[music] Welcome to Derms on Drugs. A video podcast brought to you by scholars and medicine, the best educational platform in dermatology, and totally free for anybody who hasn't checked it out yet. Derms on Drugs is where cutting edge derm meets, uh, hit her Miss Comedy. I'm Matt Zyres, and each week I'm joined by my residency buddies, Laura Ferris and Tim Patton, to use our 60 years of combined derm experience to debate, discuss, and dissect the hottest topics in dermatology. It's everything you need to know to be on the cutting edge of dermatology, and it'll be the most fun you've ever had while actually learning something useful. New episodes drop every Friday, so join us on scholars and medicine, Apple Podcasts, Spotify, or whatever your preferred platform is. Well folks, I gotta tell you, I'm so excited this week, so CTCL has long been one of my favorite topics to talk about and think about, but least favorite things to actually take care of. And we've got a great guest on this week from Memorial Sloan Kettering, Dr. Schemier-Geller, to really talk to us about some fascinating work he's done with DuPillaMab and CTCL as well as talk about CTCL in general. So we are just gonna go ahead and jump right into it with Dr. Patton, here on our taping today on St. Patrick's Day, so Dr. Patton's got his appropriate garb on, and we will let him get us started. All right, my deep dive was titled, "In a grade of epidemiology and immunotranscriptomics, uncover a risk and potential mechanism for cutaneous lymphoma, unmasking or progression with DuPillaMab therapy." This was by Cabara Perez in the November 2024 issue of Journal of Allergy and Clinical Immunology. So first, the epidemiology, the authors went through the FDA Adverse EGENT Reporting System, the Fairs Database from 2017 to 2023, mainly looking for reports of CTCL and mycosophongodes with DuPUs, but they looked at other drugs and other side effects, you know, to see if the signals were legitimate. They did some. I'm gonna jump in right there 'cause I have the Fairs, sorry, but the Fairs Database. Yeah. So Dr. Keller, you've done some work. You've published some stuff from the Fairs Database, correct? Yes, yes. So, is it like patients, doctors, anybody just calling in being like, "Hey, I was on this drug and I, you know, my left eye was itchy for two days." And that could send her. Like, how does stuff get in there? How good of a database do you think of it as being? So there's a lot of reporting bias. I mean, who gets to report there is mainly physicians and the pharmaceutical companies that run trials and other, you know, other investigations into these drugs. So it's. for sure, it's not there. It doesn't describe the incidence of prevalence of their diseases. And also the disease diagnosis, they do not have to report like how the diagnosis was made, was it made by apathyology or clinical only. So it can be very, very unclear the diagnosis sometimes that require some hypothesis. But again, it's like, it's large numbers, specifically when you deal with these zebra's, like, CTCL goes into that category. So it's easier to look into like big numbers when you go into this like. Okay. Big response. Right, because it was like for it, they wanted a negative control and so they picked hand and wrist fracture, right? That would be like, that is not associated or. There's no cause and effect with Dupy. But why would anyone. Well, like, why is there one case of that in there? Who called them up and said, "This guy broke his wrist? I'm gonna put that in with Dupy." I mean, it's weird. We're gonna put it in with any drug, like. Maybe GABA patent, like you fell. You fell, sure. Broke your wrist. Yeah, but if the patient felt while he was on the clinical trial using Dupy, then they have to report it. It's reported. It's reported. And up there. So it's mostly, most likely these are the cases. So what percentage of it. Do they have those numbers? What percentage of it is like from the clinical trial, the reporting there, and what percentage of it is, you know, if a person comes in, you can fill out the forms. Did they have any date on that? Wait, I gotta jump in. Because that is the worst whenever, like, the nurses call them from the drug company. Yeah. Bob, but, blah, you ready for your refill? Or have you been filled? Oh, you know, you've had the sniffles. And then I get a nine-page packet of that, like, just throw it away. But, yeah, I've nobody fills those out, right? I mean, if we think