Rad Onc Twitter

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ASCO has been great this year - how many spots filled in the SOAP again? I can't keep it straight...market correction will happen, right guys? Guys?
 
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ASCO has been great this year - how many spots filled in the SOAP again? I can't keep it straight...market correction will happen, right guys? Guys?
What a dramatic way to describe a blanket recommendation for trials that primarily included patients with low to intermediate risk features. I don't know about you, but I would err on the side of adjuvant for Gleason 8+, SVI, N+ patients.
 
What a dramatic way to describe a blanket recommendation for trials that primarily included patients with low to intermediate risk features. I don't know about you, but I would err on the side of adjuvant for Gleason 8+, SVI, N+ patients.
Urology Twitter is generally much more grandiose than RadOnc Twitter, it could be a Netflix limited series.
 
What a dramatic way to describe a blanket recommendation for trials that primarily included patients with low to intermediate risk features. I don't know about you, but I would err on the side of adjuvant for Gleason 8+, SVI, N+ patients.
Just means instead of treating now, well treat in a year. Of course, we won't be able to get a psma pet as we'll see em two weeks after urology starts em on bicalutamide and lupron.
 
What a dramatic way to describe a blanket recommendation for trials that primarily included patients with low to intermediate risk features. I don't know about you, but I would err on the side of adjuvant for Gleason 8+, SVI, N+ patients.
I would as well, but probably won’t see the patient.
 
Just means instead of treating now, well treat in a year. Of course, we won't be able to get a psma pet as we'll see em two weeks after urology starts em on bicalutamide and lupron.
Early salvage certainly reasonable in this population, though an argument can be made that the adjuvant setting is their window for cure. These patients are at high risk of distant failure such that when they do have a biochemical recurrence and you get a PSMA, it will show distant mets, and then the benefit of XRT is limited. The recent JCO paper (with all the caveats of retrospective studies) makes the argument for adjuvant in these high-risk patients. Of course, I fully recognize that none of this matters if there's no buy in from urologists and medoncs who control the referrals.

 
It is pretty rad if it turns out to be true

People will criticize for small patient numbers. Right now it's N=12, 100% response rate yada yada.

If you flip a coin 12 times, and get 12 heads, it's a HIGHLY significant result. It's just N=12, but you can show that the null (I expect not to find > or <6 heads) is rejected at a p-value of <0.000001. And this means the experiment WILL BE replicated at bigger N. (FWIW, 7 heads, p=0.2; 8 heads, p=0.07; 9 heads, p=0.02; 10 heads, p=0.003; 11 heads, p=0.0002.)

What I'm saying is: the small patient numbers have ~zero to do with anything. We are not exactly used to that in oncology where the delta between (hoped for, or hypothesized) experiment (outcome) vs control is usually small.
 
They will only use it postoperatively.
My impression is they won't use it all. Up front would cancel surgeries, post op would confirm what a ****ty job they did. When I get a patient for salvage whos already been started on anti androgens it feels like a cover up.
 


"This new approach of 'immunoablative' therapy uses immunotherapy to replace surgery, chemotherapy and radiation to remove cancer."

Its certainly important to further study this idea and if it really pans out (im doubtful), then that would be a great boon for patients. I think it flies in the face of several cancer biology principles (imaging CR does not mean the disease is eradicated, 1 cm tumor is 1 billion cells) and tumors are not monoclonal populations of cells. The results are worth further study, but I'm skeptical it will pan out.
 
People will criticize for small patient numbers. Right now it's N=12, 100% response rate yada yada.

If you flip a coin 12 times, and get 12 heads, it's a HIGHLY significant result. It's just N=12, but you can show that the null (I expect not to find > or <6 heads) is rejected at a p-value of <0.000001. And this means the experiment WILL BE replicated at bigger N. (FWIW, 7 heads, p=0.2; 8 heads, p=0.07; 9 heads, p=0.02; 10 heads, p=0.003; 11 heads, p=0.0002.)

