clinical cases

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Niagara trial for perioperative bladder cancer. Are we using the 40mg/m2 cisplatin (currently used in TOPAZ1 for cholangio) or are we doing 70mg/m2 (currently used for neoadjuvant bladder)? Also are you doing GCSF after D8 gemcitabine? The full paper is not out and the abstract doesn't specify
 
Niagara trial for perioperative bladder cancer. Are we using the 40mg/m2 cisplatin (currently used in TOPAZ1 for cholangio) or are we doing 70mg/m2 (currently used for neoadjuvant bladder)? Also are you doing GCSF after D8 gemcitabine? The full paper is not out and the abstract doesn't specify
Paper is out.

Same chemo backbone as usual (70 Cis C1/1000 GemD1,8), just + durva.

I wouldn't use growth factors for primary prevention unless I had a good reason to.
 
Since we’re on the topic of neoadjuvant bladder, two generic questions:

1) For CrCl 50-60, do you try to do split dose cisplatin? And for under CrCl 50, I know the textbook answer is go straight to surgery but curious if anyone is trying pembro-enfortumab (assuming insurance will pay)?
2) Does anyone do ddMVAC for young patients? Or is it just too toxic?
 
Ive been using enfortumab pembro as neoadjuvant but saying "unresectable" in my notes.

I never use ddMVAC.
 
Cisplatin ineligibility is one of the toughest decisions, especially when a patient doesn’t clearly meet the standard ineligibility criteria. I’m not sure if there have been any recent updates or refinements to these guidelines. That said, for patients with a CrCl of 50-60 who meet the rest of the criteria, I still consider cisplatin an option, whether as a split-dose or full-dose regimen.
I’ve treated patients with bladder,H&N, or testicular cancer in similar renal function scenarios. Hearing impairment, often from occupational or entertainment-related hazards, is another common challenge. Once, I had to administer sodium thiosulfate for otoprotection—not sure it did much physiologically, but it definitely helped ease a young patient’s anxiety.

I always have a detailed discussion about the risks and benefits, and in my experience, most patients are highly motivated to pursue bona fide curative therapy options when facing cancer.
I’ve been tempted to use ddMVAC on two occasions, but both times vinblastine was on national shortage (it’s frequently on the chemo drug shortage list). It’s frustrating—you don’t want to discuss a treatment plan with a patient only to have to call them later and say the drug isn’t available.
That said, I had one patient who completed 4 cycles of MVAC with no adverse effects and achieved a complete pCR.
 
Since we’re on the topic of neoadjuvant bladder, two generic questions:

1) For CrCl 50-60, do you try to do split dose cisplatin? And for under CrCl 50, I know the textbook answer is go straight to surgery but curious if anyone is trying pembro-enfortumab (assuming insurance will pay)?
2) Does anyone do ddMVAC for young patients? Or is it just too toxic?

I use ddMVAC. It's hit or miss / hard to predict who experiences the most toxicity. As Mehena said, you'll get patients who just breeze straight through it.

For folks with borderline CrCl, I'll get a 24 hour urine creatinine clearance as it's a more accurate measure of GFR and if that's also low, I'll split the dose of Cisplatin
 
Ive been using enfortumab pembro as neoadjuvant but saying "unresectable" in my notes.
I've not been lucky enough to get pembro/enfortumab approved yet in this setting. I also don't think that enfortumab is the "chemo free" picnic we sometimes pretend it is.
I never use ddMVAC.
The only people who like ddMVAC are retirement age oncologists and urologists. I'm not sure why they push so hard for ddMVAC. Maybe they're hoping to not have to operate after all.
 
I've not been lucky enough to get pembro/enfortumab approved yet in this setting. I also don't think that enfortumab is the "chemo free" picnic we sometimes pretend it is.

The only people who like ddMVAC are retirement age oncologists and urologists. I'm not sure why they push so hard for ddMVAC. Maybe they're hoping to not have to operate after all.
I think I only have 2 patients who's on the enfortumab/pembro neoadjuvant. I'm sure if it's larger sample size, I would get pushback from insurance. Agree that vedotin is no walk in the park.

