clinical cases

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guildsman said:
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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What are you doing with DPYD / UGT1A1 results? I thought there wasn’t really good data to guide dose adjustments but I’d love to find out there’s new info out
 
HemeOncHopeful19 said:
What are you doing with DPYD / UGT1A1 results? I thought there wasn’t really good data to guide dose adjustments but I’d love to find out there’s new info out
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My former institution got sued for a bad DPD mutation outcome and the result of the suit was not actually a monetary settlement, but mandatory DPD/TYMS testing prior to fluoropyrimidine treatment. Pharmacy will no longer release the drug without the test result.

IME, when I have clinical concern for DPD/TYMS I let the toxicity resolve and dose reduce by 50%. I usually send the test then, but even if it comes back negative, I keep the dose reduction.

Outside of a clinical trial (IIRC, the NAPOLI studies required it), I have not, in over a dozen years, tested for UGT1A1.
 
gutonc said:
My former institution got sued for a bad DPD mutation outcome and the result of the suit was not actually a monetary settlement, but mandatory DPD/TYMS testing prior to fluoropyrimidine treatment. Pharmacy will no longer release the drug without the test result.

IME, when I have clinical concern for DPD/TYMS I let the toxicity resolve and dose reduce by 50%. I usually send the test then, but even if it comes back negative, I keep the dose reduction.

Outside of a clinical trial (IIRC, the NAPOLI studies required it), I have not, in over a dozen years, tested for UGT1A1.
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Interesting. What does pharmacy do if patient is DPD deficient? Is there a dose adjustment guideline?

On a separate note… what’s the oldest person you’ve sent for a whipple and did you regret it? Asking for a friend…
 
HemeOncHopeful19 said:
Interesting. What does pharmacy do if patient is DPD deficient? Is there a dose adjustment guideline?
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Probably nothing. I suspect it's like the echo prior to HER2 or anthracyclines, they just want to see it, they don't care what the answer is.

To be fair, I don't actually know since this was still going live when I left. And the pharmacists are just cogs in the same machine and being tasked with dealing with risk management's f*** up. I don't blame them...they've got mortgages to pay too.
HemeOncHopeful19 said:
On a separate note… what’s the oldest person you’ve sent for a whipple and did you regret it? Asking for a friend…
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Early 70s and no. I've regretted sending younger patients though.

But TBH, who gets a Whipple is not up to me. So the regret isn't really on me if things go sideways. I'm fortunate to have access to a number of excellent HPB surgeons in the area. Some I can count on to be thoughtful about choosing who is an appropriate Whipple candidate and who isn't and explain it well. Others I will send people to when I think we need to do some total cowboy s*** and that they'll be honest about the risks and generally get the patient through it. But in the end, I tell people "this is the standard surgical treatment for the cancer you have, Dr. Whipple will talk to you about whether it's the right option for you and you two can decide on the plan".
 
HemeOncHopeful19 said:
Interesting. What does pharmacy do if patient is DPD deficient? Is there a dose adjustment guideline?

On a separate note… what’s the oldest person you’ve sent for a whipple and did you regret it? Asking for a friend…
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We adjust the doses based on similar recommendations to this article, depending on genotype (https://ascopubs.org/doi/10.1200/OP.20.00553).

We have a cohort at our institution of octogenarians who underwent Whipple. The outcomes are complex, average overall survival was 1 - 2 years following surgery. We also participated in the GIANT study (https://ascopubs.org/doi/10.1200/JCO.2024.42.16_suppl.4003) for older adults with metastatic pancreatic cancer who were deemed vulnerable by geriatric assessment and in that group OS is 5 months. I suspect that population makes up the majority of treated older adults with pancreatic cancer (resectable or metastatic).
 
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Since we seem to have at least two GI docs participating, I'll ask what everyone's thoughts are on the ESOPEC data that came out this summer for esophageal adeno. Has it changed local practices for you guys? I have seen plenty of (fair) criticism in the Rad Onc community, curious what people think here.
 
HemeOncHopeful19 said:
Since we seem to have at least two GI docs participating, I'll ask what everyone's thoughts are on the ESOPEC data that came out this summer for esophageal adeno. Has it changed local practices for you guys? I have seen plenty of (fair) criticism in the Rad Onc community, curious what people think here.
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The only real criticism I've seen from Rad Onc is that they used the CROSS radiation dosing which isn't what is used in actual practice, and that's a totally fair critique.