What I'm saying is: the small patient numbers have ~zero to do with anything. We are not exactly used to that in oncology where the delta between (hoped for, or hypothesized) experiment (outcome) vs control is usually small.
Agreed. Would not need a phase 3. Statistics is about generating a conclusion about the real world from a sample. When the answer is obvious ie antibiotics for bacteria, you don’t always need it.
Btw:they did biopsy the pts.
 
Agreed. Would not need a phase 3. Statistics is about generating a conclusion about the real world from a sample. When the answer is obvious ie antibiotics for bacteria, you don’t always need it.
Btw:they did biopsy the pts.
These types of outcomes (ie, placebo vs immunotx would give a ~0% vs ~100% ORR, and chemoRT would give ~25% vs ~100%) are almost akin to parachute/no parachute outcomes. #nohyperbole
 
These types of outcomes (ie, placebo vs immunotx would give a ~0% vs ~100% ORR, and chemoRT would give ~25% vs ~100%) are almost akin to parachute/no parachute outcomes. #nohyperbole

I know you said ORR but chemoRT definitely doesn’t give a 100 percent CR rate, which is probably what is relevant in terms of not doing surgery
 
I know you said ORR but chemoRT definitely doesn’t give a 100 percent CR rate, which is probably what is relevant in terms of not doing surgery
You have to get ORRs to get CRs and cures and OS differences. Has anyone ever died of metastatic colorectal cancer that was no evidence of radiographic disease.

2022-06-05 09_43_51-Pashtoon Kasi MD, MS on Twitter_ _#ASCO22 👇🏾See what’s now published @NEJM...png
 
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You have to get ORRs to get CRs and cures and OS differences. Has anyone ever died of metastatic colorectal cancer that was no evidence of radiographic disease.

Ok.

Point is an ORR from chemoRT not really relevant here. Not sure what you were trying to say. Also we did have a randomized trial (multiple) to show that preop chemoRT helped.

Anyways I agree we don’t need a phase III to use IO in MSI high rectal cancer (5-10 percent) , but we will need and want more patient data, which we will surely get.
 
Point is an ORR from chemoRT not really relevant here. Not sure what you were trying to say.
ORR is a marker for things that are very relevant. I am saying when you have a treatment that is giving ***100%*** ORRs, you will get a lot of pCRs. E.g., a woman with palpable breast mass and ax nodes who gets a cCR from chemo+/-immuno has a high chance of pCR. (Another arena where avoiding RT... and even surgery... is being explored, although tenuously.)
 
this is probably wrong 🙂

(edit: will freely admit this is a dumb argument at outset)
When I was a medstudent in the late 90s this was the prevailing dogma in oncology. 1 billion cells, equally clonogenic with the Immune system playing a minor role. Because of the math of log kill (10exp11 to 10exp8) it was easy for drug to show a complete radiological response without meaningful kill. The prevailing dogma was that solid malignancies could not be addressed by drugs alone nor could they cure stage 4 disease. Gave me relative confidence that radiation would be a major part of oncology for the entirety of my career.
 
These types of outcomes (ie, placebo vs immunotx would give a ~0% vs ~100% ORR, and chemoRT would give ~25% vs ~100%) are almost akin to parachute/no parachute outcomes. #nohyperbole

This is the statement you wrote again. Can you explain where in 2022 the fact that radiation makes a rectal tumor smaller is useful, interesting, or relevant?

Don’t double down on a useless post
 
This is the statement you wrote again. Can you explain where in 2022 the fact that radiation makes a rectal tumor smaller is useful, interesting, or relevant?

Don’t double down on a useless post
Lol let's see if I can explain my logic. ORRs are very associated with pCRs. I am not sure it's 1:1, but it's kind of close... for a rectal patient undergoing chemoRT who gets total cessation of bleeding, a perfectly normal DRE, perfectly normal endoscopy, and negative PET and MRI, the pCR odds are very high. We are looking at, AFAIK, "organ preservation" for chemoRT rectal patients that get a pCR (letting the chemoRT be the cure). If you can get a pCR at a MUCH higher rate WITHOUT chemoRT, this is... something. This will mean, at least for some rectal patients, the best chance for pCR will NOT be chemoRT, but something else entirely.
 