The (quite prominent) GU oncologist I trained under in fellowship told me to never use ddMVAC so I've deleted it from my brain after boards lol.
 
Also as an aside, I've never seen a regimen as controversial as ddMVAC. It's almost got a cult-like following both for and against. I feel like someone should make a sweatshirt or something haha
 
Also as an aside, I've never seen a regimen as controversial as ddMVAC. It's almost got a cult-like following both for and against. I feel like someone should make a sweatshirt or something haha
100% agree with this. It's basically a religion at this point.
 
Case: metastatic colon cancer on third-line Lonsurf. Has a history of cardiac arrest 7 years ago with pacemaker, unknown etiology for arrest.

Question: would any one add bevacizumab, or with the history of arrest, you wouldn't risk the thrombotic effects?
 
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I don't think the history of arrest by itself would rule out the bev to me but presumably there was some element of CAD investigation surrounding the event? Even if there was CAD found, I think its a risk benefit discussion mostly depending on how stable any CAD is (i.e. recent events)?
 
Case: metastatic colon cancer on third-line Lonsurf. Has a history of cardiac arrest 7 years ago with pacemaker, unknown etiology for arrest.

Question: would any one add bevacizumab, or with the history of arrest, you wouldn't risk the thrombotic effects?
For cardiac folks I'm more concerned about flouropyrimidines than I am bev.
 
Case: metastatic colon cancer on third-line Lonsurf. Has a history of cardiac arrest 7 years ago with pacemaker, unknown etiology for arrest.

Question: would any one add bevacizumab, or with the history of arrest, you wouldn't risk the thrombotic effects?
Personally, I would give ddMVAC in this situation
 
@gutonc or anyone else... have a few GI questions that have come up recently

Where do your institutions draw the line between Sigmoid / Rectal for these Rectosigmoid or "High Rectal" masses? Particularly when it comes to doing something like TNT vs Surgery up front followed by ?Colon or Rectal treatment paradigms post op?

For true PET/EUS/Dx Lap staged T2N0 Gastric, do your groups ever offer up-front surgery instead of perioperative chemo? It doesn't really make sense to me that the guidelines more or less read as "you should do perioperative chemo... unless you didn't... then you probably don't actually need to."
 
@gutonc or anyone else... have a few GI questions that have come up recently

Where do your institutions draw the line between Sigmoid / Rectal for these Rectosigmoid or "High Rectal" masses? Particularly when it comes to doing something like TNT vs Surgery up front followed by ?Colon or Rectal treatment paradigms post op?
I tend to let the surgeons and Rad Oncs duke it out over this one. I don't think that there's a strict dividing line (except for one clinical trial we have open that has a hard stop at something like 12 or 15cm above the anal verge). The way that we seem to be trending is that, if the colorectal surgeon thinks they can get it out without a temporary ileostomy, we treat that more like colon (although almost always do perioperative FOLFOX a'la the PROSPECT trial).

In all other cases, or if the patient refuses surgery, we're going full TNT --> watchful waiting.
For true PET/EUS/Dx Lap staged T2N0 Gastric, do your groups ever offer up-front surgery instead of perioperative chemo? It doesn't really make sense to me that the guidelines more or less read as "you should do perioperative chemo... unless you didn't... then you probably don't actually need to."
I tend to go the periop chemo route in these folks, mostly as a test of time. If they can't handle 4 cycles of FLOT, they're not going to tolerate a gastrectomy.
 
