The Oncology Podcast

The Oncology Journal Club S3E4: ASCO 2025 Special - Part 1

• The Oncology Network • Season 3 • Episode 4

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Welcome to The Oncology Journal Club Podcast Series 3
Hosted by Professor Craig Underhill, Dr Kate Clarke & Professor Christopher Jackson | Proudly produced by The Oncology Network

Welcome to the Oncology Journal Club ASCO 2025 Special – Part 1! This is where we take a famously different approach to oncology research.

If you're after an enlightening and entertaining take on this year’s ASCO meeting, the OJC team has you covered – blending expert analysis with trademark humour.

Our hosts go beyond the standard presentations to explore what the research really means for clinical practice.

For links to the abstracts and bios of our hosts, head to the show notes on oncologynetwork.com.au.

Subscribe to The Oncology Newsletter for regular updates on the latest cancer research and join our community at oncologynetwork.com.au.

The Oncology Podcast - An Australian Oncology Perspective

Speaker 1:

Welcome to the Oncology Journal Club ASCO 2025, special Part 1. This is where we take a famously different approach to oncology research. If you're after an enlightening and entertaining take on this year's ASCO meeting. The OJC team has you covered. Blending expert analysis with trademark humor, our hosts go beyond the standard presentations to explore what the research really means for clinical practice. I'm your producer, rachel Babin, from the Oncology Podcast, and I'm joined by our brilliant hosts, professor Craig Underhill, dr Kate Clark and Professor Christopher Jackson. You'll find links to all of the abstracts in the show notes at oncologynetworkcomau. And don't forget to check out part two. This episode is proudly brought to you by the Oncology Network's podcast team.

Speaker 2:

Well g'day kia ora, kia ora. Welcome everybody to our Trans-Tasman Perspectives on ASCO, the scientific meeting in Chicago. We're going to quickly go through quite a wide number of papers and abstracts from the meeting. Hi Chris and hi Kate, kia ora. So there was quite a lot of news out of ASCO. I saw there was 10 simultaneous publications in the New England Journal of Medicine. So that seems to be the thing to do and that adds to the probability of the discussant saying you have a practice-changing treatment if you get a simultaneous publication. There was also simultaneous publications in some other journals and one that we won't have time to go through today oh, it's Tintin from Kansas One paper published in JAMA showing some clear benefits in a randomized clinical trial for robotic surgery versus a standard of care for patients with lower and middle rectal cancer. So we might talk about that even at the next episode. I think that would be interesting to go through.

Speaker 2:

I saw a tweet from ASCO. There was 44,000 attendees. 40% of those were from outside of the US. I wondered if the numbers might be down this year because of the travel issues in the US and overnight Trump's banned people traveling to the US from quite a number of countries. I think there would have been some people hesitant to go, but I found a tweet from ASCO this time last year. Hesitant to go, but I found a tweet from ASCO this time last year which said there was 45,000, so really no significant change, maybe a bit of a plateauing. You would expect that the numbers do creep up every year.

Speaker 2:

I did notice, however, one notable attendee was spotted at the meeting and that was Steve Vogel from New York. So we had heard that he'd retired. Turns out he'd retired from his practice in the Bronx, was still doing a little bit of work in the lung space, but no longer a general oncologist, so that caused quite a flutter of excitement amongst the Twitterati. Some suggested that he should get a merit award like the gold microphone or something for asking the most insightful questions. So I hope he did get to ask a question. Interesting to know. If any of our listeners know about that, please let us know.

Speaker 3:

We could call it the Vogel Award for the best question of all of ESCO.

Speaker 2:

Exactly, and I did notice a tweet from Clifford Hudders as the ESCO CEO and he was basically advocating and talking about the President's proposed budget with the NIH and other scientific funding cuts. And Clifford said slashing federal research funding at a time when science is revolutionizing cancer care risk leaving millions of patients without the promise and potential of life-saving breakthroughs. So this is really a global issue and well done Esco for leading on that and leading on its advocacy. And it's worth thinking about, when we go through all this data, the amount of money and effort and funding that's gone into these breakthroughs, which take many years to come to fruition. So the real consequence of those cuts we're not going to see direct job losses, but the impact on scientific advances will unfold over many, many years.

