clinical cases

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Basic staging question: For localized clear cell renal cancer initial staging, do you all have a preference on CTAP versus MRI?

NCCN guidelines leave it up to the provider - I think MRI would be more helpful for assessing venous invasion into the renal vein, which might be helpful for surgical planning (?) but doesn’t actually change the plan I think.
Ask your urologist what they want (that’s what I do)
 
Basic staging question: For localized clear cell renal cancer initial staging, do you all have a preference on CTAP versus MRI?

NCCN guidelines leave it up to the provider - I think MRI would be more helpful for assessing venous invasion into the renal vein, which might be helpful for surgical planning (?) but doesn’t actually change the plan I think.
Whenever I have the choice between CT and MRI, I always choose the CT. Would a good MRI be "better"? Probably. Are they going to actually get a good MRI? Probably not. The good enough cheap and easy test is always preferable to the crap quality "right" test. And most MRIs of the abdomen are crap quality because people either can't, or won't follow directions about breath holding and not moving.
 
@gutonc Thank you for sharing this. It's a bizarre PET/CT. I was off the mark then, as I was thinking along the lines of small cell carcinoma or, second best, high-grade lymphoma.
 
@HemeOncHopeful19
Why don’t you tell us what you think it is? What’s wrong with asking that? What’s your point?
You seem like a rather malignant fella.
I disliked your post because I dislike small round and blue tumors, which historically I haven’t seen turn out well for patients, chill lol
 
@gutonc Thank you for sharing this. It's a bizarre PET/CT. I was off the mark then, as I was thinking along the lines of small cell carcinoma or, second best, high-grade lymphoma.
It was in fact a high grade lymphoma. I was expecting a sarcoma or a melanoma.
 
So you admitted him for cycle 1 promptly? What’s your approach to initiating tx in this type of clinical scenario?
I recently had a pt with similar demographics and presentation, walked into clinic with only mild to moderate pain symptoms and normal labs (maybe slight AKI). Unlike this case, radiology strongly suggested lymphoma unless proven otherwise. Unfortunately, he decompensated quickly and passed while awaiting biopsy results, with suspected multifactorial organ failure from spontaneous TLS, possibly also infection.
 
So you admitted him for cycle 1 promptly? What’s your approach to initiating tx in this type of clinical scenario?
I recently had a pt with similar demographics and presentation, walked into clinic with only mild to moderate pain symptoms and normal labs (maybe slight AKI). Unlike this case, radiology strongly suggested lymphoma unless proven otherwise. Unfortunately, he decompensated quickly and passed while awaiting biopsy results, with suspected multifactorial organ failure from spontaneous TLS, possibly also infection.
No, because I can't do inpatient chemo where I am, and he'd already left semi-AMA from the mothership hospital immediately after his biopsy was performed.

He has no end-organ damage and no evidence of TLS. He's getting an echo on Monday, port on Tuesday and R-CHOP on Wednesday. I suspect FISH and NGS will come back in a week or so and I'll know if he needs to transition to Pola-R-CHP or DA-R-EPOCH.
 
Two possibly simple cases but wanted to make sure I wasn’t totally off track.

1) 70 year old with prostate cancer diagnosed 2016. Had RT to prostate at time of diagnosis and to an oligo bone met 3 years ago. He’s been on ADT since diagnosis and kind of strangely, apalutamide for several years now - a drug which is not approved for metastatic CRPC. He had a recent PET that showed lung lesions and a new bone met, so urology now sending to med onc.

Would you consider this failure of novel hormonal agent and go to a taxane or would you say that he’s never been appropriately treated with the right novel hormonal agent and switch to enzalutamide or abiraterone? My instinct is that either a taxane or another hormonal agent are appropriate (especially if he wants to avoid chemo).

2) A 70 year old with new pancytopenia, no PMH and no strange meds. WBC 2, ANC > 1, HgB 10, platelets 90. No constitutional symptoms. I’m going to do the usual workup (nutrition, etc) - but new pancytopenia in an elderly patient is a guaranteed ticket to a bone marrow, right?
 
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Two possibly simple cases but wanted to make sure I wasn’t totally off track.

1) 70 year old with prostate cancer diagnosed 2016. Had RT to prostate at time of diagnosis and to an oligo bone met 3 years ago. He’s been on ADT since diagnosis and kind of strangely, apalutamide for several years now - a drug which is not approved for metastatic CRPC. He had a recent PET that showed lung lesions and a new bone met, so urology now sending to med onc.