they're. If somebody said, "Oh, the nurse from, you know, "regenre on call and said, "They broke their wrist. "You just don't fill it out." On air, I fill those all out. Okay. That's that. All right. So, even more complicated. They look at a bunch of. Oh, yeah. Dr. Geller would. I say, it gets even more complicated, because some of these cases, they report all of the patient's medication at the time of the incidence. So you end up with, like, 20 or 30 medications. And now, figure out which one was responsible for this fracture, or for the CTCL he presented with. And we started, like, the forest. We did two analysis, one's based on, like, like, poorly therapy or poorly medication, taking anyone who just had DUPI as associated with the CTCL. And the others were only the reports of, like, a monotherapy, saying that it was DUPI causing CTCL. And it showed similar, like, increased risk for CTCL to DUPI patients. Okay. All right. We'll watch. But we digress, Dr. Pat. Yes. I know. I'm curious. We were gressing, not digressing. Yeah. It's always good to interrupt me to be quite honest. All right. So they looked at different measures, proportional reporting ratios, reporting odds, ratios, confidence intervals, Bayesian something. I liked AE Score the best, so the AE Score it accounted for limitations inherent in the PRR and ROR by assigning higher weights to events that occur often with the drug of interest, and that are disproportionately associated with the query drug. And it assigns lower weights to events with low case counts. So we were talking before the show, "Lebry. " No. "Trail O'Kill You, Mab." Had the highest PRR. That was the proportional. proportional reporting ratio. It had the highest, but there were only two cases of CTCL when the trail of patients. So by doing this calculation of the AE Score, the AE Score wound up being very, very low for trail low. So that's the one I focused on, because they have different charts for RORs and PRRs. The AE Score, I think, kind of cleans things up a little bit. Got to say for our listers, Pat, and just pronounced it, "Trail You Kill You, Mab." "Trail." It is not "Trail O'Kill You, Mab." "Oh, Kill You, Mab." "Trail O'Kill You, Mab." "Trail O'Kill You, Mab." "Trail O'Kill You, Mab." They don't want to call it "Kill You, Mab." No, no. That's a horrible name. "Terrible." "Kill You, Mab." All right, supplementing figure one C shows where CTCL falls compared to other reported conditions in the "Deep Hill You, Mab" patient. So this was just a chart of the AE Score versus condition. And CTCL actually falls in the middle. Like the highest AE was pruritis. Do you think "Deep Because" is pure pruritis? I do not. AE for conjunctivitis was high. I think we all think "Deep Because" conjunctivitis. So it's almost like a combination of yes, maybe true side effects, but maybe also just the patients themselves, not necessarily the drug. You had higher AE scores for sunburn. I don't think that's the result of Dupy. Milliaria CTCL had an AE score similar to Karateconus, which is, I think, part of a topic term. ESinophilic granulomotosis and polyngiitis, which I don't think Dupy causes that. But I think it's in the. I don't know about that. I think those patients are hyper-easinophilic. They're kind of in that. Yeah, learning. Yeah. And morphologically, maybe they had something that looks like exoma. So it's supplementary figure 2A through D. They plot AE score versus a chi-square. So a higher chi-square means that the association is less likely by chance. So in these graphs, if you're in the upper right quadrant, that's something that happens disproportionately reported with Dupy and very unlikely to occur by chance alone. So the events that occur in those upper right quadrant are CTCL, but Erdicaria shows up in that upper right quadrant. So does pruritis. So does congenit-junctivitis. So it's very tricky, especially with this large database, like do we have a true cause and effect. But CTCL does keep showing up. They looked at other drugs, and using that same AE score, Dupy had the highest AE score, but you stick in, you map, IL-23 inhibitors, IL-17 inhibitors, they all had AE scores that were higher than 2.5, which is what the author has kind of said. That's the number where it above that, it is probably meaningful. Now, so that's the epidemiologic stuff. Do we want to say anything about that before going on to the transcriptome, or do we just go on to the transcriptome? Dive on to the transcriptome.
