because of the MRI based treatment. But we discussed if one could use smaller margins without the MRI linac too?
Similar point here. Proton RT leads to higher survival in leptomeningeal disease. But is it the protons (less side effects) or the volume (CSI vs. IFRT)? And can you facilitate CSI with photons and acceptable toxicity too? Difficult to tell.

I find the exploratory subanalysis interesting. They seem to have had a lot of patients with ovarian cancer and leptomeningeal disease. I can only recall seeing a few patients with ovarian cancer and brain metastases in my work experience and cannot recall one with leptomenigeal disease.
 
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The investigators deserve congratulations but the issue is that the trial changed two things in the experimental arm: treatment volume and technique.
The argument is, that IFRT with photons was the only possibility, since CSI with photons is too toxic, but CSI with photons is also posssible too.
So, ghe technique was a necessary change to facilitate the volume choice,
It probably comes down to patient selection too, many of these patients will die of extracerebral tumor progression and any treatment escalation to the CSI will not matter.

We had a similar discussion a few months back in an other context. You recall the trial that showed less acute toxicity with MRI linac treatment vs. CBCT based treatment? Then we found out that the MRI linac group also had smaller margins? So what led to less toxicity? MRI based treatment or smaller margins? The authors pointed out that the smaller margins were only possible because of the MRI based treatment. But we discussed if one could use smaller margins without the MRI linac too?
Similar point here. Proton RT leads to higher survival in leptomeningeal disease. But is it the protons (less side effects) or the volume (CSI vs. IFRT)? And can you facilitate CSI with photons and acceptable toxicity too? Difficult to tell.

I find the exploratory subanalysis interesting. They seem to have had a lot of patients with ovarian cancer and leptomeningeal disease. I can only recall seeing a few patients with ovarian cancer and brain metastases in my work experience and cannot recall one with leptomenigeal disease.
Great points. First involved site photon RT could conceivably include SRS to a focal area of enhancement all the way to whole brain RT + spinal RT. Second, less toxic CSI VMAT techniques have been developed that target the spinal nerve roots rather than all of the vertebrae + margin as in the past.

As a proton skeptic, I acknowledge that our field would have been unwilling to consider CSI for LMD without the promise of protons sparing the heart, stomach and some bone marrow.
 
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building off @theradiator post - for those who do do VMAT CSI for LMD - what are your tips/tricks? What is your approach in terms of contours as well as planning - how many fields?
 
building off @theradiator post - for those who do do VMAT CSI for LMD - what are your tips/tricks? What is your approach in terms of contours as well as planning - how many fields?

I believe SERO is active on this board
 
building off @theradiator post - for those who do do VMAT CSI for LMD - what are your tips/tricks? What is your approach in terms of contours as well as planning - how many fields?
Case was a couple years ago. Gave 400x 5 with vmat to canal and nerve roots with margin to 40 cm field starting from s2 making sure that anterior dose fell off to 50% within 1-1.5 cm of the ptv.

Then put in a gap and gave 300 x 10 to the rest. Zero acute complaints.
 
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I believe SERO is active on this board
Good. SERO is a good group. Happy to have them here.
 
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Well SERO is getting proton so they’re done with this
 
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We use 3 isocenters for VMAT CSI with partial arcs (120 - 240 degrees) for the spine volumes and full rotation for the head volume with feathering.
Usually we give 10 x 3 Gy, sometimes we treat with 2.5 Gy to higher doses.
We are strict when offering CSI and only do it when extracranial disease is well controlled.
My last two breast cancer patients both lived more than 1 year after CSI. Both finished treatment on outpatient basis, only side effects were hematologic toxicity (manageable).

One interesting thing I noticed is that the timepoints of your planning CT and treatment slots can confuse you. We match with CBCT, so if you did the planning CT early in the morning and choose to treat late in the afternoon, you may see mismatches. The length of the spine changes during the day (we become shorter) and you may see that when you try to match your volumes on CBCT, producing errors. We now plan and treat at a similar timepoint.
 
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We use 3 isocenters for VMAT CSI with partial arcs (120 - 240 degrees) for the spine volumes and full rotation for the head volume with feathering.
Usually we give 10 x 3 Gy, sometimes we treat with 2.5 Gy to higher doses.
We are strict when offering CSI and only do it when extracranial disease is well controlled.
My last two breast cancer patients both lived more than 1 year after CSI. Both finished treatment on outpatient basis, only side effects were hematologic toxicity (manageable).

