Peace

I want to wish a Merry Christmas to all of you who celebrate. 

And whether or not you celebrate, I want to wish you Peace. 

"Peace on Earth" is a phrase that is often associated with Christmas. It was part of the message that angels gave to shepherds in announcing the birth of Jesus. It's the one I always gravitate to at this time of year.

I've given this same message on Christmas many times to you all, and it feels like I'm just repeating myself. As much as I want there to be peace on earth every year, it seems like there is less of it. Even Pope Leo a couple of days ago asked the world for just 24 hours of peace. 

And it's not just conflicts between nations, but within nations, too. Where I live, there is so much division, so many people who won't even talk to one another because of what they see as their differences. They can't see that they have so much more in common. That turmoil in the world makes it hard to feel good inside -- to have some inner peace. 

And inner peace is what I wish for us all. 

I'm coming up soon on my 18th diagnosiversary. You'll read more about that in a few weeks.  In many ways, life as a Follicular Lymphoma patient gets easier with time. You come to believe that you really can live a "normal" life with this disease -- whatever "normal" means.

At the same time, 18 years as an FL patient means 18 years of an aging body. I was a young, healthy man when I was diagnosed at 40 years old.  I was running in 5k and 10k races, starting to train for a short triathlon, enjoying time with my young kids, and telling myself that 40 wasn't so bad. Now I'm closing in on 60, juggling three different Electronic Medical Records portals, arranging pill bottles so I don't take the wrong ones at the wrong time, and going to physical therapy twice a week for a knee problem that came out of nowhere. It's hard feel inner peace when you hurt your back just by sneezing too hard.

But I also remind myself that my wife and I walk two miles every day. I had a cardiac stress test not too long ago that the doctor described as "excellent for my age and gender." We're going to the Grand Canyon later this year, something we had planned to do almost 30 years ago. My FL is stable, and my  dermatologist didn't find any new skin cancer the last time I saw her. There's lots to be thankful for.  Lots of reasons to feel some peace.

I try to find peace in the small things. I can always find peace there.

I hope you can find some peace today, too. Maybe looking at the whole world might not do it. Maybe looking at your small part of the world might not do it, either.  

Look for the small, quiet places were peace tends to stay. Go there for a little while. Enjoy it.

I wish you a Merry Christmas, and many, many peaceful moments to come.

 

 

ASH Review: Why FL Cells Don't Go Away (Maybe)

 Another ASH review. This one is is for anstract #553: "Longitudinal single-cell profiling of the bone marrow heterogeneity identifies the T-cell niche supporting cancer persister cells in follicular lymphoma."

This is the presentation mentioned by Dr. Jessica Okosun in the Follicular Lymphoma Foundation's video, which I posted a couple of weeks ago.  Dr. Okosun was excited about this because it potentially revealed some important new information about FL biology.

I'll be honest, I don't usually focus much on the biology-related research that I come across -- the kind of articles that tell us about biomarkers, and cells, and genes, and Tumor Microenvironments.  It's all incredibly important. But, honestly, it's also hard to read (there are usually strings of acronyms and initials that I get mixed up with one another), and it's also usually information that may lead to new research, that may eventually lead to clinical trials, but that may not show up for many years. It's much more fun to write about a stage 3 clinical trial that might have implications next month than to write about a protein or a gene that might not affect my treatment until 2038.

But, as I said, this kind of research is very important, since its the basis for the things that show up in the treatment room years from now. So I'll do my best to explain this one. But keep in mind that I'm not a cancer biologist. I will almost certainly oversimplify this.

The idea behind the research is the understanding that, since FL has a way of hiding (which is why so many of us are asymptomatic) and then of coming back after treatment, there must be something called FL cancer precursor/persister cells, or CPC. A persister cell is a cancer cell that is resistant to treatment in some way, so even if it seems like the disease has been successfully treated, those CPCs are hiding somewhere and then come out again later, and the disease relapses.

In Follicular Lymphoma, researchers already know that FL is hard to treat because of the Tumor Microenvironment (TME) -- not the cancer cells themselves, but a lot of the things that are happening around the cancer cells. For example, FL cells are infleunced by Treg (Regulator T Cells, a type of immune cell), activated Tfh (T-follicualr helper cells, another immune cell), and dysfunctional cytotoxic T cells (another immune cell that finds and kills damaged cells, including cancer cells).

