Navigating the Molecular Landscape of Acute Myeloid Leukemia

The molecular landscape of acute myeloid leukemia (AML) is constantly changing. Genetic testing is crucial at diagnosis to determine the presence of specific molecular aberrations. FLT3 inhibitors are incorporated into frontline treatments on day 8, but their use depends on the genetic makeup of the AML. Additionally, molecular testing is conducted at various stages of treatment including at diagnosis to determine the initial genetic profile, remission to assess the presence of residual molecular disease, and relapse to identify the dominant clone driving the leukemia. Molecular testing helps determine prognosis and guides treatment decisions, including the need for transplant. By understanding the molecular landscape, clinicians can tailor treatments to achieve the best possible outcomes.

Here, Sangeetha Venugopal, MD, MS, physician in the Department of Medicine, Division of Hematology, at the Sylvester Comprehensive Cancer Center at the University of Miami, discusses how molecular testing factors into AML treatment protocols.

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0:05 | The molecular landscape of AML is dynamic, so we do genetic testing at diagnosis, because we incorporate FLT3 inhibitors on day 8. So we need to know the genetic makeup of the AML before we decide on whether we are going to add a FLT3 inhibitor or not. The FLT3 inhibitors are added in frontline treatments, so that is in patients with newly diagnosed AML. We do it at all time points, meaning we do a diagnosis to incorporate the molecularly targeted treatment, and we do at remission, which is treatment assessment of the bone marrow at the end of the first cycle of treatment to know if the molecular aberration is still present or absent. That would help us decide how the how the prognosis is going to be.

0:57 | Some of these patients may be going to transplant, and in those patients, we want to make sure that they don't have any of these molecular aberrations left to give a best possible outcome for transplant. And after that, we do molecular testing at any time the AML relapses in a patient, mainly because we need to know whether what is the dominant clone that is driving this leukemia? Was this the same molecular aberration that was present at diagnosis, or is this something new that will affect the change in management?