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Overview of Pathophysiology of and Progression of AML

Opinion
Video

Panelists discuss how the pathophysiology of acute myeloid leukemia has evolved from a single phenotype understanding to recognizing diverse genetic events that lead to transformation at the hematopoietic stem cell level, with treatment decisions now increasingly integrated with specific genetic mutations despite the disease’s rapid progression timeline.

Patients with acute myeloid leukemia (AML) face a complex disease that develops when genetic changes accumulate in blood-forming stem cells over years or decades, ultimately leading to bone marrow failure. While the visible symptoms patients experience—such as infections, bleeding, and fatigue—may appear similar across cases, the underlying genetic causes vary significantly between individuals. This understanding has revolutionized how health care providers approach treatment, moving away from one-size-fits-all therapy toward personalized medicine based on each patient’s specific genetic profile.

The rapid progression that characterizes AML means patients can become critically ill within days without proper treatment, making timely diagnosis and intervention essential. However, advances in genetic testing now allow physicians to identify specific mutations like FLT3 or IDH1, enabling targeted therapies that can significantly improve outcomes. For patients with acute promyelocytic leukemia, this precision approach has transformed what was once a highly fatal condition into one with excellent cure rates.

Modern AML care emphasizes the importance of comprehensive genetic analysis at specialized centers equipped with advanced diagnostics, infectious disease support, ICU capabilities, and transplant services. Patients benefit most when treated at experienced centers where multidisciplinary teams can quickly identify genetic markers and select appropriate targeted treatments. This shift toward precision medicine means that patients today have access to more effective, individualized treatment options than ever before, with survival rates continuing to improve as our understanding of the disease’s molecular foundations deepens.

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