But to answer your question, yes, I think this is practice changing. For anyone that surgery thinks might be an operative candidate, I have been starting with FLOT x4 and then restaging. If surgery remains an option, they go to the OR, if not, for whatever reason, you can transition to definitive chemoRT (whether you use carbo/taxol or Cis/5FU).

This definitely brings up one of the big issues with these treatment de-escalation or alternative trials. If you don't have everyone on board from the beginning, you're definitely going to get pushback from whichever specialty's treatment gets removed from the plan. One of the major reasons that TNT/Watchful Waiting has become a standard in rectal cancer is that it was designed and run, from the beginning, by a colorectal surgeon, and the med and rad oncs were just along for the ride. If you design a trial where you're planning to omit chemo (or radiation) from current SOC treatment, then the med onc (or rad onc) should be the one designing the trial...you need that kind of juice to convince colleagues that it's the right thing to do.

I also think that just because FLOT was "better" than CROSS in this trial, it doesn't make it the automatic right choice for everyone.
 
Actually have seen quite a few "complete pathological response" with FLOT as compared to chemo-rads, this could just be my experience though.
 
MD46 said:
Actually have seen quite a few "complete pathological response" with FLOT as compared to chemo-rads, this could just be my experience though.
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Me too. But IME, I was only using FLOT when I knew they were going to surgery and if it was a toss-up, I was using CROSS --> Surgery if appropriate. Now with the head-to-head data, I feel better starting almost anyone on FLOT and seeing how it goes.
 
Since we’re on the topic of non-metastatic esophageal, does anyone go by CALGB 80803? This study showed increased pathological CR with neoadjuvant induction FOLFOX + chemoRT compared to induction carbo/taxol + chemoRT.

Briefly, the study randomized patients to either FOLFOX or carbo/taxol for 2 cycles, at which point they got a PET. For patients with SUV >= 35% decline from baseline, they continued with the same chemo during RT. For non-responders, they crossed over to the other trial. 40% of PET responders to FOLFOX had pCR whereas only 14% PET responders had pCR to carbo/taxol.


To my fellow eyes, this certainly seems practice changing since pCR is strongly correlated with overall survival in multiple tumor types.
 
ONC2023 said:
Since we’re on the topic of non-metastatic esophageal, does anyone go by CALGB 80803? This study showed increased pathological CR with neoadjuvant induction FOLFOX + chemoRT compared to induction carbo/taxol + chemoRT.

Briefly, the study randomized patients to either FOLFOX or carbo/taxol for 2 cycles, at which point they got a PET. For patients with SUV >= 35% decline from baseline, they continued with the same chemo during RT. For non-responders, they crossed over to the other trial. 40% of PET responders to FOLFOX had pCR whereas only 14% PET responders had pCR to carbo/taxol.


To my fellow eyes, this certainly seems practice changing since pCR is strongly correlated with overall survival in multiple tumor types.
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I don't for a couple of reasons:
1. pCR isn't a validated surrogate endpoint in esophageal cancer yet (that I'm aware of).
2. FOLFOX+RT is a total s***show from a toxicity perspective.

I do love the idea of PET adapted therapy though and would like to see something like ESOPEC with PET after 4 cycles and surgery vs chemoRT based on PET result.

I don't think 80803 is necessarily the wrong thing to do though, just not my preferred plan. It's also not all that surprising that response to carbo/taxol induction chemo was low in adenos.
 
gutonc said:
The only real criticism I've seen from Rad Onc is that they used the CROSS radiation dosing which isn't what is used in actual practice, and that's a totally fair critique.

But to answer your question, yes, I think this is practice changing. For anyone that surgery thinks might be an operative candidate, I have been starting with FLOT x4 and then restaging. If surgery remains an option, they go to the OR, if not, for whatever reason, you can transition to definitive chemoRT (whether you use carbo/taxol or Cis/5FU).

This definitely brings up one of the big issues with these treatment de-escalation or alternative trials. If you don't have everyone on board from the beginning, you're definitely going to get pushback from whichever specialty's treatment gets removed from the plan. One of the major reasons that TNT/Watchful Waiting has become a standard in rectal cancer is that it was designed and run, from the beginning, by a colorectal surgeon, and the med and rad oncs were just along for the ride. If you design a trial where you're planning to omit chemo (or radiation) from current SOC treatment, then the med onc (or rad onc) should be the one designing the trial...you need that kind of juice to convince colleagues that it's the right thing to do.