Speaker 3:

Yeah, we should pay attention, Craig, on this podcast as to which of the research studies are publicly funded versus pharma funded. I mean overall medical oncology in general. About 90% of studies are pharma funded, but it'd be a shame to see the entire field too commercially.

Speaker 2:

And just the other general comment I'd make is there was a little bit about AI creeping in, which is great. Asco launched an AI tool to help interrogate their guidelines, not intended to give treatment recommendations, but as a tool to help clinicians search the guidelines more efficiently, to come to the section pertaining to the patient in front of them or the patient they're about to see, and give some guidance. So I thought that was interesting. And also there was a paper, Abstract 1116, a deep learning model being used in the pathology space to predict HER2 positivity, apparently better than pathologists at finding HER2 positivity, which, Kate, you would not understand this probably better than Chris and I. But that's now become a big issue, hasn't it? Breast cancer, Because even a little bit of HER2 positivity means patients make benefit from the anti-HER2 drugs.

Speaker 4:

It's also very labour-intensive, particularly the fish amplification readings. So if we can do that with a computer, we can save our pathologists for the tricky questions, as their workforce is under significant pressure all around the world. So I think that's really promising.

Speaker 3:

Can't wait for them to do K67 and neuroendocrine tumors.

Speaker 4:

Same problem, they're still counting.

Speaker 2:

I think all of our fears to date about AI have been mostly centered around taking jobs off us, but the suggestion to date has been that these will be very useful tools to help us in our day-to-day practice. But we'll wait and see. Kate, did you want to kick off with? There was some potential practice changing stuff in breast cancer. In fact, breast was one of the tumor highlights in this meeting, I think.

Speaker 4:

Yeah, so I'll start out front with the breasts because that's where they are. So I'm going to start with LBA-109, which is an ASCENT04 trial and also a keynote D19 trial presented by Sarah Tulaney from Dana-Farber and Harvard much in the news at the moment, poor loves. This was looking at first-line metastatic triple negative breast cancer in the population that are PD-L1 positive. So very niche group of patients but a one-to-one randomization. Sazitazimab-govertican still the hardest drug name to pronounce, which is a trope monoclonal antibody drug conjugate and Pembrolizumab versus dealer's choice of chemotherapy plus Pembrolizumab. The dealer's choices were sensible, however.

Speaker 4:

440 patients, median follow-up of some months Handwriting has let me down there. Progression-free survival has hazard ratio of 0.65, 11 months versus eight months. Median duration of response in responders Always think this is a bit naughty to report 16 and a half months versus nine months. There's a trend to OS. It's immature at the moment. I'm looking forward to seeing what the crossover plan was, because this is a combination versus not as effective as you'd like, chemo plus Pembro, but definitely the Sazetazumab is an active drug, so that was interesting. All up though, sazetazumab, which is given two weeks out of three and costs twice as much as Pembro, that's a lot of money to be spending on therapy. So until that becomes, the significant toxicity in this group is financial.

Speaker 2:

Kate, there was some commentary around that this meant the end of upfront chemo in triple negative breast cancer. Do you think that's accurate or still too early?

Speaker 4:

Oh look, I think in many jurisdictions where, once you've got something FDA approved, you get funding, great, but in those of us that live in the real world, we are decades away from sasitizumab govatican. It's also, I understand, quite tricky to ship around the world. It needs a special cold chain, which is one of the reasons it's so expensive.

Speaker 2:

Sasitizumab govatican.

Speaker 4:

Got the numbers on the end too, isn't it?

Speaker 2:

Letters on the end E-X-Z or Zed or something that's been our favorite drugs that we've been following the development of over the years on the podcast.

