clinical cases

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redeyelopez

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10+ Year Member
Hi All,

I am an oncology attending primarily seeing lung, head and neck, and GI cases.

Is there a place on StudentDoc to discuss clinical cases with other oncology attendings?

I am wondering, for metastatic colon cancer cases, do many omit the 5FU bolus? I have seen some colleagues do this and am curious about the evidence. Many thanks for any suggestions.
 
We can certainly discuss them here.

As for met colon and 5FU bolus, it's where I first turn to manage toxicity, particularly myelosuppression. There's surprisingly little (AKA no) prospective data on it's impact on efficacy, but a brand new (like, last week) registry study of >11K met CRC patients showed no impact on mOS but decreased cytopenias with bolus omission.
pubmed.ncbi.nlm.nih.gov

Omission of 5-Fluorouracil Bolus From Multidrug Regimens for Advanced Gastrointestinal Cancers: A Multicenter Cohort Study - PubMed

After adjusting for baseline clinical factors, we found that omission of the 5-FU bolus from FOLFOX, FOLFIRI, and FOLFIRINOX regimens was not associated with decreased survival, but resulted in decreased toxicity and possible health care savings.
pubmed.ncbi.nlm.nih.gov pubmed.ncbi.nlm.nih.gov

In frail patients I will omit it from day 1 for metastatic disease but otherwise I try to use it. This study might actually change my practice a bit.
 
ShuperNewbie said:
Wait this is an amazing thread. Can we have this be a "young attendings ask the old guard general questions about how they'd handle certain situations" thread? I'm sure I'll be using this a lot lolol
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Use it however you want to.

Hell, some of us geezers GenXers might even throw a question or two out there.
 
I have a case: 70F (ecog 0, but has uncontrolled T2DM) with borderline resectable pancreatic adenocx. Surgeon wants Neoadj chemo. I was thinking mFOLFIRINOX with 5FU at 1800 mg/m2, oxaliplatin 65 mg/m2 and irinotecan at 120 mg/m2. Basically a 25% dose reduction overall. Hoping she can tolerate for 6-8 cycles before restaging scans. Thoughts?
 
osprey099 said:
I have a case: 70F (ecog 0, but has uncontrolled T2DM) with borderline resectable pancreatic adenocx. Surgeon wants Neoadj chemo. I was thinking mFOLFIRINOX with 5FU at 1800 mg/m2, oxaliplatin 65 mg/m2 and irinotecan at 120 mg/m2. Basically a 25% dose reduction overall. Hoping she can tolerate for 6-8 cycles before restaging scans. Thoughts?
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Would be interested in seeing people's answers to this, as the question of how/when to dose reduce based on age seems to be one of the more subjective areas in oncology.

Also, just a fellow, but I've seen a lot of PDAC, and my attendings image after 4 cycles/8 weeks of neoadjuvant therapy for PDAC.
 
osprey099 said:
I have a case: 70F (ecog 0, but has uncontrolled T2DM) with borderline resectable pancreatic adenocx. Surgeon wants Neoadj chemo. I was thinking mFOLFIRINOX with 5FU at 1800 mg/m2, oxaliplatin 65 mg/m2 and irinotecan at 120 mg/m2. Basically a 25% dose reduction overall. Hoping she can tolerate for 6-8 cycles before restaging scans. Thoughts?
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As you know, the data for neoadjuvant chemo for BRPDAC (or even resectable) are all over the map and there's no solid data to support it...that said, we all do it. There are 15-20 active, ongoing studies looking at this but in my experience, they are hard to recruit to because everybody already has it in their head that neoadjuvant is the right answer.

There's no right answer here. You could start with a dose reduction and escalate as tolerated, or start with full-dose and reduce as needed. The advantage to the former is that you're less likely to kill them early on. Advantage to the latter is that it's the book answer. IMO, dose reductions in the 20-25% range are unlikely to reduce efficacy in any meaningful way but of course there's no data on this so you can do whatever you want.
ONC2023 said:
Would be interested in seeing people's answers to this, as the question of how/when to dose reduce based on age seems to be one of the more subjective areas in oncology.

Also, just a fellow, but I've seen a lot of PDAC, and my attendings image after 4 cycles/8 weeks of neoadjuvant therapy for PDAC.
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This is a "style point" unless on a clinical trial. I've treated a lot of pancreatic cancer in my career, and the reality is that radiographic changes on standard imaging (3-phase CT) are usually pretty minimal, even after 6 months of treatment and in cases who have gone on to have surgery and found to have a pCR. Research into imaging biomarkers is ongoing, but again, outside of a trial, the imaging timeline is whatever the treating physician decides it should be.

