sorafenib resistance in FLT3-mutated acute myeloid leukemia

Approximately 30% of acute myeloid leukemia patients have FLT3 mutations, which are associated with poor prognosis.

Knowledge gaps remain regarding sorafenib resistance driven by metabolic factors and the bone marrow environment.

Primary sorafenib resistance is described as initial treatment failure due to redundant signaling pathways and tumor heterogeneity.

Secondary sorafenib resistance develops after prolonged therapy through new genetic mutations or activation of alternative pathways.

Sorafenib resistance in FLT3-mutated acute myeloid leukemia includes both primary and secondary drug resistance.

The paper examines sorafenib resistance mechanisms involving tumor genetic changes and the bone marrow microenvironment.

FLT3 tyrosine kinase inhibitors including sorafenib show efficacy in FLT3-mutated acute myeloid leukemia, but resistance is a major challenge.