People will criticize for small patient numbers. Right now it's N=12, 100% response rate yada yada.

If you flip a coin 12 times, and get 12 heads, it's a HIGHLY significant result. It's just N=12, but you can show that the null (I expect not to find > or <6 heads) is rejected at a p-value of <0.000001. And this means the experiment WILL BE replicated at bigger N. (FWIW, 7 heads, p=0.2; 8 heads, p=0.07; 9 heads, p=0.02; 10 heads, p=0.003; 11 heads, p=0.0002.)

What I'm saying is: the small patient numbers have ~zero to do with anything. We are not exactly used to that in oncology where the delta between (hoped for, or hypothesized) experiment (outcome) vs control is usually small.
The follow up in the trial is only 6 months. In rectal cancer, one needs probably a bare minimum of 3 years of follow up.
Anyways MMR deficient rectal cancers accounts for only 5-10% of all rectal cancers.
 
The follow up in the trial is only 6 months. In rectal cancer, one needs probably a bare minimum of 3 years of follow up.
Anyways MMR deficient rectal cancers accounts for only 5-10% of all rectal cancers.
Ok, but within 10-15 yrs, radiation will disappear from rectal cancer. Presently, we don’t have any good evidence that neoadjuvant chemorads has any benefit over folfox alone. It’s hanging on by a thread (w a less than 5% absolute benefit in local control), that the next active systemic agent will cut.
 
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Oh man, I would love to hear what happened between Dr. Winkfield and ASTRO. I have my suspicions but love to hear the truth.
Karen Winkfield and Curtiland Deville were elected as ex-officio board members(meaning non-elected board members to ASTRO) because of their article in Advances in Radiation Oncology.
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Maybe she felt she could hold on as a board member life long.
Kind of interesting article where none of the co-authors include an Latina,Native american/pacific islander or an Asian
 
Karen Winkfield and Curtiland Deville were elected as ex-officio board members(meaning non-elected board members to ASTRO) because of their article in Advances in Radiation Oncology.
View attachment 355909

Maybe she felt she could hold on as a board member life long.
Kind of interesting article where none of the co-authors include an Latina,Native american/pacific islander or an Asian
For the sake of diversity, why not replace one of the totally worthless board members like Ben smith with a person of color?
 
The follow up in the trial is only 6 months. In rectal cancer, one needs probably a bare minimum of 3 years of follow up.
Anyways MMR deficient rectal cancers accounts for only 5-10% of all rectal cancers.
Are rad oncs the "true" oncologists? If some RT regimen had produced 6mo 100% CR rate it would have been tattooed on the chest of every rad onc in America today, and every rad onc would have tweeted the tat pic! Several patients followed >6 months. Yes this is niche-ish, but the mere fact that the word "immunoablative" exists for epitheloid cancers now is a big deal. I had never heard it prior to this.

I would go one step further. There now exists more of an (exciting? promising? palpable?) immunoablative paradigm than an oligometastatic (vis-à-vis SABR) paradigm.

KGUUn8w.png
 
Are rad oncs the "true" oncologists? If some RT regimen had produced 6mo 100% CR rate it would have been tattooed on the chest of every rad onc in America today, and every rad onc would have tweeted the tat pic! Several patients followed >6 months. Yes this is niche-ish, but the mere fact that the word "immunoablative" exists for epitheloid cancers now is a big deal. I had never heard it prior to this.

I would go one step further. There now exists more of an (exciting? promising? palpable?) immunoablative paradigm than an oligometastatic (vis-à-vis SABR) paradigm.

KGUUn8w.png
No doubt that we have been living through a paradigm change that started in the 1990s and coincided so ironically with peak radonc. Circa 2010 with inklings from Ipi in melanoma, there was still lots of cynicism from most MEDONC researchers regarding immunotherapy. By 2012 all parties were jumping face forward, including radonc.

