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May I ask why not cape monotherapy for 6 months?
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clinical cases
Started by redeyelopez
Mostly extrapolating from the IDEA collaborative data. If someone can't tolerate oxali, I'll just do cape.
Did you mean 3 months? I am not familiar with x 4. Either way I think this is a good middle ground in these borderline cases.
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4 cycles = 3 months
42 year old.
Bilateral renal masses, biopsy proven ccRCC (called low grade on path).
The left mass is so large it needs radical nephrectomy. The right mass is borderline.
She’s seeing me for neoadjuvant treatment to shrink them before urology goes in.
I like the idea of dual IO in young people because it’s the best chance of a durable response, but the response rate is lower than IO/TKI.
Would anyone do “neoadjuvant” dual IO, or do you prioritize the ORR of TKI’s in this setting? I’m leaning toward IO/TKI - either Cabo/nivo or if the patient is ok with the toxicity, Len/pembro.
Bilateral renal masses, biopsy proven ccRCC (called low grade on path).
The left mass is so large it needs radical nephrectomy. The right mass is borderline.
She’s seeing me for neoadjuvant treatment to shrink them before urology goes in.
I like the idea of dual IO in young people because it’s the best chance of a durable response, but the response rate is lower than IO/TKI.
Would anyone do “neoadjuvant” dual IO, or do you prioritize the ORR of TKI’s in this setting? I’m leaning toward IO/TKI - either Cabo/nivo or if the patient is ok with the toxicity, Len/pembro.
I would probably do what you’re doing. We love the idea of those sustained CRs with dual IO but in reality it’s like… 10-15%?
If it is the chance or staying off dialysis I’d probably lean toward IO/TKI. Response rates are higher and you’re still getting exposure to IO anyway.
I agree, while in the metastatic setting there is a good argument for io/io, I would do pembro lenva for cytoreduction prior to surgery, especially if there is no sarcomatoid differentiation.
I'm sure you are planning this, but would make sure he has genetic testing. Likelihood >10% you'll find something.
Just a brief Lenvatinib update regarding my earlier question on len-pembro for ccRCC: I hate this drug.
1) A CLL case (mal heme is my weak area, and I'm covering for a partner - so pardon how simple of a question this is)
- 80 year old. CLL treated with obinutuzumab and venetoclax 4 years ago with excellent response. Counts normalized for 4 years. Earlier in 2026, WBC starting rising, almost entirely lymphocytosis. 40K --> 100K. Platelets now down to 50K. ANC is now < 1. New anemia. LDH 550 and uric acid 12. No blasts on smear. Flow pending.
CT CAP with new upper abdominal nodes.
The question here is Richter's Transformation vs just relapsed CLL, right? The textbook right answer is PET him and then get excisional biopsy I believe but this is inpatient and can't get a PET. Also, he's too sick to get an abdominal surgery to go after the abdominal nodes - I don't think they're accessible percutaneously.
Would a bone marrow be an appropriate replacement?
2) ccRCC case. Good performance status 55 year.
--- Nephrectomy 2024 with 1 year adjuvant pembro ending July 2025.
-- Oct 2025, developed small thigh mas on PET with her previous oncologist.
-- PET with me 3/2026: growing thigh mass and small hip lytic lesion --> very small volume of disease.
-- Thigh mass removed, confirmed as ccRCC.
So I have a lady with oligorecurrent disease -- one of which has been surgically excised. The other area is amenable to SBRT.
My options are:
1) IO-IO ---> I am a bit concerned about IO/IO rechallenge since she relapsed so soon after end of pembro, though it's low volume recurrence
2) IO-TKI --> this is not curative (at least likely than IO/IO)
3) SBRT perhaps then "adjuvant" IO/TKI?
1) A CLL case (mal heme is my weak area, and I'm covering for a partner - so pardon how simple of a question this is)
- 80 year old. CLL treated with obinutuzumab and venetoclax 4 years ago with excellent response. Counts normalized for 4 years. Earlier in 2026, WBC starting rising, almost entirely lymphocytosis. 40K --> 100K. Platelets now down to 50K. ANC is now < 1. New anemia. LDH 550 and uric acid 12. No blasts on smear. Flow pending.
CT CAP with new upper abdominal nodes.