DLBCL question:

I have a young 30M no PMH but diagnosed with stage II nonbulky DLBCL (ABC subtype, double expressor BCL2 and MYC but not double hit). Which regimen would you pick and why? Assume you can get insurance approval for all:

1. RCHOP x3 -> PET -> RCHOP x1
2. Da-REPOCH x6
3. Pola-R-CHP x6

I am leaning towards 1 because that's the standard but I know the lymphoma docs back in my fellowship prefer Polarix for double-expressors
 
Yup, Pola-R-CHP for non-GCB double expressers makes a lot of sense, even in stage 2 non-bulky disease. The argument is mainly based on a subgroup analysis of POLARIX showing that non-GCB patients accounted for most of the benefit seen in the overall treatment arm, but this is corroborated by this NEJM letter (DOI: 10.1056/NEJMc2306105) that a lot of people cite arguing that this effect was consistent among multiple early stage trials even before POLARIX reported out. The theory that they quote is that non-GCB cell of origin large B-Cells preferentially express CD-79b and so this difference is rooted in physiology, and since a lot of these patients tend to be younger with a lot more to lose, I see a lot of hematologists gravitate towards Pola for these patients.
 
Yup, Pola-R-CHP for non-GCB double expressers makes a lot of sense, even in stage 2 non-bulky disease. The argument is mainly based on a subgroup analysis of POLARIX showing that non-GCB patients accounted for most of the benefit seen in the overall treatment arm, but this is corroborated by this NEJM letter (DOI: 10.1056/NEJMc2306105) that a lot of people cite arguing that this effect was consistent among multiple early stage trials even before POLARIX reported out. The theory that they quote is that non-GCB cell of origin large B-Cells preferentially express CD-79b and so this difference is rooted in physiology, and since a lot of these patients tend to be younger with a lot more to lose, I see a lot of hematologists gravitate towards Pola for these patients.
Let’s say the patient is 85 with Non-GCB disease.

Are we still doing mini-CHOP or going for broke with POLARIX? I guess they excluded people 80+ but not sure how fair that is.

I’m also curious if people are doing the 2 cycles or Rituximab at the end…
 
Let’s say the patient is 85 with Non-GCB disease.

Are we still doing mini-CHOP or going for broke with POLARIX? I guess they excluded people 80+ but not sure how fair that is.

I’m also curious if people are doing the 2 cycles or Rituximab at the end…
Ah yes. Complicated question.

I've found that some folks are adopting the FLYER regimen and some aren't for limited stage DLBCL. Almost all folks got 2 cycles of Rituxan at the end. Even though the trial followed most patients to the three year mark I feel like a lot of people aren't comfortable using this yet, as it kinda leaves a big question unanswered, as to whether consolidative ISRT for these patients is necessary or not, and if we're mainly limiting chemo to spare toxicity, it's hard to argue that substituting RT for chemo really spares THAT much toxicity or not.

As for mini-CHOP, I'll usually start most of my 80+ yo's on mini-CHOP with consideration of escalation if mid treatment PET doesn't get a great response. For my 80+ year olds who are fit and healthy, I'll usually start them on full dose CHOP and de-escalate to mini-CHOP if they really can't handle it. I don't really use Pola-R-CHP as much for these folks unless they're non-GCB, as the Pola is really tough to de-intensify (we get one dose reduction and then technically the FDA label says we have to take it off).
 
Ah yes. Complicated question.

I've found that some folks are adopting the FLYER regimen and some aren't for limited stage DLBCL. Almost all folks got 2 cycles of Rituxan at the end. Even though the trial followed most patients to the three year mark I feel like a lot of people aren't comfortable using this yet, as it kinda leaves a big question unanswered, as to whether consolidative ISRT for these patients is necessary or not, and if we're mainly limiting chemo to spare toxicity, it's hard to argue that substituting RT for chemo really spares THAT much toxicity or not.

As for mini-CHOP, I'll usually start most of my 80+ yo's on mini-CHOP with consideration of escalation if mid treatment PET doesn't get a great response. For my 80+ year olds who are fit and healthy, I'll usually start them on full dose CHOP and de-escalate to mini-CHOP if they really can't handle it. I don't really use Pola-R-CHP as much for these folks unless they're non-GCB, as the Pola is really tough to de-intensify (we get one dose reduction and then technically the FDA label says we have to take it off).
This trial hasn’t read out yet, but for an older/frailer non-GCB patient I’d still consider starting with mini-pola-R-CHP and possibly dose escalating if well-tolerated. S227: INITIAL SAFETY DATA FROM THE PHASE 3 POLAR BEAR TRIAL IN ELDERLY OR FRAIL PATIENTS WITH DIFFUSE LARGE CELL LYMPHOMA, COMPARING R-POLA-MINI-CHP AND R-MINI-CHOP - PMC
 
