The Chronic Lymphocytic Leukemia Channel is supported with funding from AstraZeneca (Diamond), Johnson & Johnson (Gold) and Lilly (Silver).
VJHemOnc is an independent medical education platform. Supporters, including channel supporters, have no influence over the production of content. The levels of sponsorship listed are reflective of the amount of funding given to support the channel.
ERIC CLL 2026 | Beyond BTK and BCL2 inhibitors: targeting signaling pathways in CLL
Silvia Deaglio, MD, PhD, University of Turin, Turin, Italy, discusses key takeaways from the ERIC session on targeting signaling pathways, from the B-cell receptor (BCR) and beyond, and highlights the need to move beyond current therapies for chronic lymphocytic leukemia (CLL). Dr Deaglio notes that the session covered BTK inhibitors and degraders, the BCR pathway, toll-like receptors, and CAR T-cells in CLL patients, with a focus on addressing resistance and transformation. This interview took place at the 2026 ERIC International Meeting in Barcelona, Spain.
These works are owned by Magdalen Medical Publishing (MMP) and are protected by copyright laws and treaties around the world. All rights are reserved.
Transcript
Well, you know, the session started with a question, if we even need more therapy now that we have BTK inhibitors and BCL2 inhibitors and they work wonders, alone or in combination, with fixed durations, et cetera. And the obvious starting point was yes, that we need to go beyond that. And the audience agreed that, let’s say, the areas where we need to concentrate are patients who become double-resistant, both to venetoclax and to BTK inhibitors, and patients who have a high chance to transform or experience recurrent transformation...
Well, you know, the session started with a question, if we even need more therapy now that we have BTK inhibitors and BCL2 inhibitors and they work wonders, alone or in combination, with fixed durations, et cetera. And the obvious starting point was yes, that we need to go beyond that. And the audience agreed that, let’s say, the areas where we need to concentrate are patients who become double-resistant, both to venetoclax and to BTK inhibitors, and patients who have a high chance to transform or experience recurrent transformation. And so we, let’s say, out of all the very complex scenarios, we decided together with the co-moderator Tom Kipps to explore four different areas. So we had Dr Danilov talking about BTK inhibitors and degraders. Then we had Dr Brown exploring more on the BCR pathway. So are there other targets along the pathway to star kinases, like SYK, or ERK and the MAP kinases, and so on and so forth. And then we had Dr Muzio telling us about toll-like receptors. And we ended with Marco Ruella exploring CAR T-cells in CLL patients, which is a largely unexplored area so far. Well, you know, it’s different mechanisms. At some point, BTK inhibitors lead to the development of resistance that’s usually genetically driven. And there’s a lot of mutations that have been identified, not only the C481S, which is the typical mechanism of resistance emerging from ibrutinib, but there’s also other mutations that appear. So the degraders have a very interesting alternative mechanism that could in some way bypass. So it’s a very good way to complement the inhibitors and the degraders.
This transcript is AI-generated. While we strive for accuracy, please verify this copy with the video.
Read more...