For me, the only reason I image earlier than 12 weeks (off study) is treatment intolerance, the surgeon demands it (in which case I tell them to order it) or clinical concerns for disease progression. There's nothing wrong (other than unnecessary overutilization of healthcare resources) with doing it at 8 weeks. But don't pretend there's some magic in it.
 
There's an ongoing trial right now looking at alternating FOLFOX / FOLFIRI in the neoadjuvant setting for less fit / ECOG 1+ elderly patients that this person would be great for, but the jury's out on that one
 
35M ecog 0, Gallbladder adenocarcinoma on partial cholecystectomy. Surgeon wants neoadjuvant chemo prior to more extensive complete cholecystectomy with lymph node dissection. I know there's no standard neoadjuvant tx for gallbladder cx but what have folks here used/found to be successful in your experience?

I'm thinking just doing the topaz1 regimen with cis/gem/durva. Scan/discuss with surgeon after 4 rounds and see where we stand. Also gonna get NGS on the tissue. Thoughts?
 
osprey099 said:
35M ecog 0, Gallbladder adenocarcinoma on partial cholecystectomy. Surgeon wants neoadjuvant chemo prior to more extensive complete cholecystectomy with lymph node dissection. I know there's no standard neoadjuvant tx for gallbladder cx but what have folks here used/found to be successful in your experience?

I'm thinking just doing the topaz1 regimen with cis/gem/durva. Scan/discuss with surgeon after 4 rounds and see where we stand. Also gonna get NGS on the tissue. Thoughts?
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The EA2197 - OPT-IN trial is currently investing this exact scenario. Patients are randomized to perioperative chemo vs surgery alone.

I don't think you're going to get durva approved here and there's no evidence for it anyway. I'd just use Gem/Cis off study.
 
Interesting. Curious why the surgeon wants neoadjuvant. If it was incidentally found on resection, the purpose of further surgery is full staging that neoadjuvant would confound, right? And then if it meets criteria, adjuvant capecitabine based on BILCAP.
 
ONC2023 said:
Interesting. Curious why the surgeon wants neoadjuvant. If it was incidentally found on resection, the purpose of further surgery is full staging that neoadjuvant would confound, right? And then if it meets criteria, adjuvant capecitabine based on BILCAP.
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My thoughts exactly on this one. Maybe it's just my lack of experience but it sounds like neoadjuvant would just delay surgery here and with a young patient like that, why play games? I guess it depends on how deep her tumor penetrated.
 
ONC2023 said:
Interesting. Curious why the surgeon wants neoadjuvant. If it was incidentally found on resection, the purpose of further surgery is full staging that neoadjuvant would confound, right? And then if it meets criteria, adjuvant capecitabine based on BILCAP.
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Surgeon believes tumor currently extends beyond resectable area. Was discussed in tumor board and consensus was for some sort of neoadjuvant therapy. Also patient has current infection around gallbladder, likely delaying things more
 
Oh I see. If you frame it as tumor unresectable/locally advanced, maybe that will give you better shot with insurance approving TOPAZ regimen rather than calling it neoadjuvant. That’s a trick I’ve seen attendings do

In the words of one attending, “All tumors are locally advanced.”

If you get great response, great - go to surgery. If not, continue TOPAZ until progression.
 
Neoadjuvant therapy is moving to standard of care for a lot of GI tumors, but we’re still not there yet in terms of the data, as you can see from the above discussion of pancreatic cancer. It doesn’t help that the design of some of these studies is stupid and it makes it hard to accrue.

I am a proponent of neoadjuvant therapy as it hasn’t been shown n any scenario I’m aware of to be detrimental and in many cases better than adjuvant. I would personally have no issue giving Gem/Cis in this setting but would prefer to do it on study if available.
 
For PSA recurrence after radical prostatectomy with no radiologic evidence of disease, how do you approach it?

My understanding for M0 CSPC:

First, ADT + salvage RT
And then, if PSA doesn't become undetectable, you treat it as M0 CRPC
--- so if the doubling time is < 10 months, apalutamide, darolutamide, or enzalutamide
--- if doubling time > 10 months, observe
 
ONC2023 said:
For PSA recurrence after radical prostatectomy with no radiologic evidence of disease, how do you approach it?

My understanding for M0 CSPC:

First, ADT + salvage RT
And then, if PSA doesn't become undetectable, you treat it as M0 CRPC
--- so if the doubling time is < 10 months, apalutamide, darolutamide, or enzalutamide
--- if doubling time > 10 months, observe
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This is another area of active investigation with a lot of good answers but no "right" answer (IMO).