(I could go more into these different types of T cells and what they do, but I don't think that's going to help explain anything. It will probably just confuse you and me.)  

However, as the abstract points out, with FL, researchers still haven't been able to identify the specific CPCs (those cancer cells that are hiding someplace) or the cells in the Tumor Microenvironment that might be helping the FL cells stay alive.

But they do know that the bone marrow might be a good place to look. \

So for this research, that's just what they did.  

The researchers took bone marrow samples from 19 patients who had been given Rituxan. They took a bone marrow sample at diagnosis, and another one 12 months after they had received Rituxan, so they could compare them. They also took bone marrow samples from 5 healthy donors so they culd compare results to them as well. 

What they found wasn't surprising. Remember that all of the Tumor Microenvironemnt examples were of T cells -- different types of immune cells that have some kind of influence on FL cells. They found that the "T-cell landscape" in the bone marrow was "highly heterogeneous" in the samples from FL patients. This isn't surprising to me because FL is a highly heterogeneous disease -- it acts differently in each one of us. They compared those to the "healthy" patients, whose T-cell landscapes were more uniform. 

More specifically,  they found that the samples from the FL patients had a "decrease of cytotoxic
CD8 T cells and naive CD4 T cells and an increase of IFN-responsive CD4 and CD8, Treg, Tfh-like, and
memory CD8 T cells." (I told you, it gets hard to read with all of the initials.) Those same cells that were increased are the ones that were associated with poor outcomes -- POD24 (where the disease returns within 24 months) and Time to Next Treatment less than 30 months. The things that decreased are the things that are associated with a better outcome -- longer Progression Free Survival and Time to Next Treatment.

There are more details about how some other parts of the Tumor Microenvironment and the differences they found, but I think you probably get the point. They seem to have identified some biomarkers that could show early on whether there will be good or bad outcomes, and these are potential targets for new treatments. 

And just to be clear about how they did this -- they took a sample of bone marrow and looked at it. Then they gave some Rituxan to get rid of B cells. And then they took another bone marrow sample to see what was left. And they found some important things -- a "preserved niche" in the bone marrow that could support survival of some (fairly rare) CPCs. It's not just cancer cells surviving treatment, it's also a bunch of immune cells that are protecting those cancer cells and allowing them to grow and persist. 

Is this the piece of the puzzle that we need to fix everything? It's impossible to tell at this point.

But I'm going to take Dr. Okosun's excitement about it as a very good sign. 

Still sifting through some more ASH commentaries to see if there are other things (besides Epcoritamab) that people are excited about. More soon, whether it's from ASH or someplace else.

 

ASH Review: Epcoritamab

If there was a Big Winner for Follicular Lymphoma at ASH this year, it was without a doubt Epcoritamab.

Epcoritamab is a bispecific antibody, meaning it has two mechanisms working. On one side, it attaches to a protein on the surface of the cancerous B cell, and then also attaches to a protein on a T cell, an immune cell. In this way a bispecific uses the body's immune system to treat the cancer.

The research that has everyone so excited is the results of a phase 3 clinical trial, also published in the prestigious medical journal The Lancet, as "Epcoritamab, lenalidomide, and rituximab versus lenalidomide and rituximab for relapsed or refractory follicular lymphoma (EPCORE FL-1): a global, open-label, randomised, phase 3 trial."

The results really are pretty exciting. This is a phase 3 randomized trial, which means the researchers split a large group of patients into two, so they could directly compare the results of two different  treatments. This kind of trial is considered the most accurate (rather than comparing one group to the results of a trial that happened a few years ago). In this case, one group was given R-squared (Rituxan + Lenalidomide/Revlimid), while the other was given R-Squared plus Epcoritamab. There were 448 patients in the trial (a pretty large number), and all had relapsed or refractory disease (they had already had treatment, and it didn't work or no longer worked).

With a median follow-up of 14.8 months, the Overall Response rate for the Epcoritamab group was 95% (versus 79% for the R-squared group). The Complete Response Rate was 83% for Epcoritamab and 50% for R-squared. 