I also think that just because FLOT was "better" than CROSS in this trial, it doesn't make it the automatic right choice for everyone.
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How long you would typically wait after first 4 cycles of FLOT for PET scan and do u repeat egd?
 
Might be a dumb question but figured I should ask. I'm a first year fellow currently on a busy solid onc consult service.

I get a lot of - patient has a MASS on imaging suspicious for malignancy, consult onc.

What are the must rule out things I should be aware of or rather how I do make this educational for me? I feel comfortable with new colon masses but other areas are lacking. 90% of the time I'm really just doing goals of care conversations and confirming that Management of infection per primary, but I want to make sure to get more out of it.
 
MifflinDunder said:
Might be a dumb question but figured I should ask. I'm a first year fellow currently on a busy solid onc consult service.

I get a lot of - patient has a MASS on imaging suspicious for malignancy, consult onc.

What are the must rule out things I should be aware of or rather how I do make this educational for me? I feel comfortable with new colon masses but other areas are lacking. 90% of the time I'm really just doing goals of care conversations and confirming that Management of infection per primary, but I want to make sure to get more out of it.
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Learn the basic diagnosis and staging for new tumors based on suspected primary.

For example what is important to find out for a pancreatic mass (imaging for respectability -> tumor board with your surgeons). Another one is always try to get IR to use a core needle rather than an FNA if lymphoma is on the menu!

Also my personal pet peeve but don’t be that fellow that tries to duck every consult before path is back. You’re an Oncologist, these people are in the hospital and are told they probably have cancer. They are SCARED, and just knowing you’re on board and seeing your face can be helpful.
 
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nxt170 said:
How long you would typically wait after first 4 cycles of FLOT for PET scan and do u repeat egd?
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ESOPEC trial did PET at 3w after C4. Repeat EGD wasn't part of the protocol.

My surgeons typically want to operate 6-8w after chemo (ESOPEC protocol said 4w) so PET is somewhere in the 3-4w range. EGD isn't typically repeated since it doesn't add much.
 
Slightly academic questions: For a patient with advanced HCC that has history of variceal bleeding treated with TIPS and normal platelets, would you ever consider atezolizumab/bevacizumab? Normally I would say never, but I'm wondering what you would do if the patient had TIPS 2 years ago with no bleeding since.

There's no contraindication to durva/treme, so that's likely the more correct option for first-line therapy.
 
ONC2023 said:
Slightly academic questions: For a patient with advanced HCC that has history of variceal bleeding treated with TIPS and normal platelets, would you ever consider atezolizumab/bevacizumab? Normally I would say never, but I'm wondering what you would do if the patient had TIPS 2 years ago with no bleeding since.

There's no contraindication to durva/treme, so that's likely the more correct option for first-line therapy.
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I would absolutely get a repeat EGD to confirm there are no varices anymore and if so, would feel comfortable with atezo/bev.

Durva/Trem isn’t a wrong answer either
 
82M history of RCC s/p radical nephrectomy many years ago, now with progressive pancytopenia, BMBx 6 months ago hypercellular with small B cell population (CD19, CD20, CD23) comprising <5%. All mutation testing negative and karyotype normal. Now having intermittent B symptoms. Over past 6 months has continued to be pancytopenia (WBC 2s, ANC 1-1.5, Hgb 8s, Plt 80s), but super large spleen measuring over 30cm, and recent PET demonstrated high activity in spleen (SUV 35) without any significant disease elsewhere. Only had some very small RP lymph nodes that lit up. Super high uric acid needing to be rasburicase twice in 1 week. But no other labs consistent with TLS (was actually hyperCa initially and needed denosumab). Spleen biopsy is nondiagnostic (necrotic tissue). I have a peripheral flow cytometry in-process. What is the possibilities and what would you do from here?

My thoughts: atypical Hairy cell leukemia (HCL-V), splenic marginal zone lymphoma, transformed aggressive B cell lymphoma primarily involving spleen?

Atypical HCL is my leading differential but it's just so rare..
Splenic marginal zone lymphoma is low grade and you wouldn't see such high FDG on PET (SUV 35 in spleen)
Transformed aggressive Bcell lymphoma would have obvious TLS and he should be having HypoCa (not hyperCa), hyperphos and hyperK, and elevated LDH, which he does not have any.