Would you consider this failure of novel hormonal agent and go to a taxane or would you say that he’s never been appropriately treated with the right novel hormonal agent and switch to enzalutamide or abiraterone? My instinct is that either a taxane or another hormonal agent are appropriate (especially if he wants to avoid chemo).
I'd probably re-biopsy for NGS and go to Abi/Pred. Docetaxel isn't the wrong answer, and may be the right answer once you see him. I wouldn't do enza or daro at this point
2) A 70 year old with new pancytopenia, no PMH and no strange meds. WBC 2, ANC > 1, HgB 10, platelets 90. No constitutional symptoms. I’m going to do the usual nutrition etc workup - but this is a straight to marrow station, I think. I’m not being overly aggressive by getting a bone marrow during first visit before I even get back the nutritional labs/peripheral smear, right?
Definitely needs a marrow. Whether you do it today or next week is up to you and the patient. You might find that they want to wait until getting the basic lab workup done. But if I had time, I'd offer it same day.
 
Thank you, that’s very helpful. And that makes sense about not going to enza/daro after apalutamide.
 
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2) A 70 year old with new pancytopenia, no PMH and no strange meds. WBC 2, ANC > 1, HgB 10, platelets 90. No constitutional symptoms. I’m going to do the usual workup (nutrition, etc) - but new pancytopenia in an elderly patient is a guaranteed ticket to a bone marrow, right?
I will say I did this once and my marrow results came back as “very consistent with B12 deficiency” 🤦🏼‍♂️ and they were promptly cured. I don’t think you’re wrong to go there immediately though.
 
I will say I did this once and my marrow results came back as “very consistent with B12 deficiency” 🤦🏼‍♂️ and they were promptly cured. I don’t think you’re wrong to go there immediately though.
And honestly, unless somebody has blasts on peripheral flow, this is why I usually ride it out. 95% of the marrows I do either confirm the diagnosis I already had (myeloma, lymphoma) or don't provide me any useful information at all ("moderately hypocellular marrow for age, no overt dysplasia or blasts, could be early MDS, vitamin deficiency or inflammatory process, clinical correlation recommended").
 
I'd probably re-biopsy for NGS and go to Abi/Pred. Docetaxel isn't the wrong answer, and may be the right answer once you see him. I wouldn't do enza or daro at this point
To check myself since I admittedly see very little GU: If he's clearly progressing on ADT + apalutamide, I would think he's failed ARPi and wouldn't think abi would add much for him, I'd put it in the same bucket as daro/enza. Assuming he's not incredibly symptomatic, that his disease isn't exploding (not sure of the size/extent of the lung lesions), and that there isn't anything on NGS or germline testing, I would lean towards Lu-PSMA-617 (assuming this is PSMA avid disease) since we can give that pre-docetaxel now, but if he's blowing up or just wants to rip the chemo band-aid off then would go docetaxel. Is that off?
 
To check myself since I admittedly see very little GU: If he's clearly progressing on ADT + apalutamide, I would think he's failed ARPi and wouldn't think abi would add much for him, I'd put it in the same bucket as daro/enza. Assuming he's not incredibly symptomatic, that his disease isn't exploding (not sure of the size/extent of the lung lesions), and that there isn't anything on NGS or germline testing, I would lean towards Lu-PSMA-617 (assuming this is PSMA avid disease) since we can give that pre-docetaxel now, but if he's blowing up or just wants to rip the chemo band-aid off then would go docetaxel. Is that off?
My own experience suggests you can get some mileage out of Abi after enza/apa/daro and it's well tolerated. Pluvicto or docetaxel aren't wrong either.

Much of this is down to the patient at this point. Asymptomatic and wants to prioritize QOL and not spending a ton of time in clinic/infusion? Abi/pred. Wants to "do everything"? Docetaxel +/- abi/pred (yes, I know that's first line but you could argue this guy hasn't actually been treated appropriately for first line metastatic disease) or go straight to Pluvicto.
 
Great discussion. I've felt that abi/pred post enza (and I guess extended to this weird case with apalutamide) offers very little based on this ARPI switch paper albeit a small phase II (Optimal sequencing of enzalutamide and abiraterone acetate plus prednisone in metastatic castration-resistant prostate cancer: a multicentre, randomised, open-label, phase 2, crossover trial - PubMed). Germline is often missed so would definitely check thats been done. I feel like a lot of patients want Pluvicto over taxane but I've had a few patients with long lingering cytopenias post pluvicto that make chemo difficult. More recently, I've been suggesting to fit patients to try the taxane first to ensure we aren't limited with the next line of therapy.
 
NSCLC stage IIIA, T2N2, EGFR Exon 20 insertion mutation currently undergoing ChemoRT.

How do people approach consolidation immunotherapy in the setting?

There are some evidence that these uncommon EGFR mutations do better with immunotherapy compared to the common mutations. Though there hasn’t been great evidence of this.
 
NSCLC stage IIIA, T2N2, EGFR Exon 20 insertion mutation currently undergoing ChemoRT.