Understanding the molecular basis for high MSI tumors and their high immunogenicity is a relatively recent thing. Imagine being a GI medonc (or Tim Chan) in the early 2000s. Such stories to pursue and ironies to be found. Those very molecularly heterogenous populations of tumor cells, which should make them invincible to targeted cytotoxic therapy at a population level, have invited in TILs at a remarkable level and with a little tweak of immuno-editing, you are curing certain groups of cancers. A Gleevec type story in certain cancers.

These are selected patients. But the story will be rinse and repeat and trials in earlier stages of cancers all around. Won't change what we do with 90 percent of locally advanced (low) rectal CA in the near future. But, its another 10% off our docket.

Radoncs also jumped on these molecular stories, and gathered talent and hoped that stereotactic radiation would invite in TILs and make us magicians across the board. Have only seen this in mice. Please prove me wrong.
 
No doubt that we have been living through a paradigm change that started in the 1990s and coincided so ironically with peak radonc. Circa 2010 with inklings from Ipi in melanoma, there was still lots of cynicism from most MEDONC researchers regarding immunotherapy. By 2012 all parties were jumping face forward, including radonc.

Understanding the molecular basis for high MSI tumors and their high immunogenicity is a relatively recent thing. Imagine being a GI medonc (or Tim Chan) in the early 2000s. Such stories to pursue and ironies to be found. Those very molecularly heterogenous populations of tumor cells, which should make them invincible to targeted cytotoxic therapy at a population level, have invited in TILs at a remarkable level and with a little tweak of immuno-editing, you are curing certain groups of cancers. A Gleevec type story in certain cancers.

These are selected patients. But the story will be rinse and repeat and trials in earlier stages of cancers all around. Won't change what we do with 90 percent of locally advanced (low) rectal CA in the near future. But, its another 10% off our docket.

Radoncs also jumped on these molecular stories, and gathered talent and hoped that stereotactic radiation would invite in TILs and make us magicians across the board. Have only seen this in mice. Please prove me wrong.
I don’t know how anyone can be optimistic over 10-20 year timeframe. IO is only going to improve and io modulators will be found. Much of stage 3 nsclc will disappear and almost certainly neoadjuvant chemo/io will at some point replace the cross regimen.
 
I don’t know how anyone can be optimistic over 10-20 year timeframe. IO is only going to improve and io modulators will be found. Much of stage 3 nsclc will disappear and almost certainly neoadjuvant chemo/io will at some point replace the cross regimen.
Eh, I don’t know. I don’t see surgery winning out over RT. Especially, given how sick lung cancer patients tend to be from comorbidity.
 
Eh, I don’t know. I don’t see surgery winning out over RT. Especially, given how sick lung cancer patients tend to be from comorbidity.
Three factors at work that have rad onc implications.

First, the immunotherapy. More willingness to do chemo/IO then surgery; and RT is pretty much out in postop Stage III.

Second, smoking is declining; less lung cancer.

Third, screening; rapidly declining incidence of Stage III. This means a significantly declining number of lung cancer patients under beam.

The triple hit hypothesis.
 
Three factors at work that have rad onc implications.

First, the immunotherapy. More willingness to do chemo/IO then surgery; and RT is pretty much out in postop Stage III.

Second, smoking is declining; less lung cancer.

Third, screening; rapidly declining incidence of Stage III. This means a significantly declining number of lung cancer patients under beam.

The triple hit hypothesis.
Why would anyone do surgery over RT? Many of these patients have comorbid illnesses and the trimodality studies never really provided a benefit to cutting
 
Why would anyone do surgery over RT? Many of these patients have comorbid illnesses and the trimodality studies never really provided a benefit to cutting
Because surgeons like to cut, especially in large systems. Nowhere in oncology, is the role of surgery more dubious than bladder cancer, yet it is still the treatment of choice, despite grotesque consequences.
 
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