Speaker 4:

Particularly, as I think the phase one was presented by a man who had the best accent ever. So it was says it doesn't make, which is actually how I learned to say it, because it's got rhythm, so it doesn't make. Then we are going to go to another kind of breast cancer. So LBA4 trial called Serena 6, presented by the lovely Nick Turner from Marsden, this was looking at women with advanced breast cancer Again a little niche. You had to have been on six months of an aromatase inhibitor and a CDK4-6. It could be any of the available three without progression. Then you got circulated tumor DNA and I haven't looked into what tech they used, I apologize looking for ESL1 mutations every couple of months and then if you were found to have a mutation, which happened to about 50% of patients during the trials follow-up period, you were randomized to either staying on the AI or switching to chemizestrant, which is an oral delightful vestrant but you don't have to get jabbed in the bum for it. And you sat in your CDK for six.

Speaker 4:

This is where I argue with Nick and I would probably need to do this with some significantly more mana than I have, significantly more knowledge than I have. Sorry, translate that for the Australian Primary endpoint of PFS progression of free survival. I'm not sure if you can count that from randomization if you change your drug halfway through, but anyway, you stayed on your CDK4-6 for longer if you switched your hormonal partner when it looked like you were developing a resistance to it. I think is the outcome of this trial. But curiously, pfs, which is at post-trial, also has a HADAR ratio of 0.52. So there's something going on here. Changing the biology of people's cancers or maybe getting resistance at very low volume is advantageous. Again, it's another one. I'd quite like to wade through the paper, but I would argue that it's not a PFS if you switch a drug halfway through.

Speaker 2:

Interesting. So I've had a lot of patients Kate on the original, not a lot, probably close to 10 on the original access program for fulvestrins. That was a very effective drug in women who'd failed other hormone treatments. It's quite impressive. So it's great to see there's an oral version because in fact they had deep IM injections into two buttocks once a month. They didn't seem to mind doing that because they were still alive and their disease was in remission. But yeah, great to have an oral drug.

Speaker 4:

I feel sorry for Fulvestrin, it was too late. The first tests were half dose, yeah, so it's kind of always been Johnny come lately, but it's going to be replaced by the oral cert. I went to LBA 1008, also presented by Sarah Tulaney, who's obviously had a great meeting also presented by Sarah Tulaney, who's obviously had a great meeting Destiny Breast 09,. So another trastuzumab diruxetan study, first line HER2 positive medicine at breast cancer. I'm fascinated by this. So three arms trastuzumab duroxetan alone, trastuzumab duroxetan, pitazumab and docetaxel. Trastuzumab pitazumab 50% of patients with de novo metastatic disease 50% were hormone receptor positive. The hazard ratio for PFS, comparing the combination of pitazumab and trastuzumab-duruxetan versus our traditional first-line therapy trastuzumab-pitazomab is 0.56, the numerical difference I haven't written it down hazard ratio PFS 0.56 of the pitazomab-containing trastuzumab-duruxetan arm compared with docetaxel-herceptin trastuzumab-pitazomab. The duration of response was more than three years in the combination arm compared with more than two years in the other arm. My questions are we know that we modify both HER2 expression and cancer behavior with each of these drugs in a slightly different way. So it worries me that this wasn't a sequence trial. So I'll be curious to see.

Speaker 4:

Trastuzumab to ruxetan is an incredibly active drug. It was always going to have a prolonged progression-free survival. Does it need the pitazumab? We don't know. Does it mean that these people have a shorter PFS2? We don't know, so I'm hanging out for more data in this space. It is also significantly more toxic and significantly more expensive. So pneumonitis is the problem with trituzole drug stand.

Speaker 2:

That's great and I noticed, kate. We mentioned the New England Journal papers, but I'm pretty sure all of those breast cancer trials studies that you mentioned in fact were subject to simultaneous publications.