I just I remain I remain unconvinced the fact that it's listing peritis as like For and the far upper right just like CTCL I remain unconvinced yeah All right the transcriptum stuff looked at bulk tissue single cell expression aisle 4 R a and the aisle 13 R a1 And care tenisites and DCs and healthy tissue and AD patients and CTCL I can't say I totally understood it to be honest. It was too many things going on It was like DCs have this and care tenisites and there's overlap and healthy skin and atopic and CTCL So I understood it and I was reading it, but as soon as I was done reading it I could not like Tell you what the big summary was the author summarized the forest and they say look This is how this mechanism happens care tenisites and atopic patients. They act as an aisle 13 sink When you give doopy to patients you block the care tenisites from sucking up the aisle 13 There's more aisle 13 available in the environment to drive CTCL cells I mean it seems to me that doopy would also bind to the aisle 13 receptor on CTCL cells I know that blocking them from using aisle 13 so the authors don't really go into how the CTCL cells somehow overcome this Nice little picture at the end of the supplementary just kind of going through their theory and what they think caused it I don't think doopy causes CTCL I think that there are patients who have CTCL incorrectly diagnosis atopic thermor or maybe What a any good dermatologist would say okay? This could be a topic term because of the biopsy this that the other and they give doom doopy and it unmasked CTCL I'm not buying the cause and effect Which means it is probably true that is probably true good, but I I'm not I'm not entirely convinced And we're gonna get into that in depth as we go forward. I just write this article did nothing to convince me Basically, they said there's lots of there's lots of aisle 13 in the tissue and somehow that's good to magic black box Somehow, that's how it's driving CTCL literally did nothing to convince me of anything But we'll say I think we wouldn't we have Dr. Geller's article coming up It did convince me that there may be a possibility But before we before we go that far Dr. Ferris let's let's jump over to your article Which really changed something that I've been tell it changed when I'm been telling patients since residency I'll let you go ahead All right, so my article is overall and cause specific mortality among patients with Coutaneous T. Salon Fome in the United States, shea at all. This is in the year European Journal of hematology spelled the wrong way with an A E as then instead of just an E. We just got to point that out So this was a C-R-18 registry data So almost 10,000 patients who had my co-sus fungoides Cesary syndrome primary cutaneous Plastic large cell lymphoma subcutaneous paeniculitis like T. Salon Foma So kind of all the subtypes diagnosed between 2018 As you can imagine the majority of these patients had Had MF so about 80% of them did and only about 3% had Cesary syndrome so little bits of the other ones so what were kind of the interesting things here? So one The study so you know one was that like everybody has an increased risk of mortality so Even patients with early my co-s early stage MF had increased risk of mortality a standardized More to SMR of 1.2 so not like a huge increased risk, but it was there for everybody It's 20% 20% above no more like what you would expect so that's like so it's the ratio basically of observed deaths in the study cohort Attributed to to that cause versus the expected in a control population So so this is what changed from it so wouldn't we were residents? I swear that I was caught up that inside ways that people with early stage MF had no increased mortality compared to The general population we were 100% told that right so we were told oh this is a you know a disease But it is a cancer, but you're you know your risk of death is not higher So this would tend to you know repeat that so you know other like other important things so Let's see that we that we found here so other malignancies were sort of were We're increased across all of the different subtypes CTCL was the most common cause of death across all of these groups as well, so It's you know there was a ton of hot and then a lot of Hodgkin's lymphoma particularly among the MF group I think that was the only one that really had that increased risk I would have just more mortality from leukemia to MF primary ketanus the anaphylastic large cell and socutaneous Neculitis But not in cesareous syndrome the other thing was that the risk of sepsis or Infectious death was actually pretty low. I feel like that was something that we were told was a big cause of mortality among these patients and that was actually Not not the case Most deaths from lymphoma So most deaths in the first year are actually from lymphoma, so that is probably in that first year after diagnosis the time to monitor them And not surprisingly the cesareo hoort had the pores overall survival So you know what was there kind of take home message from this is that need need for better therapies and then closer Follow-up for patients with CTCL regardless of stage. So basically we can't just say early stage disease You don't need to worry about them those were my big takeaways from This study. Yeah, it was a it's a big change for me I mean I was with my early stage people. I was like well, we're gonna send you to the CTCL