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SOHO 2025 | Optimizing therapy and extending survival in AML: balancing efficacy and toxicity
In this video, Alexander Perl, MD, University of Pennsylvania, Philadelphia, PA, comments on the potential to improve outcomes in acute myeloid leukemia (AML) by reducing treatment intensity while maintaining efficacy, particularly with the use of targeted therapies such as venetoclax, azacitidine, and FLT3 inhibitors. He highlights that achieving equally effective therapy with less toxic approaches is a key goal, and that ongoing research may re-evaluate the need for transplant in certain patients. This interview took place at the 13th Annual Meeting of the Society of Hematologic Oncology (SOHO 2025) in Houston, TX.
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Transcript
You know, extending survival is the holy grail in AML. I think what we want to do is to find ways that we can get equally effective therapy for patients who currently, again, may be over-treated with maximally intensive approaches with less toxic therapy. For example, if we look at the outcome of older patients treated with venetoclax, azacitidine, gilteritinib, it looks so promising that we would say to ourselves, can’t we do this in younger patients? And does fitness for intensive chemotherapy really matter at all? If it does not, and if the outcome with triplet venetoclax, azacitidine, say, gilteritinib, but really any of the potent FLT3 inhibitors is equivalent to what we see with intensive chemotherapy, there’s a win right there...
You know, extending survival is the holy grail in AML. I think what we want to do is to find ways that we can get equally effective therapy for patients who currently, again, may be over-treated with maximally intensive approaches with less toxic therapy. For example, if we look at the outcome of older patients treated with venetoclax, azacitidine, gilteritinib, it looks so promising that we would say to ourselves, can’t we do this in younger patients? And does fitness for intensive chemotherapy really matter at all? If it does not, and if the outcome with triplet venetoclax, azacitidine, say, gilteritinib, but really any of the potent FLT3 inhibitors is equivalent to what we see with intensive chemotherapy, there’s a win right there. And if that leads to very deep remissions in patients who don’t have adverse risk genotypes, NPM1 wild type or ELN adverse gene mutations, we may start really reevaluating, do we need transplant in every patient? And suddenly we’re in the scenario that we’re in with Ph positive ALL, where we can really dial down the intensity for a large number of patients who may be over-treated by transplanting every patient. Again, a lot of blanks to be filled in here, and I don’t think we’re ready to do that in a widespread manner. But for the question of, is it solved that we don’t need to worry about improving outcomes in FLT3-mutated AML? No, I think we really can move the bar higher. And I’m hopeful that at least for subsets of patients with optimal responses and favorable genotypes, we may be able to eliminate a lot of the intensive chemotherapy and maybe transplant for a lot of those patients.
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