My general approach in these situations is PSMA-PET (Or Axumin-PET, more on that in a second) and if negative and the patient is relatively fit and motivated, 3 months of ADT --> prostate bed XRT --> 3 more months of ADT, then monitor. I've seen people go forever on ADT or up to 2 years, but in general, if they get to undetectable at 6 months, I'll give them a break and do intermittent ADT.

If they're asymptomatic though, or not particularly fit, or don't want ADT or , then observation isn't unreasonable. You can also do XRT alone or ADT alone, recognizing that both are inferior to combined therapy but that may not be relevant in an 87yo vasculopath with cirrhosis.

What to do after this approach when you don't get a complete PSA response is also variable. Some people give an ASRI, some people use abi/pred, some just ride it out and see what happens.

I think the key in managing these cases is to find out what's most important to the patient in terms of QOL, PSA, treatment intensity, etc and tailor your treatment that way.

The PET tracer issue is getting complicated in prostate cancer (and other cancer types as well). There is data in the nuc med literature that PSMA is more sensitive for distant mets and Axumin more sensitive for prostate bed recurrence. I honestly don't know what to do with this in the real world, other than spend too much money on scans.
 
gutonc said:
This is another area of active investigation with a lot of good answers but no "right" answer (IMO).

My general approach in these situations is PSMA-PET (Or Axumin-PET, more on that in a second) and if negative and the patient is relatively fit and motivated, 3 months of ADT --> prostate bed XRT --> 3 more months of ADT, then monitor. I've seen people go forever on ADT or up to 2 years, but in general, if they get to undetectable at 6 months, I'll give them a break and do intermittent ADT.

If they're asymptomatic though, or not particularly fit, or don't want ADT or , then observation isn't unreasonable. You can also do XRT alone or ADT alone, recognizing that both are inferior to combined therapy but that may not be relevant in an 87yo vasculopath with cirrhosis.

What to do after this approach when you don't get a complete PSA response is also variable. Some people give an ASRI, some people use abi/pred, some just ride it out and see what happens.

I think the key in managing these cases is to find out what's most important to the patient in terms of QOL, PSA, treatment intensity, etc and tailor your treatment that way.

The PET tracer issue is getting complicated in prostate cancer (and other cancer types as well). There is data in the nuc med literature that PSMA is more sensitive for distant mets and Axumin more sensitive for prostate bed recurrence. I honestly don't know what to do with this in the real world, other than spend too much money on scans.
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What do you like to do when the PSMA is + but the PSA is like, 4? I struggle with whether to offer these patients intermittent ADT vs continuous tx, *especially* if they have prior had conventional CT scans that were NED
 
HemeOncHopeful19 said:
What do you like to do when the PSMA is + but the PSA is like, 4? I struggle with whether to offer these patients intermittent ADT vs continuous tx, *especially* if they have prior had conventional CT scans that were NED
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I'm a "QOL over all" oncologist when it comes to metastatic disease. So in this case I'd go with whatever the patient wanted. For my 80+ guys, intermittent ADT. For the "young" ones, maybe continuous and add and ARSI.

Again...you can't really go wrong here. Take into account what the patient wants and try not to just treat scans and numbers. No PET scanner or chemistry analyzer has ever experienced profound fatigue from iatrogenic hypogonadism, but lots of men do.
 
HemeOncHopeful19 said:
What do you like to do when the PSMA is + but the PSA is like, 4? I struggle with whether to offer these patients intermittent ADT vs continuous tx, *especially* if they have prior had conventional CT scans that were NED
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Ah yes the question of stage migration. Yeah people are really struggling what to do in this situation. Obviously Gutonc's answer is more than reasonable and I think almost everyone would agree with that approach. One of my GU attendings made the great point that if a patient like this were in STAMPEDE, they'd be treated as M0 biochemically recurrent with ADT + ARAT if the doubling time were 9m or less (+/- RT if salvage to the prostate bed were offered). That said it'd be tough NOT to offer oligometastatic RT if they have a single spot in the axial skeleton on PSMA PET esp if the patient is younger. I think it's a data gray zone but I think we'll have a better answer to this situation soon since it's a hot topic at conferences and stuff.
 