My thoughts on management:
1) can try and ask IR to repeat a spleen biopsy to see if they get viable tissue. I know spleen biopsies have high risk of bleeding
2) can see if a surgeon is willing to perform a splenectomy on this 82M with comorbidities. We would definitely get a tissue diagnosis if this is possible
3) treat with single agent rituximab and see what happens?

Thoughts?
 
osprey099 said:
82M history of RCC s/p radical nephrectomy many years ago, now with progressive pancytopenia, BMBx 6 months ago hypercellular with small B cell population (CD19, CD20, CD23) comprising <5%. All mutation testing negative and karyotype normal. Now having intermittent B symptoms. Over past 6 months has continued to be pancytopenia (WBC 2s, ANC 1-1.5, Hgb 8s, Plt 80s), but super large spleen measuring over 30cm, and recent PET demonstrated high activity in spleen (SUV 35) without any significant disease elsewhere. Only had some very small RP lymph nodes that lit up. Super high uric acid needing to be rasburicase twice in 1 week. But no other labs consistent with TLS (was actually hyperCa initially and needed denosumab). Spleen biopsy is nondiagnostic (necrotic tissue). I have a peripheral flow cytometry in-process. What is the possibilities and what would you do from here?

My thoughts: atypical Hairy cell leukemia (HCL-V), splenic marginal zone lymphoma, transformed aggressive B cell lymphoma primarily involving spleen?

Atypical HCL is my leading differential but it's just so rare..
Splenic marginal zone lymphoma is low grade and you wouldn't see such high FDG on PET (SUV 35 in spleen)
Transformed aggressive Bcell lymphoma would have obvious TLS and he should be having HypoCa (not hyperCa), hyperphos and hyperK, and elevated LDH, which he does not have any.

My thoughts on management:
1) can try and ask IR to repeat a spleen biopsy to see if they get viable tissue. I know spleen biopsies have high risk of bleeding
2) can see if a surgeon is willing to perform a splenectomy on this 82M with comorbidities. We would definitely get a tissue diagnosis if this is possible
3) treat with single agent rituximab and see what happens?

Thoughts?
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I think I want to know what your flow comes back with. It looks like HCL-v should still show CD103 so that should get answered one way or the other.

I like the IR Bx vs Rituximab idea, I’d probably lay those options out for the patient and let them decide. If they’re 82 with comorbidities you may end up just giving Rituximab alone no matter what you find so maybe since you already have proven a clonal disorder in the marrow you could make the argument to just treat. I’d just be praying the flow shows something helpful.

I doubt you’ll find a surgeon willing to take out the spleen (unless you work in Florida…)
 
osprey099 said:
82M history of RCC s/p radical nephrectomy many years ago, now with progressive pancytopenia, BMBx 6 months ago hypercellular with small B cell population (CD19, CD20, CD23) comprising <5%. All mutation testing negative and karyotype normal. Now having intermittent B symptoms. Over past 6 months has continued to be pancytopenia (WBC 2s, ANC 1-1.5, Hgb 8s, Plt 80s), but super large spleen measuring over 30cm, and recent PET demonstrated high activity in spleen (SUV 35) without any significant disease elsewhere. Only had some very small RP lymph nodes that lit up. Super high uric acid needing to be rasburicase twice in 1 week. But no other labs consistent with TLS (was actually hyperCa initially and needed denosumab). Spleen biopsy is nondiagnostic (necrotic tissue). I have a peripheral flow cytometry in-process. What is the possibilities and what would you do from here?

My thoughts: atypical Hairy cell leukemia (HCL-V), splenic marginal zone lymphoma, transformed aggressive B cell lymphoma primarily involving spleen?

Atypical HCL is my leading differential but it's just so rare..
Splenic marginal zone lymphoma is low grade and you wouldn't see such high FDG on PET (SUV 35 in spleen)
Transformed aggressive Bcell lymphoma would have obvious TLS and he should be having HypoCa (not hyperCa), hyperphos and hyperK, and elevated LDH, which he does not have any.

My thoughts on management:
1) can try and ask IR to repeat a spleen biopsy to see if they get viable tissue. I know spleen biopsies have high risk of bleeding
2) can see if a surgeon is willing to perform a splenectomy on this 82M with comorbidities. We would definitely get a tissue diagnosis if this is possible
3) treat with single agent rituximab and see what happens?

Thoughts?
Click to expand...