center, but you're gonna be fine. Don't worry about it I'm gonna have to kind of change what I'm telling people and So that's a color is the Hodgkin's lymphoma connection is that like unknown Like I guess I don't Seems those like there are two different cancers to me CTCL and Hodgkin's lymphoma like what's the is there a real connection there? So we do see a lot of patients with comorbidities and their Hodgkin lymphoma is definitely one of the other hematological conditions we see in patients with my causes for goddess and usually it's like his history of Hodgkin lymphoma There is some some there are some thoughts that the treatments for the Hodgkin lymphoma might cause some Immunomodulation of the you know of the T cells which make it easier for New clones to emerge and develop on the skin And so definitely it's something that is well known and we do get to see it other entities like lymphoma paupulosis Also get to be seen right Equently in other in with other like hematological conditions. So I mean, I completely agree with what you mentioned Also, this is what I learned that this is still what I usually tell my patients I do tell them that even in the early stage disease there is a chance of something like 10 to 15% of the disease to progress to a more advanced Disease but overall the you know the lifespan is gonna be the same as the normal population We discussed that before. I mean all of these like big data Registry is they have a lot of biases. So it depends on what was reported and you know what's there They you know the diagnostic criteria that was used and there We we do see that the early stage like 1 a1b which just had patches and plaques they have like overall great survival and Specifically nowadays that we have a lot more like offers like treatment offers to other to these patients So so I guess the other take from point for dermatologist like me who the minute that they see any sort of cutaneous lymphoma send it to somebody else Was that actually they were patients with MF word increased risk of death from skin cancer. So maybe that means you know I should still Follow them with their non CTCL issue. So I thought that was interesting too. I don't know what that again. Bye. You gotta keep them and do the biopsy And cryo generate the revenue for UNC and then send somebody else for their CTCL and let them do the 45 minute visits with no procedures That's what send those to Duke I thought that was an interesting thing but they die more from skin cancer. So yeah at Memorial We keep these patients again, and sometimes we just explained to them that it's good to be also followed by someone who knows this disease Because sometimes it there are like tricky elements there some of these patients do start like to rapidly progress and it's good to have someone So that they can contact and be seen like immediately. So even the 1A patient some of them have just like a single patient
patch the same always same area just using clobetansol I get to see them at least once a year. We you know unless the patient doesn't want to come and then he knows that if something fliers up you can always reach back but we also the early stage because it is like the small amount of patients who do develop more aggressive disease can really become very sick. So we prefer to keep them close. Alright that's funny. I do have a couple of like CTCL patch plaque diagnosed you know 15 years ago and now I do see them further other skin stuff. Do you ever see that? Do you ever see patients who have like CTCL 15 years initially diagnosed and then it blows up or if you get 15 years out from like a patch plaque diagnosis are you pretty much like yet the CTCL is not going to be a problem in those patients. Yeah usually this is the case usually if the disease becomes aggressive it happens in the first like first or second year. It's rarely to be seen like decades after that but again some of the patients as they get older the immune system probably becomes weakens and then you know things do change. And again some of them even they are from the era of getting at least like poof a treatment. They have several of these patients so even if it's not directly associated with their disease it's they do develop like very nasty non melanoma skin cancers and other things that require them to be under better control because of the adverse effects of the treatments they receive. Alright before we go into your article one one basic CTCL question just two and I like literally if I see CTCL at this point I just immediately said it was a university so I haven't thought this through in a long time. Remind me of how staging works is it stage one is skin limited disease stage two it's an Olympian node stage three it's in your blood and stage four you got tumors or like how what's the very basic thumbnail sketch of the staging. So it goes based on TNMB so it is like for the tumor for the skin compartment and then you have the nodes compartment and then you have the the B is for the blood compartment and you have M which just drives them to the highest level right metastasis if it's like in the liver in the bones in like anywhere that on the lymph lymph lymphatic system. And then for astromatologist the most important is to understand what's going on on the skin. If it's just patches and plaques up to 10% of the body surface area then the patient and the patient has no lymph nodes and no blood then is in one a stage which is