For all of you heme inclined folks, when you salvage DLBCL with R-GVP, when do you use cisplatin vs carboplatin? Is there any evidence to show a difference in efficacy? (I know this exists for bladder and H&N, but I'm unfamiliar with any evidence in the DLBCL literature, which I'm sure exists somewhere)
 
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Thoracic case:
Stage IIIA lung adeno non-op for patient comorbidities. PDL1 0%, STK11 mutation on NGS. Got carbo/taxol/radiation. Question about consolidation durva? I have typically not been giving it for PDL1 0% and probably would lean further away with the STK11 mutation. Any thoughts from the group?
 
soccerusa said:
Thoracic case:
Stage IIIA lung adeno non-op for patient comorbidities. PDL1 0%, STK11 mutation on NGS. Got carbo/taxol/radiation. Question about consolidation durva? I have typically not been giving it for PDL1 0% and probably would lean further away with the STK11 mutation. Any thoughts from the group?
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I don't care about the PDL1 level but the STK11 mutation suggests lack of response so I probably wouldn't bother. Just pretend it's 2015 and monitor.
 
ShuperNewbie said:
For all of you heme inclined folks, when you salvage DLBCL with R-GVP, when do you use cisplatin vs carboplatin? Is there any evidence to show a difference in efficacy? (I know this exists for bladder and H&N, but I'm unfamiliar with any evidence in the DLBCL literature, which I'm sure exists somewhere)
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Why GVP over ICE, GemOx, etc? No real need to use cisplatin in this setting.
 
ShuperNewbie said:
For all of you heme inclined folks, when you salvage DLBCL with R-GVP, when do you use cisplatin vs carboplatin? Is there any evidence to show a difference in efficacy? (I know this exists for bladder and H&N, but I'm unfamiliar with any evidence in the DLBCL literature, which I'm sure exists somewhere)
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My institutions always used R-ICE for whatever reason (probably habit, I don’t get the hype with inpatient admits) which has Carbo in it.
 
ShuperNewbie said:
Honestly, no real reason. I've always thought of GDP as slightly less toxic but slightly less effective than ICE but this might be more in my mind than in actual reality
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If this is their first relapse, they should move to BEAM auto if they are at least in PR.

GemOx is even milder and still effective. Don't need full efficacy at the expense of toxicity if auto is to follow
 
Had a young patient 55M no significant PMH metastatic pancreatic cancer originating in uncinate process. No obstruction on presentation and never had ERCP, only liver biopsy confirming metastatic cx. Gave one cycle of FOLFIRINOX and he almost died with bili >12 and alk phos 3000. Still hospitalized but did get ERCP and there is significant tumor obstruction, unable to be stented. His numbers are downtrending now but would you keep him on FOLFIRINOX (I'm omitting 5FU and 25% dose reduction for everything else) or switch to gem/abrax or even single agent gem?

He has nothing on his NGS, MMR-p, and no HRR/BRCA btw.
 
osprey099 said:
Had a young patient 55M no significant PMH metastatic pancreatic cancer originating in uncinate process. No obstruction on presentation and never had ERCP, only liver biopsy confirming metastatic cx. Gave one cycle of FOLFIRINOX and he almost died with bili >12 and alk phos 3000. Still hospitalized but did get ERCP and there is significant tumor obstruction, unable to be stented. His numbers are downtrending now but would you keep him on FOLFIRINOX (I'm omitting 5FU and 25% dose reduction for everything else) or switch to gem/abrax or even single agent gem?

He has nothing on his NGS, MMR-p, and no HRR/BRCA btw.
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I wouldn't do anything until his obstruction was relieved. Can he get a PTC?

Oxali and maybe Gem are the only two drugs I'd feel comfortable giving with a bili over 4. 5FU and abraxane aren't recommended and irinotecan is contraindicated. I wouldn't personally bother giving single agent Gem, but it's not the wrong answer, it just doesn't really do much.

These cases really suck.
 
gutonc said:
I wouldn't do anything until his obstruction was relieved. Can he get a PTC?

Oxali and maybe Gem are the only two drugs I'd feel comfortable giving with a bili over 4. 5FU and abraxane aren't recommended and irinotecan is contraindicated. I wouldn't personally bother giving single agent Gem, but it's not the wrong answer, it just doesn't really do much.

These cases really suck.
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He has a PTC and bili at discharge was down to 6. I won't give him anything unless bili <3. Just wondering if going for another mFOLFIRINOX with dose reduction is worth the risk. I hate pancreatic cancer
 
osprey099 said:
He has a PTC and bili at discharge was down to 6. I won't give him anything unless bili <3. Just wondering if going for another mFOLFIRINOX with dose reduction is worth the risk. I hate pancreatic cancer
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Oh yeah, in that case, with his biliary tract decompressed, in a young, otherwise fit person I'd go for mFOLFIRINOX. I never use the FU bolus with FOLFIRINOX, just way too toxic. And definitely worth easing back into it with a dose reduction.
 