How do people approach consolidation immunotherapy in the setting?

There are some evidence that these uncommon EGFR mutations do better with immunotherapy compared to the common mutations. Though there hasn’t been great evidence of this.
have you explore data regarding amiv in this setting? if it is other EGFR mutations in this setting, EGFR exon 19 deletion or exon 21 L858R mutation, we can use osi
 
have you explore data regarding amiv in this setting? if it is other EGFR mutations in this setting, EGFR exon 19 deletion or exon 21 L858R mutation, we can use osi
But ami/lazer aren't approved post-chemoRT in stage III disease.

I'd probably use IO in this setting but with the understanding that the benefit is much less than in EGFR WT (but probably more than in Exon 19 or 21 mutations).
 
But ami/lazer aren't approved post-chemoRT in stage III disease.

I'd probably use IO in this setting but with the understanding that the benefit is much less than in EGFR WT (but probably more than in Exon 19 or 21 mutations).
also, in the standard of care setting, there is nothing else you can offer. the PACIFIC trial does include small portion of patients with EGFR mutation.
 
For stage II colon cancer (pMMR, T3N0), would you count small bowel obstruction from an enlarged cecal tumor as a high risk feature that warrants considering adjuvant 5FU? Patient had ememis, but tumor was not truly fully obstructing on scope (very large but not total obstruction) and was having bowel movement. No other high risk features - no LVI, PNI, etc

If ctDNA is negative, I don’t think this would cause me to give single agent 5-FU. If ctDNA positive, probably.

Anyone think about this differently?
 
For stage II colon cancer (pMMR, T3N0), would you count small bowel obstruction from an enlarged cecal tumor as a high risk feature that warrants considering adjuvant 5FU? Patient had ememis, but tumor was not truly fully obstructing on scope (very large but not total obstruction) and was having bowel movement. No other high risk features - no LVI, PNI, etc

If ctDNA is negative, I don’t think this would cause me to give single agent 5-FU. If ctDNA positive, probably.

Anyone think about this differently?
I’m not sure I’d even get a ctDNA on this one. But I understand why you would.

I wouldn’t consider that a high risk tumor. Pre ctDNA days, I would never have given this person chemo. Now with ctDNA, it’s an easier sell if it’s positive, but I’m still not fully convinced of it’s efficacy in this setting.

ETA: If this is a 45yo, I might get the ctDNA and offer if positive. If it's a 70yo with the usual comorbidities (what I used to call "VA healthy" in residency), I don't think I'd even go down that path. I'd call it low-risk Stage II and be done with it unless they asked about ctDNA.
 
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Metastatic colon cancer on 5FU maintenance, has enlarging liver lesions after 5 months of maintenance. Tolerated FOLFOX well. Was going to restart FOLFOX to see if there’s still any benefit remaining but don’t see data doing this in the colon field.

On a similar but different note, do people do maintenance 5FU in metastatic gastric? I’ve had someone on 5FU alone for >1 year now.
 
Metastatic colon cancer on 5FU maintenance, has enlarging liver lesions after 5 months of maintenance. Tolerated FOLFOX well. Was going to restart FOLFOX to see if there’s still any benefit remaining but don’t see data doing this in the colon field.

On a similar but different note, do people do maintenance 5FU in metastatic gastric? I’ve had someone on 5FU alone for >1 year now.
I would probably switch to FOLFIRI + whatever third agent they qualify for if only to avoid the neuropathy but I don’t think FOLFOX is wrong
 
Metastatic colon cancer on 5FU maintenance, has enlarging liver lesions after 5 months of maintenance. Tolerated FOLFOX well. Was going to restart FOLFOX to see if there’s still any benefit remaining but don’t see data doing this in the colon field.
The CAIRO-3 study, which established maintenance Cape as SOC after 6 cycles of CAPOX-Bev in met colon, didn't have a cutoff for how long people had to be on maintenance before going back on CAPOX-B at progression on maintenance. So, extrapolating a bit, FOLFOX+Bev (or Pan if appropriate), isn't the wrong answer. That said, I tend to do switch therapy (FOLFIRI + something) in people who progress in <6 mos of maintenance after FOLFOX/CAPOX. Bottom line, either is fine and will depend on your particular scenario.
On a similar but different note, do people do maintenance 5FU in metastatic gastric? I’ve had someone on 5FU alone for >1 year now.
As with every other non-colorectal GI cancer that uses 5FU in some way, there are no data to support it, but lots of people do it anyway.
 
I will say I did this once and my marrow results came back as “very consistent with B12 deficiency” 🤦🏼‍♂️ and they were promptly cured. I don’t think you’re wrong to go there immediately though.
Welp, coincidentally I can now say I’ve seen this twice!
 
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