So there’s been a lot of discussion of the prognostic markers at this meeting around, you know, what effect they should have on the influence of frontline treatment choice. I would say for the low-risk patients with mutated IGHV, these are really patients who will benefit from any of these modalities, and that’s where I think specific comorbidities, patient preference can come into play...
So there’s been a lot of discussion of the prognostic markers at this meeting around, you know, what effect they should have on the influence of frontline treatment choice. I would say for the low-risk patients with mutated IGHV, these are really patients who will benefit from any of these modalities, and that’s where I think specific comorbidities, patient preference can come into play. But for most of my patients, I would recommend a venetoclax obinutuzumab-based regimen there because those patients can do exceptionally well with that treatment. For patients with the unmutated IGHV, the remission duration is a bit shorter with venetoclax obinutuzumab. So doing a venetoclax plus BTK inhibitor-based therapy is very reasonable in that group, as well as we could still consider continuous BTK therapy. And then particularly for those patients with high-risk disease, TP53 aberration, and then also patients with complex karyotype, we may want to consider still a continuous BTK inhibitor-based strategy to maximize the initial PFS until we have more data on retreatment after time-limited venetoclax-based therapies in the high-risk group.
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