This trial hasn’t read out yet, but for an older/frailer non-GCB patient I’d still consider starting with mini-pola-R-CHP and possibly dose escalating if well-tolerated. S227: INITIAL SAFETY DATA FROM THE PHASE 3 POLAR BEAR TRIAL IN ELDERLY OR FRAIL PATIENTS WITH DIFFUSE LARGE CELL LYMPHOMA, COMPARING R-POLA-MINI-CHP AND R-MINI-CHOP - PMC
POLAR BEAR might be my new favorite trial name

Edit: I've been pissed since day one that they didn't name the regimen POLAR-CHP and market it like Coca-Cola with polar bears eating Chips or something
 
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LOL oh this is a good one thanks for sharing! Hooray for collective knowledge!
 
Hey all - have a question about one of my very weak areas as a fellow, thoracic.

Good performance status woman in her 50s - stage IIIA disease previously treated with 4 cycles chemoRT followed by durvalumab per the PACIFIC regimen in 2023 (end of durvalumab was mid 2024). Smoker. No driver mutation on initial tumor profiling, PDL1 high.

Now with solitary lesion recurrence in adrenals 6 months after end of PACIFIC. All other imaging negative (PET, brain MRI). Will biopsy lesion for definitive proof.

Questions:
1) If you have oligometastasic recurrence after PACIFIC regimen, can you get away with SBRT alone?
2) If you theoretically had widespread disseminated disease after PACIFIC, do you manage as first-line metastatic - i.e., check driver mutations and treat accordingly based on presence or absence? And in particular, if someone recurs so soon after durvalumab and continues to have no driver mutations, does it still make sense to do carbo/peme/pembro?

Thank you.
 
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Hey all - have a question about one of my very weak areas as a fellow, thoracic.

Good performance status woman in her 50s - stage IIIA disease previously treated with 4 cycles chemoRT followed by durvalumab per the PACIFIC regimen in 2023 (end of durvalumab was mid 2024). Smoker. No driver mutation on initial tumor profiling, PDL1 high.

Now with solitary lesion recurrence in adrenals 6 months after end of PACIFIC. All other imaging negative (PET, brain MRI). Will biopsy lesion for definitive proof.

Questions:
1) If you have oligometastasic recurrence after PACIFIC regimen, can you get away with SBRT alone?
Potentially. The good news here is that you pretty much can't do this wrong. I'm a big proponent of local therapy for isolated oligometastatic disease. Not that it necessarily improves OS, but it does spare people potential systemic toxicity AND saves additional systemic therapy for down the road when local treatment is no longer an option. A lot of this will depend on your local climate and surgeon/Rad Onc practice patterns. I've seen folks who rigidly stick to guidelines as gospel, or worse practice "that's the way I was trained" medicine without thinking about the case in front of them.
2) If you theoretically had widespread disseminated disease after PACIFIC, do you manage as first-line metastatic - i.e., check driver mutations and treat accordingly based on presence or absence? And in particular, if someone recurs so soon after durvalumab and continues to have no driver mutations, does it still make sense to do carbo/peme/pembro?
Depends on the recurrence timeline and first-line therapy. If <6 mos since end of therapy, I would absolutely try something different. If >12 months, I'd feel comfortable going back to what worked the first time. For that middle ground, choose one based on toxicity profile and patient characteristics. If she got platinum/etop or platinum/taxane with RT up front, I'd use platinum/pem/pembro now (assuming no new treatment options based on repeat biopsy/NGS). If pemetrexed was part of the chemoRT, I'd use a different partner drug (taxol is my go to, but the ancient LACE data say it doesn't really matter what the platinum partner is...even if this was in the adjuvant setting).
 