The Progression-Free Survival for the Epcoritamab group was higher, with estimated PFS of 16 months in 85.5% of that group versus 40.2% in the R-squared group. (They had to use an estimate because some patients hadn't reached the median time yet.)

With a "triplet" -- a combination of three different treatments -- like this one, safety is always an issue. Three treatments might mean three times the effectiveness, but can also mean three times the side effects or adverse events. Grade 3 (serious) adverse events were higher for the Epcoritamab group (219 of 243, or 90% of that group, versus 161 of 238, or 68% of the R-squared group), which was to be expected. Cytokine Release Syndrome, which can be very dangerous, was low grade for the Epcoritamab group, and was managed by the doctors.

I was going to link to a few videos of Lymphoma experts talking about the results, but they're kind of all the same thing, with the expert repeating the numbers and talking about how exciting this could be (like this one from OncLive). And I do think it's exciting, having finally seen all of the data.

Any skepticism I have comes from whether or not patients will have access to it. It does seem to me that bispecifics are probably more accessible than CAR-T (the two are often talked about together, including by me). CAR-T is great, but more expensive (as one recent bit of research pointed out), which is going to make bispecifics a more popular choice for those who make those decisions about cost. But there are going to be still less expensive options for R/R patients, probably. I hope FL patients can get the best treatment available, no matter the cost.

This isn't the last we're going to hear about Epcoritamab. There were many ASH presentations on this treatment, for many different types of Lymphoma. Two that I thought were interesting were the results of a phase 2 trial of Epcoritamab and Rituxan for untreated FL patients (97% Complete Response Rate in a small trial), and Epcoritamab and R-squared in untreated FL patients (95% Overall Response Rate). 

But it's that randomized, phase 3 trial that really makes me think that Epcoritamab will be around for a while. A large number of patients over a long period of time. It seems pretty likely that it will be a regular part of treatment programs. It might take a while to get to that point, but it probably will.

I'm still looking at ASH abstracts and watching and reading commentaries. I'll have more soon. 

ASH Review from the Follicular Lymphoma Foundaton

The ASH meeting ended yesterday, so no more previews. Now we're into reviews. Over the next few weeks, there will be lots of Lymphoma experts writing articles and making videos that talk about what they found most exciting at ASH. They're helpful. They often provide more detail and analysis than I could get from the abstracts, and it's usually easy to see patterns when they all talk about the same thing.

For this first review, we'll look at a video sponsored by the Follicular Lymphoma Foundation. It features Dr. Jessica Okosun, a Lymphoma specialist and professor at Bart's Cancer Institute in London. (Prof. Okosun was one of the panelists for the FLF's webinar, "Charting Our Progress Toward a Cure" last summer.) 

You can watch Dr, Okosun's video here on YouTube, or go to the FLF's website and see it there with some additional commentary. 

The thing that excited Dr. Okosun the most was the research on Epcoritamab and R-Squared (Rituxan + Revlimid or Lenilidomide). If there was a standout for FL reseach at ASH this year, it was this one. Since it was presented a few days ago, I've seen about 20-30 articles about it, with phrases like "game changer" and "new standard." (I'm always a little skeptical about new treatments being talked about so excitedly. I'll get more into that at some point.) The results were also published in the prestigious medical journal The Lancet a couple of days ago, which is a bigger deal, since it means the data has been peer-reviewed by other experts. 

As Dr. Okosun says in the video, the research was a randomized trial with about 400 patients, half of them getting R-squared and the other half getting R-squared + Epcoritamab. The R-Squared group had a Progression Free Survival of about 11 months, with the Epcoritamab group had not reached its median after almost 15 months (meaning fewer than half of the patients had their Lymphoma return). 

She was excited about bispecifics in general -- there was additional research at ASH on Mosunetuzumab as well -- but she also pointed out some safety concerns. Bispecifics tend to increase the risk of infection in some patients, so as with any treatment, there needs to be some caution when giving it. 

Dr. Okosun was also excited about the research on the biology of FL that was presented at ASH. We still have some basic questions that we don't have answers to, like why FL comes back after it seems to have been treated successfully. She was excited especially about research by Dr. Karen Tarte, who presented data that looked at differences between FL cells at diagnosis and then at relapse. You can see that abstract here; I'll try to look at it and comment on it soon. 