One interesting thing I noticed is that the timepoints of your planning CT and treatment slots can confuse you. We match with CBCT, so if you did the planning CT early in the morning and choose to treat late in the afternoon, you may see mismatches. The length of the spine changes during the day (we become shorter) and you may see that when you try to match your volumes on CBCT, producing errors. We now plan and treat at a similar timepoint.

Remarkable. Any publication supportive of the bolded here? Sometimes trying to set up these VMAT CSI patients is a huge pain and I'd consider recommending this to the more frequent CSI'ers in my group if there was something published on it.

I just don't see the utility of routine use of CSI in solid tumor LMD.
 
CSI on a tomo therapy machine seems to work well
 
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Remarkable. Any publication supportive of the bolded here? Sometimes trying to set up these VMAT CSI patients is a huge pain and I'd consider recommending this to the more frequent CSI'ers in my group if there was something published on it.

I just don't see the utility of routine use of CSI in solid tumor LMD.
Unfortunately, we have not published that. And I am not aware of anyone else who has done it. But perhaps we should! :)

I believe it has to do with the sequence we do the matches and treatment too.
Some will probably do the first CBCT, then match and treat. Then go to the second isocenter, do the CBCT, match and treat.
This does not allow you however to understand what is happening where the volumes meet.

We set up the first isocenter, do the first CBCT, match, but do not treat yet. Then move to the second isocenter by shifting the couch using the values that the TPS gave us. Then we do the second CBCT and see if it matches. Ideally, if you had matched the first isocenter correctly, you should be landing at the second isocenter now. If this is the case, then we move to the third isocenter with the value from the TPS and perform the third CBCT. If that works out well, then we treat that volume and then work our way up again.
I know this is very complex and time consuming, but we wanted to make sure that the feathering would be correct. If you were treating a shorter patient in the afternoon using a plan that was calculated for a longer patient in the morning, you could produce an overlap where the two volumes would meet. If this worked out well the first couple of fractions, we were confident that the positioning was good and then skipped it for the rest of the fractions.

It's during the first shift using the value from the TPS that we saw, that were we not at the place where we were supposed to be. And when we looked at the length of the spine on the CBCT, it became apparent that it has to do with the overall length of the spine depending on the timepoint during the day.
 
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do proton centers seek out CSI cases?
it used to be a huge no-no a decade ago, as these take up too much machine time which could be used for prostates
 
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Quite important results for RT in irresectable pancreatic cancer. Another negative trial.

i mean… negative trials aren’t so bad. There are enough wisps of benefit here that rad oncs will probably continue chemoRT. Just think: EORTC 22922 was a negative trial too, but rad oncs focused on the happy outcomes and BOOM the negative experimental arm became the standard of care! Where there’s a will there’s a way.

#cynicaltake
 
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i mean… negative trials aren’t so bad. There are enough wisps of benefit here that rad oncs will probably continue chemoRT. Just think: EORTC 22922 was a negative trial too, but rad oncs focused on the happy outcomes and BOOM the negative experimental arm became the standard of care! Where there’s a will there’s a way.

#cynicaltake
It's striking how you once managed to shift the discussion over to BREAST!

I REFUSE TO GO DOWN THAT PATH AGAIN!

I am calling for a ban on breast discussions for 30 days, effective immediately.
:giggle::giggle::giggle:
 
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It's striking how you once managed to shift the discussion over to BREAST!

I REFUSE TO GO DOWN THAT PATH AGAIN!

I am calling for a ban on breast discussions for 30 days, effective immediately.
:giggle::giggle::giggle:
I have come here to chew bubblegum and kick a$$.... and I'm all out of bubblegum

But in all seriousness. Just reading the conclusions (NB: doesn't expressly state "NEGATIVE TRIAL," but of course it is) from 20,000 feet I can foresee many a GI rad onc in tumor board USING this data to lobby for chemoRT still. Don't you think, or no?
 
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Don't you think, or no?
Absolutely. This is an example of a trial that will not change SOC much.

Surgery is often not helpful. In a younger, healthier patient, R0 and margin benefit alone likely to push these patients towards chemorads prior to surgery unless real chip-shot in surgeon's mind.

The surgeons will end up our biggest advocates.
 
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I have come here to chew bubblegum and kick a$$.... and I'm all out of bubblegum

But in all seriousness. Just reading the conclusions (NB: doesn't expressly state "NEGATIVE TRIAL," but of course it is) from 20,000 feet I can foresee many a GI rad onc in tumor board USING this data to lobby for chemoRT still. Don't you think, or no?
I agree- this is probably the best or close to the best we could hope for in pancreatic cancer.
 
