EHA 2026 | Clinically relevant advances that have been made in HL biology and the value of ctDNA

You know, I think we’ve learned a lot about Hodgkin biology over recent years. Probably 25 years ago, we weren’t even sure exactly what kind of cell a Reed-Sternberg cell was. Since then, we’ve learned a lot. We’ve learned that it’s a crippled germinal center B cell. We’ve learned that there are a lot of genomic and genetic changes that drive its survival and growth. And so because of that, even though it should be destined to die, it doesn’t. And it grows and recruits a lot of other immune cells around it. We’ve also learned that those immune cells, while they’re normal, are not just innocent bystanders. They’re actually contributing to the activity of the tumor in general. And so that’s where I think we’ve learned a lot around blocking that interaction, specifically as we’ve learned about the genetics of PD-L1 and PD-L2. That’s allowed us to switch off that mechanism. And I think more recently, we’re also learning a lot about circulating DNA and how we can actually monitor the disease through that process. So it’s been an exciting time probably in the last 20 to 25 years. One of the things that’s been very exciting in recent years is the ability to actually use circulating DNA as a metric of what is happening in the disease. Previously, we had used sort of single molecules like TARC, like CD30, even IL-6 as other kinds of mechanisms of testing whether a patient was destined to have a badly behaved type of Hodgkin or more recently, whether or not it was going to be a good one that responded well to treatment. However, circulating DNA has really allowed us to actually identify three different subtypes driven either by genomic changes, the immune environment, or even a viral process. And because of that, we can see how patients respond well to treatment. And most of the patients, as I say, will benefit. But this is a way in which we, along with PET scans, can actually determine whether patients are doing as well as what we would hope. I would also say that TARC, along with PET scans, has been another mechanism. Using those two together, we’ve been able to say that if you’ve had a good response in both, you’re likely to stay in remission for the long term.