the lowest. One beats if he has patches and plaques which are up to 80% so between 10 to 80% meaning he's not a retrodermic so then he's like 1b. If he does develop lymph nodes that will bump him up to 2a. Now what if they are just feeling lymph nodes get you to 2a because they could be reactive does it have to be a biopsy proven? Sometimes we try to get a biopsy but sometimes it's you know it's very you do a patch can you see that it's a clear cut and that will just put them into the 2a. And again 2a is just based like you said on a clinical palpation and if the biopsy does show that there is like involvement then it will be like a 3 stage 3. But for the skin if it's 2 more or a retroderma then that will make them into like stage 2b which is the first part of the advanced stage disease. They have much poorer prognosis and interestingly they even have a poor prognosis compared to the stage 4 which is their retrodermic patients. And within that you know the ones who do have like lymph nodes that will put them into stage 3 as well and the ones who have blood involvement that will put them into stage 4. So it's like it's an integration of the 3 compartments. So usually when we see I mean for one a you don't need to do all of the staging but for usually 1b and above we do sent them to PET scan or CAT scan. We do a blood work to see if there is like any circulating clone in the blood which is a clonalities testing and flow cytometry. And based on that you can say if the patient is like early stage versus advanced stage. And we can kind of think of it as early stage as skin limited maybe some reactive lymph nodes late stage. It is definitely malignant cells in your lymph nodes your blood somewhere and 2 more or every 2dermac. Okay. If he has even 1 tumor that will up stage in their prognosis is much worse. Okay. All right. So let's go ahead and get into our Dr. Gellers paper here that again just a Dr. Ferris' paper really changed the way that I think about. Sort of early stage CTCL and I'm going to be a little less you know I don't worry about it. So I'm going to kind of give our audience the very brief summary of CTCL and Dupy. So early on people thought Dupy might be a treatment for CTCL so the group out of Northwestern treated a number of people with known CTCL and they got worse. And so then it was like, "Woo, go!" Maybe Dupy makes CTCL worse and then we didn't hear a whole lot about it with your case reports for a while. Then about a year and a half, two years ago study started coming out that were basically like let's look at a big database and see if people who go on Dupy are more likely to get CTCL and these were all saying yes. People who went on Dupy were more likely to get CTCL than people with AD who didn't go on Dupy but all of those are just dumb studies because they didn't control for the severity of disease. So the real fundamental question is there's some number of people who clinically and histologically it's you cannot tell that it is not a topic dermatitis. You should look at it and it looks like dermatitis, you buy up some, come back dermatitis even if you buy up so them and say I think this might be CTCL, it comes back dermatitis. And you're not going to find out that it's CTCL for some predefined period of time. Now those are generally people with relatively widespread disease and so the assumption has been that it's that if you go on Dupy it means you've got over 10% BSA, over 10% BSA is probably a risk factor that maybe you've got CTCL that is masquerading as a topic, Derm. And then when you go on the Dupy the AD is going to clear up and now the CTCL is diagnosable that's been the general idea and there hasn't been a single study that really you know deviated from that pattern at all. And then Dr. Galler published back in the very beginning of 2025 this year looking at all of his all of their patients in memorial Sloan Kettering and essentially turned out there were 30 cases of maybe 32 cases I think of people who got diagnosed with a topic Derm then got treated with a systemic then got diagnosed with CTCL. And of the 32 cases every single one of them had been on Dupy now some of them had also been on a Jack two of them had been on a Jack at some point as well but the other 30 every single one had been on Dupy not a single person on trailow not a single person on a Jack inhibitor without ever having been on Dupy. And at this point right so this came went up through 2024 in their clinic like we've had Jack inhibitors for several years we've had trailow for a number of years there been enough people on those drugs now that if this was just you know, a CTCL masquerading is a D it seems like pretty unlikely that every single case would have been treated with Dupy and so that is the first it's the first thing that makes me say well maybe this is like not just a class effect of systemic drugs for a D but nothing related to Dupy and I'm going to kind of you know that was my interpretation of the study let me just read the title of the study here so that if anybody wants to look it up and we always forget to mention this but the scholars and medicine platform and on are the sites where the podcast is running we have slides that go along with this or the key visuals and tables for most of the articles that we talk about are there. But so it was diagnosis of Coutaneous T. Sellum Phoma following exposure to biological agents for a topic during a retrospective cohort study from a single tertiary cancer center first off there was a medical student last name Leo and Dr. Geller our guest was senior author so Dr. Geller I'm going to kind of open it up to you what you know it was a great idea and so I'm assuming you started doing this study thinking geez pretty much everybody we've seen who's got this story has been on Dupy and just you know you're a CTCL guy to how do you read this whole situation at this point. So you mentioned like the farest database before and we discussed that also before before the broadcast but you get all of these loud data sets and then you start us
