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ESH CLL 2026 | How targeted therapies shape clonal evolution and resistance in CLL
Romain Guièze, MD, PhD, CHU Clermont Ferrand, Clermont Ferrand, France, discusses how targeted therapies shape clonal evolution in chronic lymphocytic leukemia (CLL), highlighting how different treatments select for distinct resistance mutations and how monitoring these subclonal changes may help guide optimal treatment sequencing. This interview took place at the ESH CLL 2026 congress in Stockholm, Sweden.
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Transcript
We know that each targeting therapy differentially shapes the subclonal architecture in CLL, promoting distinct subclones. So, for example, we have BTK mutation resulting from treatment with covalent BTKi and non-covalent BTKi. And you have BCL2 mutation and amplification 1q in patients with resistance to venetoclax. So through the study and the follow-up of this alteration in subclones, you can optimize the treatment...
We know that each targeting therapy differentially shapes the subclonal architecture in CLL, promoting distinct subclones. So, for example, we have BTK mutation resulting from treatment with covalent BTKi and non-covalent BTKi. And you have BCL2 mutation and amplification 1q in patients with resistance to venetoclax. So through the study and the follow-up of this alteration in subclones, you can optimize the treatment. For example, for patients with BTK-mutated clones, we have shown that treating these patients with venetoclax decreased the variant allele frequencies of this BTK-mutated clone. And in addition, within the patients treated with BTKi, there is diverse BTK mutation depending on each of the covalent BTK inhibitors and of course with other mechanisms emerging for non-covalent BTK inhibitors or even BTK degraders.
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