AI Article Synopsis
- The development of molecularly targeted therapies for acute myeloid leukemia (AML) is rapidly advancing, with new treatments targeting FLT3, IDH1, IDH2, and BCL2 approved in the last 5 years.
- While these therapies aim to exploit certain biological weaknesses in leukemia cells, resistance mechanisms, such as genetic mutations and changes in enzyme activity, can emerge, making treatments less effective.
- By better understanding when and how resistance develops, clinicians can create more effective treatment plans that involve combining and sequencing different therapies to enhance patient outcomes.
Article Abstract
The development of molecularly targeted therapy for acute myeloid leukemia is progressing at an accelerated pace. Therapies targeting FLT3, IDH1, IDH2, and BCL2 have been approved in the last 5 years. As we exploit these biological vulnerabilities, various mechanisms of resistance arise. Emergence of competing clones with different genetic drivers and acquisition of constitutional mutations in the target renders therapies ineffective, and enzymatic isoform changes can lead to reappearance of the disease phenotype. Understanding the timing and circumstances of resistance origination will allow clinicians to develop combinatorial and sequential therapeutic approaches to deepen responses and improve survival. The objective of this review is to illustrate the biological underpinnings of each therapy and the landscape of resistance mechanisms and discuss strategies to overcome on- and off-target resistance.
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| http://dx.doi.org/10.1007/s12185-024-03827-8 | DOI Listing |
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