The more pancreatic cancer I see, the more my mortal fear of pancreatic cancer is stoked. Ooof I feel so sorry for this dude. Hopefully those novel KRAS inhibitors / degraders prove effective
 
Question: 56 m met crc, left primary in sity , 2 liver and bilateral small lung mets . kras wt braf wt msi-stable. 9 x folfox avastin with pr.

Do most of you drop oxaliplatin at this time? He is not having major toxicity but I am not sure of the additonal benfit of continuing .

I would appreicate your thoughts many thanks
 
redeyelopez said:
Question: 56 m met crc, left primary in sity , 2 liver and bilateral small lung mets . kras wt braf wt msi-stable. 9 x folfox avastin with pr.

Do most of you drop oxaliplatin at this time? He is not having major toxicity but I am not sure of the additonal benfit of continuing .

I would appreicate your thoughts many thanks
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I usually drop oxaliplatin after 6 months, or if neuropathy is G2. Just curious, if left sided and kras/braf WT, why not FOLFOX panitumumab instead of FOLFOX bev?
 
redeyelopez said:
Question: 56 m met crc, left primary in sity , 2 liver and bilateral small lung mets . kras wt braf wt msi-stable. 9 x folfox avastin with pr.

Do most of you drop oxaliplatin at this time? He is not having major toxicity but I am not sure of the additonal benfit of continuing .

I would appreicate your thoughts many thanks
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I go 12 cycles as tolerated and then drop to 5FU/Bev, Cape/Bev or a treatment holiday if they've had a great response.

I also know people who will just dose reduce oxaliplatin 10% at a time once toxicity starts until they titrate it off. I think that's stupid once you get below 50%, but it's not "wrong" per se.
 
osprey099 said:
I usually drop oxaliplatin after 6 months, or if neuropathy is G2. Just curious, if left sided and kras/braf WT, why not FOLFOX panitumumab instead of FOLFOX bev?
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Thanks ,yes I think a fair point-I thought that myelf. Another Doctor was looking after this patient and moved recently so I have just taken him over this week. As he was already started on the avastin -I wonder it it worth switching at this stage?
 
redeyelopez said:
Thanks ,yes I think a fair point-I thought that myelf. Another Doctor was looking after this patient and moved recently so I have just taken him over this week. As he was already started on the avastin -I wonder it it worth switching at this stage?
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I wouldn't. You're getting a good response. Stick with it. Save EGFR directed therapy for when you need it. Yes, it should have gone first, but that horse is out of the barn already.
 
redeyelopez said:
Thanks ,yes I think a fair point-I thought that myelf. Another Doctor was looking after this patient and moved recently so I have just taken him over this week. As he was already started on the avastin -I wonder it it worth switching at this stage?
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On progression, would try FOLFIRI panitumumab
 
osprey099 said:
I usually drop oxaliplatin after 6 months, or if neuropathy is G2. Just curious, if left sided and kras/braf WT, why not FOLFOX panitumumab instead of FOLFOX bev?
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I usually stop FOLFOX BEV after 6 - 8 cycles and transition to maintenance therapy. The risk of neuropathy is too high as a quality of life factor here. Remember there is a coasting phenomenon and neuropathy will worsen for up to 2 months from stopping Oxaliplatin. The benefit of first line EGFR is mostly bulky/extensive disease for response and left side hyperselected patients by liquid biopsy (if you can get it, thought provoking - https://dailynews.ascopubs.org/do/p...gene-alterations-metastatic-colorectal-cancer) or fit patients who do not mind rash (don’t forget doxy prophylaxis).

Also as above, do not use the 5-FU bolus in the metastatic setting for FOLFOX, FOLFIRI, FOLFIRINOX/FOLFOXIRI (Omission of 5-Fluorouracil Bolus From Multidrug Regimens for Advanced Gastrointestinal Cancers: A Multicenter Cohort Study) #banthebolus
 
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osprey099 said:
He has a PTC and bili at discharge was down to 6. I won't give him anything unless bili <3. Just wondering if going for another mFOLFIRINOX with dose reduction is worth the risk. I hate pancreatic cancer
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We have used FOLFOX with bilirubin as high as 5+ in appropriate circumstances with fit patient (it can be done, one of many case series, Chemotherapy in the Setting of Severe Liver Dysfunction in Patients with Metastatic Colorectal Cancer). It's best to use it in this circumstance if as above when you have adequate biliary drainage and it is already dropping and then we add Irinotecan on to make it FOLFIRINOX once it is safely below 1.5. We also check DPYD + UGT1A1 for patients, germline, NGS. Don't forget to cut the 5-FU bolus.
 
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