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Quite important results for RT in irresectable pancreatic cancer. Another negative trial.

I hate abstracts that don't define acronyms. I'm guessing CRM = circumferential resection margin? What's the difference between an R0 surgery and an R0 CRM- surgery? And isn't an R0 CRM+ surgery just...an R1 surgery?

Also, I'm pretty surprised that there was a higher rate of heme toxicities and a similar rate of non-heme toxicities. Also, is Gem now the SoC for CRT rather than 5-FU or Xeloda?

I'm not sure what everyone else's experience has been but my patients tolerate ChemoRT for pancreatic cancer extraordinarily well. Personally, I would view this as a positive trial for RT if 3 months of additional chemo can be replaced by 6 weeks of chemoRT with similar outcomes at worst and potentially improvement in PFS/OS.
 
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I'm not sure what everyone else's experience has been but my patients tolerate ChemoRT for pancreatic cancer extraordinarily well. Personally, I would view this as a positive trial for RT if 3 months of additional chemo can be replaced by 6 weeks of chemoRT with similar outcomes at worst and potentially improvement in PFS/OS.
I'd rather have 3 months of Gemcitabine mono than 6 weeks of Chemo-RT, if I had irresectable pancreatic cancer and the results would be the same in terms of PFS/OS.
 
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I'd rather have 3 months of Gemcitabine mono than 6 weeks of Chemo-RT, if I had irresectable pancreatic cancer and the results would be the same in terms of PFS/OS.
Did they break it down by systemic therapy? We already know folfirinox beats gem. I suspect a comparison of all folfirinox vs 80% folfirinox 20% gem would show no difference.
 
I'd rather have 3 months of Gemcitabine mono than 6 weeks of Chemo-RT, if I had irresectable pancreatic cancer and the results would be the same in terms of PFS/OS.
Unless I'm missing something, the randomization was to either continuing chemotherapy or proceeding with CRT, not to Gemzar vs. CRT.

402 pts received IC with FOLFIRINOX and 93 pts with Gem. We know FOLFIRINOX is superior to Gemzar, so can't really say based on this that 3 months Gemzar monotherapy is equivalent to 6 weeks CRT.
 
I hate abstracts that don't define acronyms. I'm guessing CRM = circumferential resection margin? What's the difference between an R0 surgery and an R0 CRM- surgery? And isn't an R0 CRM+ surgery just...an R1 surgery?

Also, I'm pretty surprised that there was a higher rate of heme toxicities and a similar rate of non-heme toxicities. Also, is Gem now the SoC for CRT rather than 5-FU or Xeloda?

I'm not sure what everyone else's experience has been but my patients tolerate ChemoRT for pancreatic cancer extraordinarily well. Personally, I would view this as a positive trial for RT if 3 months of additional chemo can be replaced by 6 weeks of chemoRT with similar outcomes at worst and potentially improvement in PFS/OS.
I'd rather have 3 months of Gemcitabine mono than 6 weeks of Chemo-RT, if I had irresectable pancreatic cancer and the results would be the same in terms of PFS/OS.
These results are just like Julia Roberts' character in 'Pretty Woman'...
Richard Gere: What's your name?
Julia Roberts: It's whatever you want it to be.

You want to support chemoRT? Use this trial. You want not to use chemoRT? Use this trial. This trial is whatever you want it to be!
 
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I hate abstracts that don't define acronyms. I'm guessing CRM = circumferential resection margin? What's the difference between an R0 surgery and an R0 CRM- surgery? And isn't an R0 CRM+ surgery just...an R1 surgery?

Also, I'm pretty surprised that there was a higher rate of heme toxicities and a similar rate of non-heme toxicities. Also, is Gem now the SoC for CRT rather than 5-FU or Xeloda?

I'm not sure what everyone else's experience has been but my patients tolerate ChemoRT for pancreatic cancer extraordinarily well. Personally, I would view this as a positive trial for RT if 3 months of additional chemo can be replaced by 6 weeks of chemoRT with similar outcomes at worst and potentially improvement in PFS/OS.
Chemotherapy works so well that 190 of 525 enrolled patients dropped out (and were not randomized) due to progression or toxicity.
 
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Unless I'm missing something, the randomization was to either continuing chemotherapy or proceeding with CRT, not to Gemzar vs. CRT.

402 pts received IC with FOLFIRINOX and 93 pts with Gem. We know FOLFIRINOX is superior to Gemzar, so can't really say based on this that 3 months Gemzar monotherapy is equivalent to 6 weeks CRT.
That is true, I am sorry, I missed that!
 
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