For stage III colon cancer post chemoRT, when do you get the first imaging? Do you start durvalumab before imaging or wait for imaging? I typically get CT CAP ~3-4 weeks after chemoRT, and then start durvalumab 1 week later - is this what you have been doing as well?
 
For stage III colon cancer post chemoRT, when do you get the first imaging? Do you start durvalumab before imaging or wait for imaging? I typically get CT CAP ~3-4 weeks after chemoRT, and then start durvalumab 1 week later - is this what you have been doing as well?
I'm sorry, what the what?!?! ChemoRT and durvalumab for colon cancer?

If you mean lung cancer (and I really hope you do), I typically start within 4 weeks and try to get the CT somewhere in the middle there. The PACIFIC trial mandated imaging at the completion of chemoRT (week 8) and starting durvalumab at week 10 (2w later).

Understand that the point of the post RT CT scan is to ensure that there has not been the development of metastatic disease, NOT to assess the treated disease. So what you're really looking at here is contralateral lung, liver and bones. I don't get a PET scan at this point because there will be uptake in the radiated area and it just freaks everyone out.
 
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For stage III colon lung (...right?) cancer post chemoRT, when do you get the first imaging? Do you start durvalumab before imaging or wait for imaging? I typically get CT CAP ~3-4 weeks after chemoRT, and then start durvalumab 1 week later - is this what you have been doing as well?

I like this question because it falls under the category of "things that felt so routine and straightforward that I never even thought twice about them in fellowship but then as soon as I got out I was immediately like how do I not know the answer to this?" Which still happens to me approximately every other day as I'm only 2+ years out, but is thankfully becoming at least slightly less common. Does it ever stop?

If the patient is doing well, I typically get the CT one week after completion of chemo-RT (just to check the "chest is not a complete disaster" box prior to moving on as mentioned above) and then aim to start durvalumab two weeks after chemo-RT if the patient is doing well/is game. The PACIFIC trial was amended from the original 14 day timeframe and allowed durvalumab to start up to 42 days after chemo-RT so there's a lot of leeway, ultimately only ~25% of patients started within 14 days when it was all said and done.

If you want to do the hand-wavy academic oncology navel gazing thing, the exploratory subsets in PACIFIC trend towards better HR for both PFS and OS in those that started within 14 days of chemo-RT completion. That has to be taken with a massive, massive grain of salt (exploratory subset blah blah no statistical significance blah blah patients who were healthy enough to get immunotherapy within 14 days of treatment are much more likely to do better than those who weren't blah blah) to the point where it very well may be meaningless, but when I was trying to decide on my approach I figured if a patient was cruising and had no contraindication I might as well go for that timeframe. But if they're roughed up or we can't get the scan or run into insurance issues or they just want to spend some time away from clinic for a hot sec I lose no sleep over starting them 4ish weeks out.
 
I like this question because it falls under the category of "things that felt so routine and straightforward that I never even thought twice about them in fellowship but then as soon as I got out I was immediately like how do I not know the answer to this?" Which still happens to me approximately every other day as I'm only 2+ years out, but is thankfully becoming at least slightly less common. Does it ever stop?

If the patient is doing well, I typically get the CT one week after completion of chemo-RT (just to check the "chest is not a complete disaster" box prior to moving on as mentioned above) and then aim to start durvalumab two weeks after chemo-RT if the patient is doing well/is game. The PACIFIC trial was amended from the original 14 day timeframe and allowed durvalumab to start up to 42 days after chemo-RT so there's a lot of leeway, ultimately only ~25% of patients started within 14 days when it was all said and done.

If you want to do the hand-wavy academic oncology navel gazing thing, the exploratory subsets in PACIFIC trend towards better HR for both PFS and OS in those that started within 14 days of chemo-RT completion. That has to be taken with a massive, massive grain of salt (exploratory subset blah blah no statistical significance blah blah patients who were healthy enough to get immunotherapy within 14 days of treatment are much more likely to do better than those who weren't blah blah) to the point where it very well may be meaningless, but when I was trying to decide on my approach I figured if a patient was cruising and had no contraindication I might as well go for that timeframe. But if they're roughed up or we can't get the scan or run into insurance issues or they just want to spend some time away from clinic for a hot sec I lose no sleep over starting them 4ish weeks out.
I’m not sure I believe there’s nearly anything we do in our field that really matters if we start in 2 weeks or 4 weeks.
 