The question here is Richter's Transformation vs just relapsed CLL, right? The textbook right answer is PET him and then get excisional biopsy I believe but this is inpatient and can't get a PET. Also, he's too sick to get an abdominal surgery to go after the abdominal nodes - I don't think they're accessible percutaneously.
Would a bone marrow be an appropriate replacement?
2) ccRCC case. Good performance status 55 year.
--- Nephrectomy 2024 with 1 year adjuvant pembro ending July 2025.
-- Oct 2025, developed small thigh mas on PET with her previous oncologist.
-- PET with me 3/2026: growing thigh mass and small hip lytic lesion --> very small volume of disease.
-- Thigh mass removed, confirmed as ccRCC.
So I have a lady with oligorecurrent disease -- one of which has been surgically excised. The other area is amenable to SBRT.
My options are:
1) IO-IO ---> I am a bit concerned about IO/IO rechallenge since she relapsed so soon after end of pembro, though it's low volume recurrence
2) IO-TKI --> this is not curative (at least likely than IO/IO)
3) SBRT perhaps then "adjuvant" IO/TKI?
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Really tough case and an area where there is not much data. Just thinking out loud:
1. Is this imdc favorable risk (assuming the rest of the lab values are normal)? Who knows... recurrence was relatively quick after adjuvant IO, but did the pembro change the natural history of this disease (i.e. how do we measure time to systemic therapy - from diagnosis or from end of adj therapy)? Who knows...
2. After sbrt, you have no measurable disease. What are you treating and how do we measure efficacy/overtreatment? Is active surveillance a reasonable option? (For the record I agree with SBRT)
3. Real world data post adjuvant pembro followed by io combination - looked like we may be converging on 6 months as a reasonable target for rechallenge. However, this person recurred 3 months post but is now >6 months when they will receive treatment. Where does this patient's benefit lie in rechallenging with IO/tki or io/io? (Im guessing towards less benefit)
3. Low volume disease - as you point out, is this the type of patient where you have the luxury of a trial of io/io whether it works or not? But the risk of life altering toxicity is not negligible...
4. I think the biology of this disease is aggressive and I would advocate for treatment rather than active surveillance.
If it were my patient, I would explain the above and get a feel for what they want. We have time as they will get SBRT and then come back with repeat CT. If truly nothing, the convo will be long. If tiny lung nodules start appearing, I would guide towards 1L IO/IO -> 2L cabozantinib in a 55 yo who tolerated pembro well.
Would love to hear others' thoughts!
Def want to r/o richters. PET with excisional as you mentioned is gold standard. Sure go for marrow but it’s subject to sampling error just like a random nodal bx is (without pet)
Medonc_fellow
New Member
When giving FOLFOX/FOLFIRI and skipping 5-FU bolus, do you guys still give leucovorin?
I told you.
Too sick for an excisional biopsy and hospitalized? Probably too sick for aggressive treatment too. Marrow is an answer, but I don't think it's a good one. If I could get rituximab as an inpatient (which I can't), I'd give a dose of that, maybe some steroids and hope to temporize him enough to get discharged and the appropriate workup done.
SBRT and observe? That's probably where I'd go, especially since you know she's going to get more systemic therapy relatively soon. Save it for when local therapy isn't an option anymore.
78F, ECOG 1. Met serous ovarian cancer. BRCA1 only targetable mutation (somatic, not germline). Has progressed on carbo/taxol/bev --> olaparib/bev maintenance (18 months on that regimen); Carbo/Doxil (only 3 months), then switched to Cytoxan/Pembro/Bev but had to stop after C3 because of Grade 3-4 immune mediated aplastic anemia (probably should have admitted her but she refused). Currently on a long pred taper with decent response but has persistent anemia. WBC and plts have normalized.
CT scan after just those 3 cycles showed a pretty good response. I'm planning another one once I get her off steroids, probably another month or so.
I do tend to re-challenge most of my irAEs when clinically appropriate, but I'm fairly hesitant about this one since I'm worried about her ability to survive me nuking her marrow a 2nd time.
Where would people turn for 4th line therapy in a case like this. I know there are about a dozen things I can choose, most of which won't work. I don't treat a ton of gyn stuff so appreciate folks' input.
CT scan after just those 3 cycles showed a pretty good response. I'm planning another one once I get her off steroids, probably another month or so.