Interesting case, definitely sounds like you have the differential correct.

Why not repeat another bone marrow biopsy and may be send a NGS on it again.

Talk to IR about spleen biopsy however in my experience its hard to get as IR will need general surgery cover in case the spleen starts to bleed profusely.

CD 20 population was small on BMB but could be much higher in the spleen, I think trying to give some Rituxan if patient agrees is still a good idea. Also if diagnosis starts to lead towards HCL you can add Clardribine to rituxan.

Good luck and keep us updated.
 
MD46 said:
Interesting case, definitely sounds like you have the differential correct.

Why not repeat another bone marrow biopsy and may be send a NGS on it again.

Talk to IR about spleen biopsy however in my experience its hard to get as IR will need general surgery cover in case the spleen starts to bleed profusely.

CD 20 population was small on BMB but could be much higher in the spleen, I think trying to give some Rituxan if patient agrees is still a good idea. Also if diagnosis starts to lead towards HCL you can add Clardribine to rituxan.

Good luck and keep us updated.
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No harm in repeat marrow. Send Braf and ngs.

I get single agent ritux but will be insufficient if truly HCL. If repeat marrow doesn’t give you additional answers splenic bx is your only (bad) option and would consider just following scans.
 
Yeah like everyone else has been saying, Rituxan should at least be partially effective for everything on your differential (I'll add splenic red pulp lymphoma to that, which should be very sensitive to rituxan).

Weird thing about hairy cell is that it should've shown up on your peripheral flow, esp if the spleen is that big and the patient has reciprocal cytopenias. But then again atypical cases do arise.
 
There was an earlier case in the thread about STK11 mutations in NSCLC and IO. I wanted to follow-up on this. Wanted to ask about the POSEIDON study showing that STK11, KEAP, and KRAS mutated NSCLC respond significantly better to dual IO (CTLA4/PD + chemo) than chemo alone.

For metastatic STK11/KRAS/KEAP NSCLC, is anyone using chemo + dual IO?

These are the five-year survivals (first number is dual IO plus chemo)
  • KRAS subset: 21.7% vs 8.1%
  • KEAP1 subset: 10% vs 0%
  • STK11 subset: 12.9% vs 0%
www.onclive.com

POSEIDON Update Confirms OS Benefit of Tremelimumab/Durvalumab Plus Chemo in mNSCLC

A limited course of tremelimumab added to frontline durvalumab and chemotherapy provided a sustained overall survival benefit vs chemotherapy alone in patients with previously untreated metastatic non–small cell lung cancer.
www.onclive.com www.onclive.com
 
ONC2023 said:
There was an earlier case in the thread about STK11 mutations in NSCLC and IO. I wanted to follow-up on this. Wanted to ask about the POSEIDON study showing that STK11, KEAP, and KRAS mutated NSCLC respond significantly better to dual IO (CTLA4/PD + chemo) than chemo alone.

For metastatic STK11/KRAS/KEAP NSCLC, is anyone using chemo + dual IO?

These are the five-year survivals (first number is dual IO plus chemo)
  • KRAS subset: 21.7% vs 8.1%
  • KEAP1 subset: 10% vs 0%
  • STK11 subset: 12.9% vs 0%
www.onclive.com

POSEIDON Update Confirms OS Benefit of Tremelimumab/Durvalumab Plus Chemo in mNSCLC

A limited course of tremelimumab added to frontline durvalumab and chemotherapy provided a sustained overall survival benefit vs chemotherapy alone in patients with previously untreated metastatic non–small cell lung cancer.
www.onclive.com www.onclive.com
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For the right patient. I have a patient who is STK11, but has significant comorbidities so I'm not using this. I know it's only 2 cycles of chemo, but during those 2 cycles where you're getting chemo + IO doublet, it is rough
 
I have a 60F widely metastatic disease on imaging, showing a large lung mass.
Pathology:undifferentiated SMARCA4-deficient thoracic tumor.
Does anyone have experience with this or know of effective therapies? No lung panel or PD-L1 results are back yet.She is unwell.
 
redeyelopez said:
I have a 60F widely metastatic disease on imaging, showing a large lung mass.
Pathology:undifferentiated SMARCA4-deficient thoracic tumor.
Does anyone have experience with this or know of effective therapies? No lung panel or PD-L1 results are back yet.She is unwell.
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Interesting case, data is lacking in these tumors and there isnt a good concensus on treatment either. If it is metastatic and you cannot wait on NGS due to patient clinical status worsening, I would consider giving a platinum based therapy in the in patient setting while you wait for results. If NGS supports use of immunetherapy, there is date on Opdivo single agent in some case reports showing a good amount of tumor regression. Also I would consider sending tissue for cancer type ID, ideally another area of metastatic disease if you are able to biopsy. Good luck and keep us posted.
 