Speaker 4:

As a New Zealand public health medical oncologist without an academic post, you'll be shocked. Due to my intellect I have no access to New England Journal of Medicine outside of the abstract where the hospitals have cancelled all of those very expensive journal accesses. So if you don't think you can run medicine in the abstract and you live in New Zealand, please help us protest. Lba5 Matterhorn, presented by Yelena from MSK Gastric GOJ adenocarcinoma perioptive one-to-one FLOT versus FLOT Divalumab, and the Divalumab is very conveniently given Q4 weekly so you only need two pre-op doses and then 10 post-op doses alongside your post-op therapy. Stratification included PD-L1.

Speaker 4:

I couldn't find a mention of MMR status, but you wouldn't expect it to be as big as the. Delta is Median follow-up 32 months. Median event-free survival not reached in the Davalium-Arb arm versus 32.8 months in the Control arm. Median OS not reached compared with 47 months. Respected hazard ratio is 0.71 and 0.78, both statistically significant. 24-month OS 76 versus 70%. There is a relatively big PCR benefit 19 versus 7% but there does also seem to be some disease control pushing beyond a PCR increase. So I'd be curious to see when we are going to get final readout from that. I'm also curious that that managed to get a plenary within the mature data, but it is what it is. It was an upper GI in the plenary, so I should shut up and be excited about that.

Speaker 3:

The EFS, though, in that study was pretty strong, wasn't it? And with gastric cancer, the issue of crossover is perhaps less pertinent than it might be in melanoma or other diseases where the salvage therapy is effective, because it's a pretty ineffective salvage therapy really, unless you've got squames, which you don't with gastric.

Speaker 4:

So that is one of my problems with FLOP. I like it Like FLOP. Flop's development actually is. Even worse is actually when these people relapse. You've got jack, you've used all of the good stuff and you're literally just left with bad players and you say actually your time is short, or maybe we could segue into something that might be useful in the future.

Speaker 3:

Yeah, yeah, we could do. We could segue straight into the HER2 positive studies or the Clawdon 18.2s. Should we finish off with the lead lights? I was looking for the subtitles of that. Yeah, you're done with the lead lights. The breast highlights.

Speaker 4:

Dr Jackson sat in the same lecture as I did when the anatomy professor pointed out that breasts are in fact not like headlights.

Speaker 2:

You mentioned the vep digrestrant, the protech estrogen receptor degrader, and I thought, no, we won't go through this. But a couple of other interesting molecules we're probably going to hear more about is the camisestrin in ESR1 mutated advanced breast cancer, which understands about half of women with ER-positive, HER2-negative breast cancer have this ESR1 mutation. And then also the inovolacib in the PIK3CA mutated advanced breast cancer. Again, that got a positive study, small benefit but simultaneous publication. So we'll hear more about this drug and just highlighting now how, like other tumors, we're seeing there's way more subcategories of breast cancer now than we just had with the based on each hormone receptors and HER2 receptors. We're going to be following, I think, more complicated treatment algorithms in the years ahead.

Speaker 4:

I think, very complicated, because ESR1 is almost exclusively an induced mutation, craig. So it's something that we cause by our therapy, so that's something you watch emerge. So in my head our older oncologist is saying use your best stuff up front, but it's the clever sequencing that's going to be where the future is, particularly in those disease types where we know a little bit more about how the cancer is changed by our therapy.

Speaker 2:

All right. So we heard about the Matterhorn, Chris, and I think you're going to, as usual, lead off on some other practice-changing potentially stuff in GI, and the first one you sent me a message about we've got to cover exercizumab.

Speaker 3:

This is, to me, the highlight of the entire meeting, really, and I think the biggest scandal of ASCO 2025 was that this wasn't in a plenary, let alone not even in the colorectal orals. This was at a clinical science symposium. Jeez, who would have thought? Anyway, this was the academic cooperative group study, not farmer-funded CCTG and AGITG study. Co21, dov in 2007 by Chris Booth, who's been on the OJC before, of course, who's got an excellent first name.