I’m not sure I believe there’s nearly anything we do in our field that really matters if we start in 2 weeks or 4 weeks.
Outside of maybe starting treatment on an aggressive lymphoma or AML, I 100% agree with this. Now if only we could get literally every other person in the world onboard, that would be great.
 
Young (50s) lady with metastatic pancreatic cancer got 4 cycles of mFOLFIRINOX (basically no bolus 5FU) and now with disease progression including peritoneal carcinomatosis. Having abdominal pain now but still motivated and wants more treatment. Nothing on original NGS and nothing on genetics. Would you just go for gem/abraxane or is there a more aggressive regimen you have found to be particularly beneficial in this type of aggressive disease?
 
Gem/abraxane is what I've seen used regularly if nothing targetable.
 
Young (50s) lady with metastatic pancreatic cancer got 4 cycles of mFOLFIRINOX (basically no bolus 5FU) and now with disease progression including peritoneal carcinomatosis. Having abdominal pain now but still motivated and wants more treatment. Nothing on original NGS and nothing on genetics. Would you just go for gem/abraxane or is there a more aggressive regimen you have found to be particularly beneficial in this type of aggressive disease?
I would just do gem/abraxane in the absence of high PD-L1, high TMB or MMRd.
 
I would just do gem/abraxane in the absence of high PD-L1, high TMB or MMRd.
I agree with the above two, doesn’t seem like we have much other than FOLFIRINOX and Gem/Abraxane in this crappy disease

While we’re on the subject of Pancreatic, I’m curious your thoughts (or maybe a rant) on NALIRIFOX or alternating Gem/Abraxane and FOLFOX
 
I agree with the above two, doesn’t seem like we have much other than FOLFIRINOX and Gem/Abraxane in this crappy disease

While we’re on the subject of Pancreatic, I’m curious your thoughts (or maybe a rant) on NALIRIFOX or alternating Gem/Abraxane and FOLFOX
Pretty sure I've ranted about NalIRIFOX here before, but to paraphrase myself "more toxic, more expensive and no more effective? What's not to love?".
 
Is there a KRAS? There are a TON of new trials open for KRAS inhibitors in pancreatic and between you and me, I've seen some pretty wild responses to those (wild by pancreatic standards)
 
Not exactly a "clinical case" but just a "JFC, can my people get a break around here" kind of venting post. I've been out of the office for a week (was supposed to be on vacation in Florida but instead I've been home nursing a dog dying of sarcoma...but that's a different issue). I have 2 days in clinic this week. They're not even all that busy. But in them I have:
- 81M with b/l hydronephrosis, one kidney that doesn't even appear to work anymore, diffuse FDG uptake throughout the chest and a bronch scheduled in 3 weeks...he came in with 5 family members all rarin' to go about what I'm gonna do about all of this (situation defused, should get a bronch next week but still exhausting)
- 49F has had 2 IIIC melanomas resected and treated with adjuvant IO in the past 5 years. CT yesterday shows new liver mets. Oh...and her kid works in my clinic
- 59M with GERD like sxs for ~6 mos finally gets a CT scan and has numerous retroperitoneal and splenic masses. Fortunately, it's just garden variety DLBCL...he'll be OK
- Two different 70 year old guys with Stage II-III esophageal cancer who got FLOT x4 per ESOPEC (sailed through chemo). One developed bony mets (biopsy proven) on treatment. The other was found to have aortic invasion at the time of (aborted) surgery.
- 69M who got a directed/living donor kidney transplant last month, found to have widely metastatic pancreatic cancer on a CT scan done POD10 for a wound dehiscence. And just for fun, his graft hasn't picked up function so he's back on dialysis and his creatinine and bilirubin are vying for "worst prognostic factor" (both >3 on Monday).
 