I do tend to re-challenge most of my irAEs when clinically appropriate, but I'm fairly hesitant about this one since I'm worried about her ability to survive me nuking her marrow a 2nd time.
Where would people turn for 4th line therapy in a case like this. I know there are about a dozen things I can choose, most of which won't work. I don't treat a ton of gyn stuff so appreciate folks' input.
If grade 3 requiring long term steroids or grade 4 A/E then I won't rechallenge with IO. Can bring it later if you run out of options.
That being said, check for FOLR1 IHC - Mirvetuximab soravtansine is an option (ocular s/e hence baseline eye exam), relacorilant with Abraxane (new approval), single agent chemos (gem, Abraxane etc.).
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So I am relatively early in my career and have had a few asking me about Daraxonrasib for Pancreatic Cancer, I guess it was recently approved for “expanded access” FDA Permits Expanded Access for Investigational Pancreatic Cancer Drug
Does anyone have experience with programs like that and whether a community or PP Onc doc could realistically get their patients on these drugs?
Does anyone have experience with programs like that and whether a community or PP Onc doc could realistically get their patients on these drugs?
No FOLR1 or anything targetable. I completely forgot about relacorilant/abraxane. Thanks for the reminder.
I sent a request for a patient of mine last week and got the reply with the paperwork yesterday afternoon. I'll get to work on it next week.
I've never personally done it, but do know some folks in academ-ish practice that have been successful with it in the past.
I think this one is going to be a horse of a different color though. If these data are real, this drug is absolutely game changing in pancreatic cancer. In my experience, met panc clinical trials are phenomenally easy to recruit to because the available options suck so badly and it's such a terrible disease. This company is going to be absolutely pummeled with these requests. We'll see how they hold up under the pressure.
I also put in a request this past week emailing [email protected] which I found on the Revolution Medicines Website
I finally got around to reading the email they sent me. It wasn't actually the paperwork, it was an email connecting me to the 3rd party that's administering the EAP. So...we wait.
Appreciate the input, are you guys waiting for progression on 5FU-based + Gem/Abraxane? Or just after 1 line?
The study was 2nd line or beyond so I'm going to request it on anyone who's progressed on at least one line of therapy.
The one I've got in the pipeline already is actually on 5FU maintenance after a pretty good response to FOLFIRINOX for 6 months.
I rarely do maintenance in pancreatic but he couldn't keep going on FOLFIRINOX and didn't need to change treatment yet. I suppose if they really pushed me, I could spin this as 2nd line when he fails.
Since I have no idea what the timeline or amount of work it's going to take to get this available is yet, I'm just doing it somewhat proactively on a couple of people. I think I'll have better luck than many in getting EAP access since I can plead "poverty" since it's only supposed to be for people with no access to active clinical trials. Since I'm rural CAH, I'm going to use that to my advantage.
Yeah this is where I am
I kind of feel like I should just submit this for every one of my met pancs currently on treatment.
I mean, that's 10 minutes and $250 where I am.
Stupid waste of time? Yes. A boat payment (or more reasonably a nice dinner out)? Also yes.
Have you gotten any farther? Realized when I got the paperwork how much it was going to entail. I then reached out to the mothership to ask about it and they're already 3/4 of the way through the process. Threw my name on the form and we're off to the races...soon.
Have you started switching your metastatic/unresectable pancreatic cancer patients on second-line therapy to daraxonrasib today? Or are you planning to do it very shortly? Just wondering if your institutions have started carrying this drug and if it realistically will be available in the next couple of weeks for patients to start.
It's not FDA approved yet. So you can't just "order it from pharmacy". Until FDA approval, EAP is the only way to get it. After it's approved, it's going to be phenomenally expensive.
Two cases:
1) 22 year old man, poor risk non-seminoma (brain, liver, lung mets). Had CNS met resected + RT. I then saw him and tried to give him BEP x 4. He repeatedly missed visits, and instead of getting BEP x 4 over 12 weeks, he got ~60-70% dose intensity over about 16 weeks. I tried multiple direct admit to hospital to help with adherence to only partial success. He did NOT get all his bleomycin, and he got his 4 cycles of days 1-5 BEP spread out of 4 months. (Yes, I know, a disaster).