Speaker 3:

This was a randomized phase three study in 889 patients with resected stage three or high-risk stage two colon cancer who are randomized to either health education materials about exercise or structured aerobic exercise and behavioral support. The primary endpoint was disease-free survival, which, as we know, is a validated surrogate for overall survival in stage 3 colon cancer. The secondary endpoint was overall survival, but, importantly, we have some very amazing results Now. The structured exercise program was exactly that. There were about 12 sessions a year for three years and you had to do 10 met hours per week, which is about two and a half hours of sweaty exercise that you have to do, which is a significant amount of exercise. There was behavioral support and supervised sessions, which decreased in frequency over three years and overall adherence was around 63 to 83 percent for behavioral sessions and 44 to 79 percent for exercise sessions, which shows that attendance and adherence deteriorates over time, as you expect for a behavioral intervention. But despite that, we have got some results.

Speaker 3:

And can I please have the ASCO OJC drum roll please? The drum roll please. The five-year DFS was positive for plus 6.4% for the primary endpoint of DFS. My goodness, dfs positive in a colon study. But wait, there's more. I feel like I really am a salesperson for a cheap concrete box shop. The eight-year overall survival was 83.2% in the control group, which is as you'd expect for a stage two, stage three post-chemo population, and the exercise group was 90.3%. That's plus 7% overall survival. I'll say that again plus 7% improvement in overall survival.

Speaker 3:

Now, let's just get that in context. What does plus 7% in in overall survival? Now, let's just get that in context. What does plus 7% in overall survival mean? Well, adjuvant pituzumab in breast cancer is 1.8% at 10 years. Perioperative pembrolizumab in triple negative breast is 5% at 5 years. Adjuvant trastuzumab in breast cancer is 5% at 5 years. Adjuvant oxaliplatin is 5% at 10 years and adjuvant trastuzumab in breast cancer is 5% at five years. Adjuvant oxaliplatin is 5% at 10 years and adjuvant exercise is 7% at eight years. This is a really significant improvement in overall survival and, in fact, the only improvement in overall survival we've seen in stage two or three colon cancer since the mosaic study of back, when I was a trainee. This is really impressive and I think if it was a drug it would get registered and implemented straight away, which is why I think we should fund Exercisermab. So a really important practice-changing study.

Speaker 2:

So it's not a drug but there is a cost, and the exercise programs, the exercise physiologists do come at a cost. But I reckon we should discuss this in a bit more detail, chris, maybe on the next regular episode and maybe get Chris Booth in, because it is a really interesting area and I've always worried about not so much the cost but the ability of the patients who are selected. Obviously, you know they're not superhuman, but they obviously have to be able to do the exercise and the benefits seem to be in that sort of moderate to intense exercise group.

Speaker 3:

They certainly do. And you saw the characteristics of the patients enrolled in the study reflected the adjuvant characteristics of a standard adjuvant trial, which is age 61, whereas we know in our practice it's actually 67, right? So they're a younger, fitter population than you would get in your general practice.

Speaker 2:

Yeah, but it's fantastic to see.

Speaker 3:

Yeah, it really is. And if you did a quick back of the envelope calculation, craig, if you said that an exercise session, even if you said it costs 200 bucks, you know it's a reasonable amount for an exercise session. Sure, 200 bucks for an hour? Okay, times that by 12 sessions a year, that's 2,400 a year. Or what's that? Six $7,000 over the course of three years, which is less than a single dose of Pembroke.

Speaker 3:

Yeah, that's right, it's nothing really less than a single dose of Pembro. Yeah, that's right. It's nothing really. Yeah, it's really not. So I think that was a really important study. It got a standing ovation from the people who were there and a simultaneous presentation in the New England Journal of Medicine's overall survival not often to see it in a strong effect.