Is there a KRAS? There are a TON of new trials open for KRAS inhibitors in pancreatic and between you and me, I've seen some pretty wild responses to those (wild by pancreatic standards)
For mutations other than G12C? Because I have yet to see a G12C in a GI cancer. G12Ds and G12Vs for days though.
 
For mutations other than G12C? Because I have yet to see a G12C in a GI cancer. G12Ds and G12Vs for days though.
Yup exactly! Not Sotorasib but new ones specifically for G12Ds and G12Vs
 
Not exactly a "clinical case" but just a "JFC, can my people get a break around here" kind of venting post.
Holy moly that sounds like a really rough clinic panel. Not rough from a workload perspective but emotionally rough. Geez. Never really gets easier does it? I'd probably be a puddle of tears in a dark corner if I saw those cases back to back

- 49F has had 2 IIIC melanomas resected and treated with adjuvant IO in the past 5 years. CT yesterday shows new liver mets. Oh...and her kid works in my clinic
Oh my gosh this is so sad. Hopefully there's an escape hatch with a BRAF or a c-KIT mutation but it sounds like her best bet is TIL therapy with some sort of a bridge like Opdualag or Ipi/Nivo. Oh man the young ones really get to me; I'm not very good at detaching myself emotionally from these sorts of cases and the scary thing is I'm not sure if I ever will be. Just gotta figure out how to not let it bleed into home life.
 
Yup exactly! Not Sotorasib but new ones specifically for G12Ds and G12Vs
Fingers crossed. I have seen and worked on so many negative met panc trials over the past 10 years (even helped write an IIT) that I have a hard time getting my hopes up.
 
Holy moly that sounds like a really rough clinic panel. Not rough from a workload perspective but emotionally rough. Geez. Never really gets easier does it? I'd probably be a puddle of tears in a dark corner if I saw those cases back to back
Fortunately, they're evenly split. I saw 3 of them yesterday and the rest are today.
Oh my gosh this is so sad. Hopefully there's an escape hatch with a BRAF or a c-KIT mutation but it sounds like her best bet is TIL therapy with some sort of a bridge like Opdualag or Ipi/Nivo. Oh man the young ones really get to me; I'm not very good at detaching myself emotionally from these sorts of cases and the scary thing is I'm not sure if I ever will be. Just gotta figure out how to not let it bleed into home life.
Repeat PET and biopsy are cooking. She had a BRAF mutation initially but didn't tolerate targeted therapy (before my time with her so I'm still willing to go back to the well). Really hoping for a c-kit or NTRK but I've not seen a single one of those in the past 12 years so I'm not going to hold my breath. Plan for now is ipi/nivo --> TIL...already alerted the melanoma team at the mothership.
 
Not exactly a "clinical case" but just a "JFC, can my people get a break around here" kind of venting post. I've been out of the office for a week (was supposed to be on vacation in Florida but instead I've been home nursing a dog dying of sarcoma...but that's a different issue). I have 2 days in clinic this week. They're not even all that busy. But in them I have:
- 81M with b/l hydronephrosis, one kidney that doesn't even appear to work anymore, diffuse FDG uptake throughout the chest and a bronch scheduled in 3 weeks...he came in with 5 family members all rarin' to go about what I'm gonna do about all of this (situation defused, should get a bronch next week but still exhausting)
- 49F has had 2 IIIC melanomas resected and treated with adjuvant IO in the past 5 years. CT yesterday shows new liver mets. Oh...and her kid works in my clinic
- 59M with GERD like sxs for ~6 mos finally gets a CT scan and has numerous retroperitoneal and splenic masses. Fortunately, it's just garden variety DLBCL...he'll be OK
- Two different 70 year old guys with Stage II-III esophageal cancer who got FLOT x4 per ESOPEC (sailed through chemo). One developed bony mets (biopsy proven) on treatment. The other was found to have aortic invasion at the time of (aborted) surgery.
- 69M who got a directed/living donor kidney transplant last month, found to have widely metastatic pancreatic cancer on a CT scan done POD10 for a wound dehiscence. And just for fun, his graft hasn't picked up function so he's back on dialysis and his creatinine and bilirubin are vying for "worst prognostic factor" (both >3 on Monday).
Forgot the 50F with met leiomyosarcoma in liver, lungs and bones.
 