Imaging still shows lung masses, negative brain mets. AFP, LDH, and HCG all normalized throughout treatment EXCEPT once about 3 weeks ago when AFP was 25 but came down after a 5 day BEP course.
Also PFTs with terrible DLCO now, so can't give bleo.
So here's my problem: for a poor risk non-seminoma incompletely treated at sub-optimal intensity, do I switch to observation due to negative tumor markers or do I switch to VIP? Since TIP is technically a second line regimen, I am leaning towards VIP since he didn't technically fail BEP (he just didn't get enough)?
2) My question is for a small but unresectable atypical lung carcinoid management -- NCCN says you can observe vs cape/tem vs lanreotide. Assuming low Ki-67 of 3% in a good PS 60 year old with no life-limiting comorbidities, what factors would make you give cape/tem? (This is a very complicated case that I simplified to ask the salient question -- basically no surgery or RT is possible, so I have to decide on indefinite medicine vs observation).
1) 22 year old man, poor risk non-seminoma (brain, liver, lung mets). Had CNS met resected + RT. I then saw him and tried to give him BEP x 4. He repeatedly missed visits, and instead of getting BEP x 4 over 12 weeks, he got ~60-70% dose intensity over about 16 weeks. I tried multiple direct admit to hospital to help with adherence to only partial success. He did NOT get all his bleomycin, and he got his 4 cycles of days 1-5 BEP spread out of 4 months. (Yes, I know, a disaster).
Imaging still shows lung masses, negative brain mets. AFP, LDH, and HCG all normalized throughout treatment EXCEPT once about 3 weeks ago when AFP was 25 but came down after a 5 day BEP course.
Also PFTs with terrible DLCO now, so can't give bleo.
So here's my problem: for a poor risk non-seminoma incompletely treated at sub-optimal intensity, do I switch to observation due to negative tumor markers or do I switch to VIP? Since TIP is technically a second line regimen, I am leaning towards VIP since he didn't technically fail BEP (he just didn't get enough)?
2) My question is for a small but unresectable atypical lung carcinoid management -- NCCN says you can observe vs cape/tem vs lanreotide. Assuming low Ki-67 of 3% in a good PS 60 year old with no life-limiting comorbidities, what factors would make you give cape/tem? (This is a very complicated case that I simplified to ask the salient question -- basically no surgery or RT is possible, so I have to decide on indefinite medicine vs observation).
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Asymptomatic, low grade and not amenable to local therapy? I'd just watch. If this is an "I hate cancer" person who has to do something, lanreotide. And don't bother to image more often than every 6 months or so.
What was the proportion of teratoma in the original specimen?
I personally favor observation, but the patient does not sound particularly compliant or motivated. If there is concern for residual teratoma rather than viable tumor, I would not expect a meaningful radiologic response to additional lines of chemo. I would recommend referral to a high-volume testicular cancer center for a second opinion, if you are not already practicing in one.
I would add that, in selected cases, aggressive pulmonary resection of residual germ cell tumor metastases may be considered. However, the phenotype and overall clinical picture of this patient do not appear to meet the usual criteria for such an approach.
If the AFP really rose three weeks ago and that’s from disease, he’s in trouble since that would have happened while on chemotherapy even if it was intermittent. Would check markers monthly (and observe for now but with bates breath) and consider referral to a high volume center in case 2L systemic therapy is needed.
Patient with history of chronic thromboembolic pulmonary hypertension (CTEPH) status post pulmonary thromboendarterectomy (PTE) approximately 10 years ago. The patient is currently asymptomatic with complete resolution of pulmonary arterial hypertension and no residual clots on imaging. The patient is currently on a vitamin K antagonist (VKA) for lifelong anticoagulation.
Is it safe and appropriate to transition this hemodynamically cured, asymptomatic post-PTE patient from a VKA to a direct oral anticoagulant (DOAC)?
Is it safe and appropriate to transition this hemodynamically cured, asymptomatic post-PTE patient from a VKA to a direct oral anticoagulant (DOAC)?
Yes.
Went back and forth with our "mothership" for a while and then they eventually landed on, "just refer these patients to us"
Have a 78 year old woman. Two synchronous primaries.
- triple negative breast, 1.4 cm. No suspicious axillary adenopathy on breast MRI imaging
- stage III unresectable lung adeno. No driver mutations.