Speaker 3:

The other study that caught my eye, which I think will impact on our practice in the very near immediately. Really, really, it's a breakwater study which is a follow-on from the BEACON study. Now, what the breakwater study is is a study looking at mutated BRAF colon cancer, either left or right-sided, not DMMR. So only BRAF mutants who are not DMMR, who were randomized to one of three arms either encorefinib, a BRAF inhibitor, with cetuximab, or encocetux with Folfox 6, or dealer's choice chemotherapy, which mostly was just a doublet chemotherapy with bevacizumab, I think it was. So that was mostly what it was. And again they had hierarchical testing PFS first. If that was positive they went on to do OS. The encocetux was dropped at an interim analysis. Now the headlines there are the median PFS, which was the primary endpoint, was increased from 7.1 months to 12.8 months. That's a 5.7-month approval with a hazard ratio of 0.53. When you look at median overall survival. The median overall survival was 15 months in the control arm versus 30 months in the intervention arm with a hazard ratio of 0.49. Now I don't think the overall survival gain is actually that big because the intervention arm did what I would call skimming the median and so the curve separated and the intervention arm was just sort of drifting along at the median point for quite some time. With a little bit of maturity I think we'll see that overall survival gain shrink back. But nonetheless a five-month gain in PFS with a hazard ratio of less than 0.65 makes a grade of a good ESMO score, at least three plus. Then you have to look at your PFS and your tox data to get an upgrade from there. So it's probably going to be an ESMO four at least. So that's a meaningful practice-changing benefit there. The toxicity was ASCO bingo card, which was manageable with no new safety signals seen and fortunately a four-drug combination. In this situation this patient population did seem to be reasonably tolerable and I think people will regard that as a new standard in a difficult-to-treat population.

Speaker 3:

Other ones to go through briefly the CHIRO-6 study, which was perioperative chemotherapy in peritoneal metastases. This was an important question. We don't actually know the benefit of chemotherapy and peritoneal metastases? This was an important question. We don't actually know the benefit of chemotherapy and peritoneal metastases only from single institution retrospective studies. We know about HIPEC versus cytoreductive surgery alone, but not perioperative chemotherapy, even though we're asked to do it. This included quite high risk patients, including PCI of up to 20, and randomized people to either periodic chemotherapy or surgery alone. And when you looked at the hazard ratios there was only a small separation of the curves at the tail. So the majority of patients really didn't benefit that much from periodic chemotherapy at all. But there is a slight increase in the tail of the curve and the subgroup analysis showed that right-sided primary patient's head has a ratio of 0.2, and that was an effect of synchronous presentation but not on metachronous presentation. So I think that's a study that will reinforce prejudice, but it goes to show that perioperative chemotherapy in periphenyl metastases isn't actually all that effective, even though we're asked to do it all the time.

Speaker 3:

Another death knell for perioperative chemotherapy and resectable metastatic colon cancer. Really, unfortunately, medical oncologists are not trumping these surgeons. We did have Destiny Gastric 04, which is LBA 4002, which was for her two positive gastric or gastroesophageal adenocarcinomas. Those who've got extraordinary memories will remember that Destiny Gastric O1 was a study which showed an improvement of an overall survival of 4.1 months in late-line therapy with a 10% incidence of ILD. Destiny Gastric O4 was comparing TDXD to the standard of care in second line or a standard of care which was paclitexel with remserumab. Patients are HER2 positive by IHC or ish local or central.

Speaker 3:

And getting onto the punchline, there was some crossover there in the control arm and the median overall survival went from 11.4 months up to 14.7 months. So the control arm performed quite well. In the rainbow study of PECRAM, the PECRAM arm did 9.6 months. This was 11.4, so there's no control arm suppression there and TDXD got up to 14.7 months with a hazard ratio of 0.7. 12-month overall survival was up by 9% and 24-month up by about 16%.

Speaker 3:

Ild occurred in 14% of patients of any grade and, importantly, one of the figures I always look for in palliative studies is what's the any grade fatigue, because that's really important in people who've got incurable illnesses. And that went up by 9%, from 39% to 48%. Proms were similar. So you'd have to say that TDXD is now becoming an accepted option for HER2 positive second line or later gastric cancer at that higher dose than we use in breast, and that's at 6.4 mg per kg, understanding that ILD can be a problem for those guys. So three months of gastric cancer is reasonable. Hazard ratio is okay, not an earth shattering improvement, but it is small progress there.

