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ESH CLL 2026 | Genomic predictors of outcomes in CLL: insights from the SEQUOIA and ALPINE trials
Jennifer Brown, MD, PhD, Dana-Farber Cancer Institute, Boston, MA, discusses genomic analyses from the Phase III SEQUOIA (NCT03336333) and ALPINE (NCT03734016) trials evaluating zanubrutinib in chronic lymphocytic leukemia (CLL). She highlights emerging predictors of outcomes in treatment-naive patients and how these findings may help guide the use of combination therapy strategies. This interview took place at the ESH CLL 2026 congress in Stockholm, Sweden.
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Transcript
We’re working on exome sequencing analysis on all the baseline samples from all the patients on Sequoia and Alpine, the registration trials for zanubrutinib. And it’s still a work in progress, but we found a number of predictors of outcome in the treatment-naive setting for patients being treated with zanubrutinib alone. But interestingly, in the relapse/refractory setting in Alpine, there are no predictors that we’ve identified of outcome...
We’re working on exome sequencing analysis on all the baseline samples from all the patients on Sequoia and Alpine, the registration trials for zanubrutinib. And it’s still a work in progress, but we found a number of predictors of outcome in the treatment-naive setting for patients being treated with zanubrutinib alone. But interestingly, in the relapse/refractory setting in Alpine, there are no predictors that we’ve identified of outcome. We’re still working on this, though. For example, we haven’t evaluated karyotypic complexity yet. Particularly interesting is that TP53 mutation is significant in treatment-naive, but not relapsed refractory. And we’re working on combining the TP53 mutation data with deletion 17p data because RMC of Sequoia was all deletion 17p defined by FISH. But over half the patients actually had low percentages of FISH, 7 to 20%. So that was not the dominant clone in their disease. And so we’re trying to understand the implications of that. I think the more we identify predictors of patients who do less well on single-agent therapy, that gives us an opportunity to offer them dual-drug therapy, which is likely to reduce the development of resistance and help control their disease better long-term.
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