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ASH 2024 | Understanding the drivers of resistance in AML in order to improve targeted therapy
In this video, Samuel Urrutia, MD, Washington University in St. Louis, St. Louis, MO, briefly comments on how resistance to approved therapies emerges in acute myeloid leukemia (AML). Dr Urrutia notes that understanding the mechanisms of resistance to current treatment options, such as FLT3, IDH, and BCL2 inhibitors, is crucial to developing targeted strategies to prevent relapse. By identifying the drivers of resistance, such as the proliferation of RAS-mutated clones, Dr Urrutia believes that it is possible to develop more effective therapies to target these clones at relapse or early in treatment to prevent resistance from developing. This interview took place at the 66th ASH Annual Meeting and Exposition, held in San Diego, CA.
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Transcript (AI-generated)
So we looked at the approved therapies that we currently have for AML, mainly at FLT3 inhibitors, IDH inhibitors, and BCL2 inhibitors. So most of these therapies have been in development for about five to ten years, and we’ve come to understand how these therapies, how these patients develop resistance to these therapies over time.
So just to give a few examples, in the case of FLT3, some of the initial drugs, we would see resistance developed by the development of TKD mutations when patients were treated with type 2 inhibitors like quizartinib...
So we looked at the approved therapies that we currently have for AML, mainly at FLT3 inhibitors, IDH inhibitors, and BCL2 inhibitors. So most of these therapies have been in development for about five to ten years, and we’ve come to understand how these therapies, how these patients develop resistance to these therapies over time.
So just to give a few examples, in the case of FLT3, some of the initial drugs, we would see resistance developed by the development of TKD mutations when patients were treated with type 2 inhibitors like quizartinib. Patients would develop TKD resistance mutations. For BCL2 and for IDH, we would see RAS-mutated clones, which have become important in other cancers right now with better targeted therapies. So these RAS-mutant clones would take over the phenotype and despite the initial blockade of IDH, BCL2 or FLT3, we would see RAS take over that patient phenotype and start into the process of proliferation once again. And so by understanding what drives the mechanisms of resistance, we can better have an idea of how to target that at the time of relapse or to target that at the time of the start of the therapy to avoid that from happening in the future.
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