As I said, there will be more commentary from Lymphoma experts in the next few weeks about what they found exciting at ASH. And I'm sure a lot of it will be about Epcoritamab. I have no doubt that it has the potential to make things better for Relapsed and Refractory FL patients. It will be a matter of getting it to them. 

More ASH reviews to come.  

 

ASH Preview: The Leonard List

This post is the next one in a series of previews for the ASH meeting, one of the largest gatherings of blood cancer specialists in the U.S. The abstracts (or summaries) of the presentations come out a few weeks before the meeting, so while they don't give all of the details of the research, they do give enough for me to see if it is interesting or significant enough to focus on and write about.

For this post, I'm going to do something I have done in the past -- look at The Leonard List. Every year, Dr. John P. Leonard, a Lymphoma specialist in New York, gives a list of what he thinks are the Top 10 abstracts related to Lymphoma at the year's ASH meeting. It's always interesting to see which of his Top 10 are focused on Follicular Lymphoma, and  which of them were on my list as well.

(And, to be clear, Dr. Leonard is one of top Lymphoma specialists in the world. I'm not saying my list is as accurate as his, in terms of significance of the abstracts. If it's important to you to know which research at ASH really matters, go with Dr. Leonard, not with me. I'm just a guy with a blog.)

These will be shorter discussions from me than the previous ASH posts, since we have several to talk about.

Number 10 on The Leonard List is abstract #52:  EZH2 and CREBBP mutation status identify a subset of patients who benefit from bendamustine- over CHOP/CVP-based immunochemotherapies in follicular lymphoma: Findings from the GALLIUM trial and validation in a large international cohort. This one was actually on my list of abstracts to review. It looks at data from the GALLIUM trial, which involved 1202 patients with Follicular Lymphoma who had not been treated yet. Half received Rituxan + chemotherapy (either Bendamustine, CHOP, or CVP) and the other half received Obinutuzumab + chemo (the same three possiblities). A few years ago, data from this trial showed that Bendamustine led to longer Progression-Free Survival than CHOP or CVP, but also showed that Bendamustine led to more high grade infections than the other two chemos. This led to the idea that Bendamustine might make CAR-T less effective if the CAR-T comes later, since the Bendamustine affects the T cells that CAR-T relies on. For this presentation, the researchers look at gene mutations in the data they collected to try to identify which patients might benefit from taking Bendamustine, and which might be better served with a different treatment. They found that mutations in EZH2 and CREBBP could help predict success with Bendamustine. Patients with CREBBP and wild-type EZH2 benefit most from Bendamustine, with much longer PFS and Overall Survival than other patients in the trial. The others had similar PFS no matter which chemo was given. Still some more research needed to confirm this, but it's they type of biomarker research that's been so difficult to find lately.

Number 8 on the Leonard List is abstract #5515 CD19 expression is preserved following CD19-directed monoclonal antibody therapy with tafasitamab. This is a fairly small study that focuses on one of the problems that comes with CAR-T. If you've been reading the blog for a while, you know that many FL treatments rely on targeting proteins on the surface of the cancer cell. Rituxan, for example, targets the CD20 protein, which is very common on B Lymphocytes (the white blood cell that turns cancerous in FL). Another common protein is CD19, and that's the one that CAR-T goes after. The problem is, for about 30% of CAR-T patients who relapse after CAR-T treatment, their B Lymphocytes no longer have the CD19 protein, which means a whole bunch of FL treatments won't work on them anymore (though there are plenty that will work since they don't work by targeting that protein). The research in this presentation looked at Tafasitamab, an anti-CD19 monoclonal antibody. The research looked at patients who had one of several B Cell cancers, including FL. They wanted to know if taking Tafasitamab had the same effect as CAR-T, resulting in losing the CD19 protein. They found that most patients did not lose the protein. The conclusion has to do with sequencing of treatments -- patients who are CD19-positive should receive a treatment like Tafasitamab first, and then CAR-T if necessary. It's a small study and a small piece of the puzzle, but for those of us with a cancer that often returns, that kind of planning is important. 