I'm thinking:
- First, 6 weeks of weekly low-dose carbo/taxol for concurrent chemoRT for the lung. The carbo/taxol will give me some breast coverage.
- Second, breast surgery.
- Third, adjuvant immunothery consolidation for the lung.
Questions:
- should I extend the carbo/taxol to 12 weeks to make it more breast appropriate and add pembro to it?
- would anyone do the breast surgery up front, not give neoadjuvant for a T1c TNBC breast, and start chemoRT for lung after? The carbo/taxol for the chemoRT would act as adjuvant.
- triple negative breast, 1.4 cm. No suspicious axillary adenopathy on breast MRI imaging
- stage III unresectable lung adeno. No driver mutations.
I'm thinking:
- First, 6 weeks of weekly low-dose carbo/taxol for concurrent chemoRT for the lung. The carbo/taxol will give me some breast coverage.
- Second, breast surgery.
- Third, adjuvant immunothery consolidation for the lung.
Questions:
- should I extend the carbo/taxol to 12 weeks to make it more breast appropriate and add pembro to it?
- would anyone do the breast surgery up front, not give neoadjuvant for a T1c TNBC breast, and start chemoRT for lung after? The carbo/taxol for the chemoRT would act as adjuvant.
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I like your approach. The lung cancer is the thing that's most likely to kill her if un/under-treated, at least in the near term. So I'd start there with the carbo/taxol+RT.
I also like the idea of doing an extra 6w of carbo/taxol, and you can add Durvalumab then for both the breast and the lung. This is in line with the recently published GeparNuevo trial which used neoadjuvant abraxane-->Epi/Cytoxan combined with durvalumab (basically the Eurotrash version of KN-522) and found nearly identical outcomes in pCR, DFS and 5y BCSS compared to the KeyNote regimen.
I think you'd have a hard time getting pembro approved for a T1c TNBC anyway, since KN-522 only include stage II-III. But you can get durva for the lung no problem, and GeparNeuvo included cT1b-4, N(any).
Medonc_fellow
New Member
Hey all, Im a fellow and would appreciate your input for this case:
51 y/o female with oligorrecurent breast cancer, ECOG 0 and no residual neuropathy:
- 08.2022 Original diagnosis . Two biopsies with discordant IHC:
— Bx 1: IDC NST G3. DCIS+. ER- PR- HER2 3+ Ki-67 50%.
— Bx 2: IDC with mucinous component (10%). G2. DCIS+. ER 40% PR 70% HER2 3+. Ki-67 40%
- Neoadjuvant TCHP x6.
- 04.04.23 Modified radical mastectomy, non pCR.
— Path: IDC NST G1. 1 cm residual disease. 3/9 LN+. ER 80% PR 0% HER2 neg (1+), Ki-67 10%
- 14C adjuvant T-DM1.
- 3 y 4 mo of adjuvant endocrine therapy.
- July this year, isolate cervical lymph node recurrence corroborated w/ PET-FDG.
— Path: IDC ER- PR- HER2 3+ Ki-6 40%. Androgen receptor 90%.
I was thinking on doing CLEOPATRA, we have no access to T-DXd atm and I feel it would be overkill for such low volume disease.
Taking the case to tumor board to consider isolated node resection.
Would you stop adjuvant endocrine therapy? I understand that the disease that recurred and that will most likely dictate prognosis is the HER2 enriched clone, however given that these patients now live much longer I wouldn't like to see disease progression from the HR+ clone in the coming years...
51 y/o female with oligorrecurent breast cancer, ECOG 0 and no residual neuropathy:
- 08.2022 Original diagnosis . Two biopsies with discordant IHC:
— Bx 1: IDC NST G3. DCIS+. ER- PR- HER2 3+ Ki-67 50%.
— Bx 2: IDC with mucinous component (10%). G2. DCIS+. ER 40% PR 70% HER2 3+. Ki-67 40%
- Neoadjuvant TCHP x6.
- 04.04.23 Modified radical mastectomy, non pCR.
— Path: IDC NST G1. 1 cm residual disease. 3/9 LN+. ER 80% PR 0% HER2 neg (1+), Ki-67 10%
- 14C adjuvant T-DM1.