MD46 said:
Interesting case, data is lacking in these tumors and there isnt a good concensus on treatment either. If it is metastatic and you cannot wait on NGS due to patient clinical status worsening, I would consider giving a platinum based therapy in the in patient setting while you wait for results. If NGS supports use of immunetherapy, there is date on Opdivo single agent in some case reports showing a good amount of tumor regression. Also I would consider sending tissue for cancer type ID, ideally another area of metastatic disease if you are able to biopsy. Good luck and keep us posted.
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@redeyelopez I was literally coming to ask about this same thing, which I did not even know existed until this week.

I’m curious why inpatient setting? Nothing (of the very limited information available) that I have read seemed to indicate a high response rate that would worry me for TLS, or are you just assuming their patient is still admitted?

I was reading that PDL1 status may not necessarily be a good predictor of response, any thoughts on platinum based chemoimmunotherapy instead?
 
You have valid points, OP would need to tell us what Unwell means? for me when asked to proceed asap means patient is admitted and would need to start asap while in patient. Otherwise would try out patient. PDL status may not be a good predictor however in order to get the therapy approved by insurance you will need something to support your judgment. Some of these cases behave similar to small cell, hence platinum based therapy should work. I couldnt find data on chemoimmunetherapy for these patients, in theory should work but most places I have worked at don't like giving immunetherapy inpatient.
 
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MD46 said:
You have valid points, OP would need to tell us what Unwell means? for me when asked to proceed asap means patient is admitted and would need to start asap while in patient. Otherwise would try out patient. PDL status may not be a good predictor however in order to get the therapy approved by insurance you will need something to support your judgment. Some of these cases behave similar to small cell, hence platinum based therapy should work. I couldnt find data on chemoimmunetherapy for these patients, in theory should work but most places I have worked at done like giving immunetherapy inpatient.
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Apologies yes she is still inpatient. She has diffusely met disease involving t spine with cord compression.She required decompression 9 days ago and is paraplegic but systemically stable. She will have high care needs going forward.

She is going for palliative t spine rt. Its challenging because I know the prognosis is poor with these cancers but to meet her she appears very comfortable/alert. I am not sure if we would add substantial time or quality with chemo-io.
 
redeyelopez said:
Apologies yes she is still inpatient. She has diffusely met disease involving t spine with cord compression.She required decompression 9 days ago and is paraplegic but systemically stable. She will have high care needs going forward.

She is going for palliative t spine rt. Its challenging because I know the prognosis is poor with these cancers but to meet her she appears very comfortable/alert. I am not sure if we would add substantial time or quality with chemo-io.
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Is there more disease in the thorax than the lung mass? How large? Does she really need emergent treatment for this?

All questions I'd want to know the answer to before deciding on a treatment.
 
gutonc said:
Is there more disease in the thorax than the lung mass? How large? Does she really need emergent treatment for this?

All questions I'd want to know the answer to before deciding on a treatment.
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Many thanks All,
Yes I think she is stable enough to wait for the NGS and PD-L1 results.

PET: 2 cm lesion in the left upper lobe (LUL), bulky hilar lymphadenopathy, diffuse bone metastases, and single metastases in the liver and adrenal gland.
no cns met

many thanks for all your input
 
redeyelopez said:
Many thanks All,
Yes I think she is stable enough to wait for the NGS and PD-L1 results.

PET: 2 cm lesion in the left upper lobe (LUL), bulky hilar lymphadenopathy, diffuse bone metastases, and single metastases in the liver and adrenal gland.
no cns met

many thanks for all your input
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One other thing that I'll say is that I have always found this discussion and decision making to be really difficult to do in the inpatient/acute setting. You're seeing this person at their worst (to date) and it's impossible to say how things will change over the next few weeks after surgery. Based on what you told us, she's ECOG 3+ right now and chemo in this setting is going to push that number higher. This is someone that I would have get post-op RT and then spend a few weeks in rehab before I brought her back to clinic re-evaluate her fitness for chemo.
 