Number 4 on The Leonard List is abstract #5385  Evaluating the clinical outcomes of GLP-1 receptor agonists in untreated indolent non-Hodgkin's lymphomas undergoing active surveillance. I'll be honest -- I talked to my wife about this one and I wasn't sure I wanted to even write about it, for reasons you will see. But I'm going to follow The Leonard List here and add my commentary about it. This presentation looked at the possible effects of GLP-1 agonists (that is, medications like Ozempic, Wegovy, and Mounjaro) on watching and waiting. These are given to help control diabetes and, increasingly, for weight loss. The research looked at patients with indolent, slow-growing Lymphomas (including FL) who had been taking a GLP-1 before or after their cancer diagnosis, and who were able to watch and wait. In looking only at the whole group, they found that patients who had received GLP-1, about 17.3% required treatment during the study, versus 20.3% who had not taken a GLP-1. The patients in the GLP-1 group had a lower risk of acute cardiac events including myocardial or heart attack (4.9% vs 7.3%) and a lower risk of heart failure (10.6% vs 15.2% ). Looking only at FL patients, the results were similar, but also included analysis that showed that there was "a reduction in those who progressed to DLBCL" (which I assume means transformation) -- 4.5% vs 8.3%. The abstract does not say why the GLP-1s might contribute to these results, though in the introduction, they hint that it might be more about weight loss and controlling diabetes than about the medication acting on the cancer cells directly. Both contribute to inflammation and heart issues, so reducing them will reduce other problems.

So why am I reluctant to write about it? Well, I'm always extra careful when I write about something that that's kind of "in the news" and is also controversial, and I think both of things are true about GLP-1s. The one thing I absolutely do not want anyone to think is that taking a GLP-1 will somehow cure their FL. There's no evidence in this study that such a thing would happen. This study looks at a very particular population -- FL patients who are watching and waiting -- and makes conclusions about particular things -- increasing time to treatment, reducing heart issues, and possibly reducing transformation. Should you be taking a GLP-1? I have no idea. Talk to your oncologist about how much they know about whether or not it will have an influence on your cancer, and talk to your other doctors about whether it will have an effect on any other health issues you are experiencing. Your doctors are the best people to help you make those decisions. As I wrote above, I'm just a guy with a blog.

(I'm guessing this is going to be one of those ASH presentations that people talk about after all of the details are presented at the meeting. I'll share if I see anything with good analysis.) 

Finally, Number 2 on The Leonard List is abstract #117 "Lymphovision: A lymphoma-specialized foundation model for histology-based lymphoma classification and subtyping." I already wrote about this one. I guessed number 2 correctly! 

So that's The Leonard List for this year. In the past, Dr. Leonard has gone into a little bit further detail about his picks during a special podcast episode. However, that podcast was sponsored by his old institution, and he's switched jobs since last year. I haven't seen any notice on his Twitter/X feed that he's got a podcast episode coming up, but I'll keep looking. I'll post a link if there is one,

The ASH meeting starts very soon -- it runs from December 6 to 9. That means we'll start to see press releases, articles, and videos with more detail about some of the presentations. That means I might be moving soon from "ASH Preview" to "ASH Review," but I'll probably still be sharing some ASH content either way for a few more weeks. So stay tuned.

 

ASH Preview: Zevalin

As I said I my last post, when I do previews like this for the ASH meeting, I'm not trying to be comprehensive. If something seems important, I'll look at it. (You'll see a few of those coming up.) But if something seems interesting t me personally, I'll look at that, too.

This is one of those "interesting to me personally" previews. It's for session #1825 "Real-world outcomes of Y90-ibritumomab tiuxetan (Zevalin) in low-grade B-cell non-Hodgkin lymphoma: A single-institution experience."

Zevalin is a type of RadioImmunoTherapy, or RIT. You don't see much about RIT anymore, at least not in the U.S., and there's a reason for that. RIT treatments were created to solve a problem with blood cancers in using radiation. Radiation can be an effective treatment, particularly for cancers with solid tumors. A beam of radiation can be aimed directly at a tumor. But that's not the case with blood cancers -- the cells are always moving around in the bloodstream, so it is literally a moving target. RIT works by taking a monoclonal antibody (something like Rituxan), which targets a protein on a cancer cell (CD20 is the target for both Rituxan and Zevalin). It also includes a small bit of radiation. So when the RIT finds a CD20 target, it attaches itself to the cancer cell, putting the little bit of radiation onto the cancer cell and killing it. And even better, at least in theory, because the radiation is aimed at a very specific target, there is less chance of it affecting healthy cells, so there should be fewer severe side effects. 