- 3 y 4 mo of adjuvant endocrine therapy.
- July this year, isolate cervical lymph node recurrence corroborated w/ PET-FDG.
— Path: IDC ER- PR- HER2 3+ Ki-6 40%. Androgen receptor 90%.
I was thinking on doing CLEOPATRA, we have no access to T-DXd atm and I feel it would be overkill for such low volume disease.
Taking the case to tumor board to consider isolated node resection.
Would you stop adjuvant endocrine therapy? I understand that the disease that recurred and that will most likely dictate prognosis is the HER2 enriched clone, however given that these patients now live much longer I wouldn't like to see disease progression from the HR+ clone in the coming years...
T-DXd is the "right" answer, but if you can't get it, that's sort of irrelevant. THP isn't the wrong answer, but she's already had it (granted, 4 years ago). If you have access to them, capecitabine with any of neratinib (not my favorite) or trastuzumab/tucatinib or tras/lapatinib are options. Can also use tras/lapatinib without chemo. You could even just try HP or T-DM1 and see what happened. It's been 4 years so you might get some mileage. I agree that THP might be a little aggressive for a solitary nodal recurrence (that you can measure).
Although NCCN guidelines suggest it, the data for metastatectomy in breast cancer is pretty poor, but it might not be a terrible idea in this case, recognizing that it won't be a cure, but will just kick the can down the road.
I wouldn't stop endocrine therapy at this point. Just because the HR negative clone is what recurred doesn't mean there's not HR+ stuff out there that the endocrine therapy is keeping in check. If you wind up giving chemo, I'd hold it then but would resume it once the cytotoxics are done.
And if you don't already have it, tumor genomics and germline testing.
I don’t do a lot of breast but I feel like some of my breast colleagues would say something something cut it out / radiate it and ctDNA here
Given the inability to get T-DXd, I assumed the poster was in a lower resource environment, possibly outside the US, where ctDNA may also be hard to get done.
But yes, ctDNA for sure.
Recurrent laryngeal SCC, CPS >50, ECOG 2–3, bleeding airway — inpatient pembro without trach?
Late-50s man with recurrent laryngeal/right vocal cord SCC after definitive CRT ~1 year ago. Locoregional recurrence with extralaryngeal extension/cervical nodal disease, no distant mets. PD-L1 CPS >50.
Now recurrent admissions with tumour-related haemoptysis/high-risk airway, severe COPD, feeding-tube dependence/cachexia, recent complex PCI; antiplatelets reduced to aspirin due to bleeding. Salvage laryngectomy and further RT not felt feasible. Currently inpatient/HDU under ENT airway monitoring, on TXA nebs/steroids. ECOG around 2–3.
ENT feel prophylactic trach has high morbidity/prolonged admission risk and would prefer inpatient pembrolizumab monotherapy with HDU monitoring and rescue airway plan if he deteriorates.
Would you offer inpatient pembro monotherapy as a palliative time-limited trial here,if I dont -my understanding from the ENT team is it will be palliation? really appreaciate your thoughts @gutonc
Late-50s man with recurrent laryngeal/right vocal cord SCC after definitive CRT ~1 year ago. Locoregional recurrence with extralaryngeal extension/cervical nodal disease, no distant mets. PD-L1 CPS >50.
Now recurrent admissions with tumour-related haemoptysis/high-risk airway, severe COPD, feeding-tube dependence/cachexia, recent complex PCI; antiplatelets reduced to aspirin due to bleeding. Salvage laryngectomy and further RT not felt feasible. Currently inpatient/HDU under ENT airway monitoring, on TXA nebs/steroids. ECOG around 2–3.
ENT feel prophylactic trach has high morbidity/prolonged admission risk and would prefer inpatient pembrolizumab monotherapy with HDU monitoring and rescue airway plan if he deteriorates.
Would you offer inpatient pembro monotherapy as a palliative time-limited trial here,if I dont -my understanding from the ENT team is it will be palliation? really appreaciate your thoughts @gutonc
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I didn’t read every detail but when I see the words high risk and teach I wouldn’t think IO monotherapy is going to work fast enough
This case sucks.
LOL at inpatient pembro. If you can get that approved, you're the real MVP. Also, agree with @HemeOncHopeful19 that it's unlikely to have any meaningful benefit on a timeline that is clinically relevant to him.
