AI Article Synopsis
- Acute myeloid leukemia (AML) is a severe disease mainly affecting adults, marked by an overproduction of immature myeloid cells that can't develop into healthy white blood cells, leading to a low five-year survival rate of 24%.
- Over half of AML patients have mutations in the FLT3 gene, making it a key target for emerging small-molecule treatments, though some mutations render these treatments less effective.
- The text emphasizes the importance of identifying biomarkers to better categorize AML patients based on their specific FLT3 mutations, as well as exploring new strategies to overcome resistance to FLT3 inhibitors.
Article Abstract
Acute myeloid leukemia is a disease characterized by uncontrolled proliferation of clonal myeloid blast cells that are incapable of maturation to leukocytes. AML is the most common leukemia in adults and remains a highly fatal disease with a five-year survival rate of 24%. More than 50% of AML patients have mutations in the FLT3 gene, rendering FLT3 an attractive target for small-molecule inhibition. Currently, there are several FLT3 inhibitors in the clinic, and others remain in clinical trials. However, these inhibitors face challenges due to lack of efficacy against several FLT3 mutants. Therefore, the identification of biomarkers is vital to stratify AML patients and target AML patient population with a particular FLT3 mutation. Additionally, there is an unmet need to identify alternative approaches to combat the resistance to FLT3 inhibitors. Here, we summarize the current knowledge on the utilization of diagnostic, prognostic, predictive, and pharmacodynamic biomarkers for FLT3-mutated AML. The resistance mechanisms to various FLT3 inhibitors and alternative approaches to combat this resistance are also discussed and presented.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8909069 | PMC |
| http://dx.doi.org/10.3390/cancers14051164 | DOI Listing |
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