asking yourself how accurate are they? Is there how much confounding there is, how much biases are into them? And then you go back to your clinic which you know you control very well. You know exactly what the patient has and other exposures and for how long they've been on all of these drugs. And then I wanted to go back and see, if indeed I see this increased risk that you that is well described in the case series and case studies but also in these big data sets. And we ended up doing this. We just took all of the patients that we saw with any biologic therapy and we tried to understand what are the patterns that we see. So of course you cannot make causality based on that but there is like some story that you can make out of it. And I think that more than the fact that it's only Dupri that we found that is like an exposure that it is associated in these cases with the CTCO. It's also the fact that it's only Dupri for a topic dermatitis. So many people ask me, you know, so Dupri is a very CTCL and I say immediately no 'cause if it was causing that it's nowadays it's given for a lot of other like etiologies. So I would expect to see patients with CTCL who got it for like as a phylic acid for gyrids or for asthma and we don't see that. And we don't see that in the literature either and we don't see that also in some of the literature that like the paper that was published by Hassan et El I think you talked about that in the JAD that looked into trynet X about like Dupri and CTCL. It was only in a topic dermatitis patient. So it's something specific about this like triad of a topic dermatitis, Dupri Lumab. And I would say a CTCL that is at the background. I don't think that the Dupri is actually driving a topic dermatitis into CTCL. Although there is a lot of epidemiological studies showing that patients with a topic dermatitis they have much increased risk of developing cutanoclinforma based on like the long term like a like antigenic exposure and antigenic and so I'm gonna do one of my normal interruptions here. So when we were residents we were taught that the majority of cases is CTCL. I don't know if that's hit the majority, but often it was chronic dermatitis, chronic stimulation of your lymphocytes. And I think I mentioned to you in an email that maybe that I was almost, I almost have thought of it the same way you think of a Marjolins ulcer. Right. If you got a chronic wound and you're constantly your keratinocytes or turning over, trying to heal that eventually one of them mitosis one time too many and it's that a general getting stepping away from the Dupri to Pillermab or Dupix and aspect of this. Like how do people think of chronic dermatitis is driving CTCL at this point? - So yeah, it's still the same ideas are still exist. I would just say that there are some ideas recent in recent years also about the microbiome effect on that. But that also works the same way, just that this chronic like stuff infection and chronic infection, skin infection in general, they're just also serving as a super antigen, causing this chronic like chronic inflammatory process that is keep the T cells and the lymphocytes secreting this cytokine and having this high profile inflammatory conditions that eventually causes the emergence of this monoclonal population that is getting out of control and populates the skin and you end up with a lymphoma. But you see that also not with cutanis lymphoma, you see that also with non-hotchkin lymphoma that is other than skin lymphoma 'cause some of the studies, epidemiological studies, they try to rule out these cases of cutanis T cell lymphoma just because it's so hard sometimes to differentiate. 'Cause even if you do clonality tests, you we know that some of the topic dermatitis, you have these entities of like clonal dermatitis, you end up with a clone that is like dominant in a inflammatory or reactive process. So it's very complicated. So some of the studies just looked into the informers without the CTCL component. But here like several studies done both in the US and also international showing that there is an increase in these cases and now the thoughts are that these are probably patients, either it's like clearly like misdegnosis but not necessarily these are all the cases, right? 