Honestly, if there's no local therapy to consider for the active bleeding, this is a hospice situation.
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Thanks both @gutonc and @HemeOncHopeful19 — really appreciate the replies. After speaking with him directly and confirming capacity, he very clearly understood the risks/benefits and opted for hospice.
My ENT surgeons are excellent, but I think in these airway/bleeding cases “pembro” can sometimes get treated as if it is magic. Your comments were very helpful in confirming my concern that it was unlikely to work quickly enough to matter clinically here.
My ENT surgeons are excellent, but I think in these airway/bleeding cases “pembro” can sometimes get treated as if it is magic. Your comments were very helpful in confirming my concern that it was unlikely to work quickly enough to matter clinically here.
It also costs the hospital about twice what the DRG will pay for that entire hospitalization. So only a pharmacist looking to get fired will give it as inpatient.
At tumor board, someone may bring up getting a brain MRI, which I think is reasonable.
If it unfortunately does show CNS metastases, that would obviously factor into how you tailor the treatment approach.
Not asking for input on this, just kind of a cool case from top to bottom.
82F, sent by PCP to our infusion unit for Prolia for osteoporosis. My RN checks BP on right arm and it's 80s/50s. Patient says she usually checks her left arm in the morning and it was 140s/70s this morning. So RN checks left arm and, sure enough, 140s/80s. Calls PCP office and says "this is weird, thought you should know".
PCP orders CTA chest same day, gets done 2d later. Shows near complete occlusion of right brachiocephalic artery but also shows 8mm RUL and 3cm LUL lung nodules. Gets sent to pulm who orders a PET which is hot in the b/l nodules and the rectosigmoid colon. Pulm bronchs her. Gets tissue from both nodules.
Right: Adeno. TMB high. MMR proficient. PDL1 50%. No first tier mutations but has MSH6 mutation.
Left: Squam. TMB high. MMR proficient. PDL1 0%. No first tier mutations but has same MSH6 mutation as right adeno.
So I see her yesterday. ECOG 1. Not at all interested in even talking to a thoracic surgeon, which is cool because her PFTs are borderline at best and she'd need a left lobectomy and a right wedge. But totally fine with SBRT. And on questioning, turns out mom had endometrial AND colon cancer, doesn't know dad's history and has a brother with prostate cancer and colon polyps.
So I'm pretty sure she's got a germline MSH6 mutation and likely an MMRd colon cancer. Sent her for colonoscopy and we'll see how it goes.
82F, sent by PCP to our infusion unit for Prolia for osteoporosis. My RN checks BP on right arm and it's 80s/50s. Patient says she usually checks her left arm in the morning and it was 140s/70s this morning. So RN checks left arm and, sure enough, 140s/80s. Calls PCP office and says "this is weird, thought you should know".
PCP orders CTA chest same day, gets done 2d later. Shows near complete occlusion of right brachiocephalic artery but also shows 8mm RUL and 3cm LUL lung nodules. Gets sent to pulm who orders a PET which is hot in the b/l nodules and the rectosigmoid colon. Pulm bronchs her. Gets tissue from both nodules.
Right: Adeno. TMB high. MMR proficient. PDL1 50%. No first tier mutations but has MSH6 mutation.
Left: Squam. TMB high. MMR proficient. PDL1 0%. No first tier mutations but has same MSH6 mutation as right adeno.
So I see her yesterday. ECOG 1. Not at all interested in even talking to a thoracic surgeon, which is cool because her PFTs are borderline at best and she'd need a left lobectomy and a right wedge. But totally fine with SBRT. And on questioning, turns out mom had endometrial AND colon cancer, doesn't know dad's history and has a brother with prostate cancer and colon polyps.
So I'm pretty sure she's got a germline MSH6 mutation and likely an MMRd colon cancer. Sent her for colonoscopy and we'll see how it goes.
As an anaesthesiologist/intensivist I have no oncological input into this fascinating and impressive thread (hats off to your breadth of knowledge), but that has to be the most brain dead airway plan I’ve ever heard of.
I have seen airway centered lesions temporarily swell after immunotherapy administration more than once so you either secure the airway early or not at all. The path suggested by ENT is a recipe for a horrible middle of the night death due to an airway that can’t be secured.
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