Hey - another fellow question. Question about oligometastatic prostate cancer recurrence.

80 year old with prostate cancer diagnosed in 2020. High-risk by criteria. Received ADT for at least 2 years + prostate RT in 2021. Now with rising PSA and PSMA PET shows two single sites of osseous disease, nothing in the prostate.

The way I'm thinking of this is as a low-volume mCSPC. Based on that, ADT + a novel hormonal agent is indicated - and then you can add RT to the prostate again based on data showing that low-volume CSPC benefits from prostate RT.

This is my first oligometastatic prostate cancer recurrence after SBRT, so my main question is, assuming the above answer is correct, what alternative approaches would be considered appropriate?
1) Could you do just ADT + SBRT to the osseous mets?
2) If theoretically someone has a single osseous met recurrence, can you do SBRT alone and call it a day if the PSA decreases?

Thank you
 
81M CKD newly diagnosed multiple myeloma (high risk from gain 1q). Transplant ineligible. I would like to use Dara CyBorD rather than CyBorD alone. Has anyone had success with insurance authorization for this quadruplet? Closest paper I can find to support the quadruplet use in this population is from the Lyra study
 
Hey - another fellow question. Question about oligometastatic prostate cancer recurrence.

80 year old with prostate cancer diagnosed in 2020. High-risk by criteria. Received ADT for at least 2 years + prostate RT in 2021. Now with rising PSA and PSMA PET shows two single sites of osseous disease, nothing in the prostate.

The way I'm thinking of this is as a low-volume mCSPC. Based on that, ADT + a novel hormonal agent is indicated - and then you can add RT to the prostate again based on data showing that low-volume CSPC benefits from prostate RT.
These are my favorite kinds of cases, because you almost can't do anything wrong. The above is the board answer to this question. And for the right patients, definitely the way to go.
This is my first oligometastatic prostate cancer recurrence after SBRT, so my main question is, assuming the above answer is correct, what alternative approaches would be considered appropriate?
1) Could you do just ADT + SBRT to the osseous mets?
Absolutely! This is often my approach in older people with comorbidities or who want a minimalist approach. SBRT+ADT, watch the PSA and if it starts to rise, repeat PSMA-PET and assuming more than solitary, radiatiable (not a real word, but you know what I mean), disease, add novel hormonal agent then.
2) If theoretically someone has a single osseous met recurrence, can you do SBRT alone and call it a day if the PSA decreases?
Yes you can! I love this idea because it "keeps your powder dry". You don't burn any bridges, you have minimal AEs and you save ADT, all your novel agents AND chemo for when you need them. It might be 6 months or it might be 6 years. And for an 80y old, you may never need any of them.
 
81M CKD newly diagnosed multiple myeloma (high risk from gain 1q). Transplant ineligible. I would like to use Dara CyBorD rather than CyBorD alone. Has anyone had success with insurance authorization for this quadruplet? Closest paper I can find to support the quadruplet use in this population is from the Lyra study
I have. Typically I get these folks after they've started CyBorD as inpatients at time of diagnosis. I usually add dara at that point and have never gotten pushback (N=4 in the last year).
 
81M CKD newly diagnosed multiple myeloma (high risk from gain 1q). Transplant ineligible. I would like to use Dara CyBorD rather than CyBorD alone. Has anyone had success with insurance authorization for this quadruplet? Closest paper I can find to support the quadruplet use in this population is from the Lyra study
I'd be surprised if Dara-CyBorD got rejected by insurance. It is a regimen listed in NCCN as "useful in certain circumstances" and this certainly seems to fall under a circumstance where it would be useful!
 
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