'Cause eventually we do see end for example in this study that we are discussing now about 70% of the patients who received DUPI were patients who had like a biopsy before they received the DUPI. So the outside dermatologist did great and they wanted to confirm the diagnosis before starting biologic and ended up with a result showing a topic dermatitis. And some of these biopsies also were reviewed by our pathologist and they agreed was a topic dermatitis. So is that any point? - So is that any point at any of those cases to see if there was a clonal T cell population prior to starting this? Like I mean could there be that there's, you know, this antigenic stimulation you start to develop a clonal T cell population that's not malignant and then you shift sort of the tumor microenvironment by putting in, you know, DUPI and now that we know that TH2 responses are maybe important and protection against some kinds of skin cancer and then you shift that tumor microenvironment and now that clone can transform. Like so was the clone ever there before the DUPI and then did it just go back? - We are one of the studies we are ongoing, like ongoing and we definitely looking to that. I mean for us it's we need to get the material from outside. This is the difficulty in dealing with such rare disease 'cause you need to get like the blocks and to hope that there is still some activity that will show up in the TCR. - I saw in your study that you guys of the 20 some biopsies, you guys were able to get five of them to review. Which and I'm sure you had medical students like calling the path labs, going to the path labs, knocking on the, yeah, it's hard to get the outside block a lot of the time. - So since we have thousands of dermatology listeners on our podcast. (laughing) If anybody has a case of a patient who was developed CTCL and DUPI, should they reach out to you if they have the biopsy pre-treatment? Maybe we'll funnel, we'll feed research here on Derms and Drugs. - So everybody, I hope you really enjoyed that conversation with Dr. Geller and we go even more into depth on CTCL, but only over on the scholars and medicine platform. So if you wanna hear the rest of the content and hear an even deeper dive, go over to scholarsinmedicine.com. You can Google that and you will be able to find our full discussion on CTCL. We're gonna cut it off there and move over to our trivia section of the show. And last, Pat, and Ferris, either of you guys have any additional questions for Dr. Geller. - Now, trivia is. - Patent? - All right. Yeah, let's go. - All right, so Dr. Geller, we gotta let Pat and finish the question, but as soon as he's done reading the question, you can jump in, just shout out the answer as soon as you got a guess. - Okay, we're sticking with the theme of my co-sus fungoities. What agent received approval on March 15th, 1949? That's right, 1949 for the treatment of multiple malignancies, including my co-sus fungoities. - Nitrogen mustard. - It was nitrogen mustard. - Woohoo. - Oh, technically mechlorethamine. It was approved to treat malignancies of lymphoid tissue way back then CTCL did fall under that. I mean, they didn't know what they were treating and it was IV back then. But some of those patients were my co-sus fungoities people. - Is mechlorethathine actually nitrogen mustard or is that a different thing? - No, that's it. - No, that's it. - Okay. - Yeah. - Cool. All right, one, one, nothing serious. This could be my first win. - Yeah, that's strong out of the gate. I like it. All right, Albeiro-Sezerie described the patient with a Rithriderma and cancerous cells in the skin and blood. The French term that he used to describe these cells could be translated to what scary sounding English term? So now he call them Cezerie cells, but what did he call them? - Scary sounding English term. A cerebral form. - No, that's not terribly scary there, man. - He's kind of a woman, that's scary, see ya. - He called them monster cells. - Oh, that is kind of scary. - All right. - I mean, he said it in French. - Well, that's right, there's something, yeah. - Most of you say, "Is that you, Leim-Molst-Thorl-Sé?" - Monstrous cells if you wanna be technical. But yeah, that was what we called them, I guess before we started calling them Cezerie cells, which is kind of cool. - Which is kind of cool, actually. - Wait, what does cerebral form nuclei in again? - Those are them. - What's them? - Okay, all right. - Cezerie cells, yeah. - Okay. - Okay. All right.
Last one on tack. That's the brand name. It was approved in 1999 for the treatment of CTCL. It was withdrawn from the market in 2014, but reintroduced to the market as lymphere in 2024. Lymphere is a fusion protein of interluchin two and what talks about diphtheria toxin. It's diphtheria. That's a tie. I got a tie. That's the best. That's why I had to yell it out really. Yeah, I want to see how well you know your seat. It was TV. It was all CTCL. It was just too easy for him. All right, that's it. All right. I would. Shemeer, thank you for coming on the show. This was great. And I feel like I am caught back up on the world of CTCL. And this was this was just a lot of fun. I'm having like another three physicians who are excited about CTCL. That's you know. It's a brand that's Dupy and DTCL. You're the parents every day. Yeah. To our listeners, thank you for joining us this week. If you got questions, comments, ideas for topics we cover on the show, shoot us an email at
[email protected]. If you got any of those cases of CTCL following Dupy, don't hesitate to shoot me an email. And I can connect you up by our shoot us an email. We can connect you up with Dr. Geller and whether that goes anywhere or not, who knows. But it's an interesting area. I hope you learned a few things this week. I hope you left once or twice and most of all, I hope in your plan and to join us next week. And until then, I'm Matt Zyrus. I'm Tim Patton. And I'm Laura Ferris and we are Derms on Drugs.
PodcastTranscript AI