I don't have a question here, but I need to tell somebody that, after 13 years in community practice, and taking care of hundreds of people with lung cancer, I got my first ever ALK fusion mutated case this week. I was beginning to think that it was a made up phenomenon.
 
LOL I have yet to see one but I can't wait to start someone on lorlatinib and just watch them stabilize forever
 
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redeyelopez said:
I have a 60F widely metastatic disease on imaging, showing a large lung mass.
Pathology:undifferentiated SMARCA4-deficient thoracic tumor.
Does anyone have experience with this or know of effective therapies? No lung panel or PD-L1 results are back yet.She is unwell.
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I've had a few of these. Almost always a late/aggressive presentation. Very poor prognosis. Does not typically respond well with usual platinum doublet. These is some scant data that suggests checkpoint inhibitors may be more successful here (think PDL1 +/- CTLA4). Either way sadly these patients have never done well with me. Maybe you will get something lucky on the NGS.
 
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Anyone seen a patient for positive Galleri Grail test yet? Got my first one this week. This is going to break our system.
 
HaemOnculus said:
Anyone seen a patient for positive Galleri Grail test yet? Got my first one this week. This is going to break our system.
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The institution I used to work for was the leading recruiter to their first two (both negative) clinical trials. I've seen more of these than I care to think about. At the beginning of the study, the PI (who subsequently left to work at Exact) agreed to manage all of the positive tests himself. That quickly became his entire practice, so he backed out on that and punted it to the universtiy's community based group (us) to manage. Also in the early studies (first people with active, known cancer, 2nd people with a history of cured cancer in the prior 5 years), the sponsor agreed to pay for all of the workup that a positive test resulted in. All of that of course is completely off the table now that it's in the wild.

It doesn't help that the people seeking out this test are the same entitled d-bags who request a full body MRI for a cough that lasts more than 2 days.
 
Myeloma Case Suggestions:
82 y old ecog 2, non transplant pt, diagnosed with standard risk IgA lambda in 2023, started on VRd, developed neuropathy and switched to Rd, developed disease progression and switched to DRd. Initially responded but now progressing. Planning to start Pom/Dex. Debating about adding cyclophosphamide. Thinking about tolerance in this old guy. Advise please.
 
nxt170 said:
Myeloma Case Suggestions:
82 y old ecog 2, non transplant pt, diagnosed with standard risk IgA lambda in 2023, started on VRd, developed neuropathy and switched to Rd, developed disease progression and switched to DRd. Initially responded but now progressing. Planning to start Pom/Dex. Debating about adding cyclophosphamide. Thinking about tolerance in this old guy. Advise please.
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I'd either continue the dara or add isa but pretty much the same thought process here.
 
nxt170 said:
Myeloma Case Suggestions:
82 y old ecog 2, non transplant pt, diagnosed with standard risk IgA lambda in 2023, started on VRd, developed neuropathy and switched to Rd, developed disease progression and switched to DRd. Initially responded but now progressing. Planning to start Pom/Dex. Debating about adding cyclophosphamide. Thinking about tolerance in this old guy. Advise please.
Click to expand...
I’d probably do DPd or KPd.

I’m relatively young but I’ve had one patient who progressed on basically all the Imids/Proteosome inhibitors over an 18 month period then had a somewhat miraculous turnaround on Cytoxan so I will probably always at least give that a shot if all else fails.
 
nxt170 said:
Why continue dara? He progressed while he was on Dara
Click to expand...
That's a really fair point I guess I would want to know how long they had been on Dara and how obvious/clear the progression was. I think my main point is I would do a triplet instead of just Pom/Dex personally
 
HemeOncHopeful19 said:
That's a really fair point I guess I would want to know how long they had been on Dara and how obvious/clear the progression was. I think my main point is I would do a triplet instead of just Pom/Dex personally
Click to expand...
And my thought process was, perhaps the Rev was the problem. If tolerating Dara well, I don’t see much harm in continuing it for another month or two while switching to Pom/Dex and see if the disease is controlled.

I should also go back to the OP and ask what “progression” means and what the goals of care are? If the light chains just bumped a little bit, that’s one thing. If he developed anemia and renal failure, that’s a completely different scenario. And in an 82 yo with borderline performance status, an incurable disease and rapid intolerance/progression on 3 lines of therapy, a GoC conversation is clearly indicated.
 
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