Zevalin was approved by the FDA for Relapsed and Refractory Follicular Lymphoma in 2002, and another RIT called Bexxar was approved right around the same time. I was diagnosed in 2008, so there were lots of follow-up studies being conducted and reported on in those first few years after I was diagnosed. And it was all very exciting to me. I remember the first article from a medical journal that I really got excited about was a report of R-CHOP and Zevalin, where Zevalin was used a salvage therapy (that is, it was given after R-CHOP to kind of clean up any leftover cancer cells). The idea of using three different treatment types -- a monoclonal antibody, traditional chemotherapy, and an RIT -- that work on the cancer cells in different ways, just made so much sense to me. 

So Zevalin has been on my mind for almost as long as I have been an FL patient. And those early studies showed that it was very effective. I remember communicating with two or three folks who had been in trials for Zevalin, and who had been in remission for years.

So why do we hear so little about it now?

Well, at least in the U.S., it's for a couple of reasons, but the biggest was a ruling by the FDA about how Zevalin had to be administered. Because it involves some radiation, the FDA ruled that it could only be administered by a Radiation Oncologist, someone with about 400 hours of specialized training. So while Rituxan or CHOP can be administered right in the treatment room at an oncologist's office, they would need to send you to a specialist if they thought RIT was the best option. And even in 2008, there were already a number of other options for FL treatment, so there wasn't much reason to send a patient to another specialist, or to do 400 hours of specialized training themselves. 

Soon after that ruling, the maker of Bexxar pulled the treatment from the market.But Zevalin has stuck around.  I have no idea how often it is used these days, but as far as I know, it's still available. Interestingly, a few years ago, there was another attempt at getting an RIT approved. It was called Betalutin, and it was pulled after a phase 2 trial. I kind of predicted that was going to happen when I first started reading about it.  

So what is this particular ASH presentation about?

Well, it looks at "real world" outcomes for people who received Zevalin -- patients who were not in a clinical trial. Some of those folks were followed for 22 years, from the time Zevalin was approved by the FDA.

A total of 122 patients with B Cell Non-Hodgkin's Lymphoma (most of them had FL) from one cancer center were followed. 72 of them had received one previous treatment, 43 used it as a salvage therapy after chemo, and 6 used it as a first treatment. The median age was 64 years old. 

The Overall Response Rate was just under 78%, which is pretty great for an FL treatment -- 70.8% ORR for the R/R patients, 88.4% for the salvage patients, and 100% for the first treatment patients.

The media Overall Survival was just under 10 years for the whole group. (Remember, Overall Survival measures dying from any cause, not just something Lymphoma-related, and "median" means that half of the group lived less than the median number, but half lived more than the number.) The median OS was 6.5 years for the R/R group, 15.2 years for the salvage group, and 8.4 years for the first line group. The median time to next treatment was 7.4 years, and 18 patients developed a secondary cancer.  

In their conclusion, the researchers say that Zevalin still has a place in the treatment options for certain patients. That's probably true, especially considering it is about the same cost (maybe even a little cheaper) than something like Rituxan. But I also think it's very unlikely that it's going to suddenly get popular, given all of the other treatment options we have now.

It's always interesting to look back and think about what might have been. I certainly don't have any regrets about being treated with Rituxan instead of something else. But I also can't help but wonder what the path for other FL patients would have been if Zevalin had become more popular. It's not a perfect treatment, by any means, but it might have helped a lot more people than it was able to.

More ASH previews soon.

 

 

 

 

 

ASH Preview: LymphoVision

I'm finally getting around to looking at ASH abstracts.