Speaker 2:

Oh my God, are you okay, chris? You just recommended small benefit in an expensive drug.

Speaker 3:

Well, I think it's cost benefit. It's small and I think it'll become an option. It's certainly not an option in my practice because TDXD at that costs $50,000 a dose which no one I've ever met can afford.

Speaker 2:

I'm just going to translate for the general people listening. So that's trastuzumab Duruxtacan.

Speaker 3:

Early in Craig.

Speaker 2:

Trastuzumab, what Duruxtacan, duru, what I don't know. You say it Sounds like a pelican.

Speaker 3:

Yeah, and ILD being interstitial lung disease which is one of the features of some of these emerging innovative antibodies. Speaking of expensive therapies that don't do very much, I did want to mention the Chlordon 18.2 study. So Chlordon 18.2 is a cell surface protein expressed on the surface of stomach cancer cells, adenocarcinomas, and depending on how you score it you score it by IHC you can get Chlordon 18.2 positivity rates of either 40 odd percent or 70 odd percent, depending on your scoring system. These guys used a 40 percent threshold of staining and IHC, which about half the patients have. So around about half the patients with gastric cancer would be Chloridin 18.2 positive by this definition. This used autologous car T cell therapies against Chloridin 18.2.

Speaker 3:

Autologous CAR T-cell therapies against Chloridin 18.2, chinese study. Open label RC2, rct I've not had my dinner yet. Following a failure of two or more lines of therapy and randomized two to one, 150-odd patients randomized and showed an improvement in PFS from 1.77 months to 3.25 months, six-month PFS of 18% to 24% and the secondary endpoint of overall survival improved by 2.4 months, which was not significant. The commentary was that it's a signal and will likely be tested in earlier lines of therapy. But what I think it really shows is that CAR T-cell therapy in solid tumors really is pretty ineffective, even if you've got a good target and we have to do an awful lot more work before we accept it for its cost and its toxicity in solid tumors. So even when you've got a biomarker like 18.2, it's still nothing like it is that we would see in hematological malignancies.

Speaker 2:

I think that's right, chris. I probably take the glass half full approach here. It's really the first steps and I think there'll obviously be more work in CAR T-cell and other T-cell therapies and cellular therapies and hopefully we'll see some of the advances in solid tumors in years ahead, like we have in hematological malignancies. But yeah, it's very much a wait and see.

Speaker 3:

Yeah, I mean at that cost, though even a check. Car T cell therapy is a quarter of a million bucks, and most of them are a million plus once you take into account the toxicity, so they have to be really good before we start and think I don't disagree, but I'm saying I don't think we can say on the basis there's one study, that's the end of the story.

Speaker 2:

I think it's probably-.

Speaker 3:

Oh, absolutely not. There's so much work to be done in that area. But what I'm saying, I think, craig is that it's very disappointing and that's a great shame because you know, car-t's worked so well in hematological malignancies but really we're not seeing it in solid tumors at this point.

Speaker 2:

All right, so we're just going to take a short break in this somewhat chaotic first episode of the post-ASCO meeting special and thank you for all your work in putting us together, Kate and Chris, and we're going to come back with some other tumour streams in episode two.

Speaker 1:

Thank you for tuning in to the Oncology Journal Club podcast, proudly brought to you by the Oncology Podcast. Part of the Oncology Network For healthcare professionals seeking regular news updates and insightful discussions, we invite you to join our community at oncologynetworkcomau. Your free registration includes a complimentary subscription to our weekly publication, the Oncology Newsletter, a valuable resource to stay updated on the latest advancements in the field. We value your input and welcome your feedback and paper recommendations via our social media channels, email and website. Your insights help shape the conversation and drive the direction of future episodes. This is Rachel Babin signing off for the Oncology Journal Club podcast.