For those of you who are new around here, ASH stands for the American Society for Hematology, the organization for doctors who specialize in blood disorders, including blood cancers. Every year in early December, they hold their annual meeting, and it's where some of the biggest news about Follicular Lymphoma gets shared. About a month or so before they meeting, they publish the abstracts -- the summaries of the research that will be presented at the meeting. If you're interested in reading on your own, you can find the abstracts here. You can enter a search term like "Follicular Lymphoma" or the name of a particular treatment, and you'll get the list of every abstract that deals with that thing.

Every year, I like to do a little ASH preview, and talk about some of the abstracts that I'm interested in. To be clear -- these aren't necessarily the most important abstracts (though I do try to guess what those will be, which is usually easy because of all the talk online about them). Usually it's just something that I find interesting. Like, this year, there's some research being presented about the long term success of Zevalin, an ImmunoRadioTherapy that I first wrote about in 2009. If you search for "Zevalin" in the blog, you'll see that I wrote about a whole bunch. But it never really gained acceptance as a treatment, for a specific reason. I'll write more about all of that soon when I do a preview of that ASH presentation. 

My point is, I usually write about things that interest me, not necessarily the things that experts find important. Some medical conferences end up featuring some groundbreaking research that really changes things for us as patients. But most of the time, it's the kind of small, incremental moves forward that are typical of cancer research. Science tends to move in inches (or centimeters) over many years, rather than in miles (or kilometers) all at once. 

At a meeting like ASH, that means lots of new research about treatments that are already in use, and maybe a few reports from phase 1 or phase 2 clinical trials that are very hopeful but still a long way from showing up in the treatment room. I read an article a couple of days ago where someone gave an ASH preview, looking at research for a whole bunch of blood cancers, not just FL. He says there is lots of research about "rival BTK degraders," as well as bispecifics and CAR-T treatments. Not necessarily big news about something new. But lots of Presentations showing that one company's version of a treatment might be a little better than someone else's. That's not a bad thing. Keep moving forward, inch by inch, centimeter by centimeter.

So all of that brings us to the first abstract that I want to talk about: "#117: Lymphovision: A lymphoma-specialized foundation model for histology-based lymphoma classification and subtyping."

I'll be honest -- I went through all of the abstracts and marked a bunch to look at more closely later on, and the only reason I marked this one was because the name "LymphoVision" made me laugh. It's definitely something that a hero from the Marvel Universe would have as a super power. Lympho Bob loves Lympho Anything. 

But it's actually a very cool presentation.

The research looks at Image Foundation Models, a type of huge AI-powered database. For cancer research, Image Foundation Models can be trained to look at tissue samples and determine if one is cancerous. They aren't used much with Lymphoma cells yet, but in research on other cancers, Foundation Models have actually been able to look at a sample that seems normal but that they accurately predict will mutate and become cancerous in the future. The researchers for this abstract have developed a Foundation Model that looks specifically as Lymphoma samples -- and they call it LymphoVision.

(They actually call it Lymphovision, without the upper case V, but I think it looks cooler that way.)  

For their research, they used 37 million tissue samples to train the program to recognize Lymphoma. They asked the program to perform several specific tasks, including finding FL in the sample and then classifying it as either grade 1-2 or grade 3. For that particular task, the program found 660 cases of FL -- 500 cases of grade 1-2 and 166 cases of grade 3, for an accuracy of 89.2%. When asked to identify a range of different types of Lymphoma, it had "high diagnostic accuracy" (you can see the results in the abstract). If you're wondering how all of that compares to humans, the abstract says "Based on historical
benchmarks from the 1997 International Lymphoma Study Group classification project, expert
hematopathologists achieved diagnostic agreement rates of 55% to 84%" using the same methods. 

The researchers know that more work on this is necessary, but they see a lot of promise in using tools like this for diagnosis in the future.

I don't know how much you all deal with Artificial Intelligence, but I think there is a general ambivalence about it -- one that I share. Research like this is wonderful, and shows how an AI program can save time and cut down on human error. But the technology is still in its very early stages and make lots of mistakes. That 89.2% accuracy still leaves 1 out of 10 patients getting an incorrect diagnosis. So it's not perfect. 

But I do agree that it holds some promise, and it will likely get better over time. (I'm in that weird space where I want some AI to improve quickly to make my health better, but other AI to improve slowly so I can hang on to my job for a few more years until I'm ready to retire.)

More ASH previews to come soon.