This research aims to explore the therapeutic potential of Selinexor in targeting homologous recombination in acute myeloid leukemia through the XPO1-E2F7 pathway.
Investigated the effects of Selinexor on the XPO1-E2F7-HR axis in acute myeloid leukemia cells.
Analyzed the influence of E2F7 nuclear export on homologous recombination efficiency.
Integrated Selinexor with DNA-damaging agents to assess combined treatment efficacy.
Combination treatment with Selinexor and DNA-damaging agents enhances therapeutic outcomes in AML models.
Abstract
The XPO1-E2F7-HR axis represents a potential therapeutic vulnerability, supporting the rational combination of Selinexor with DNA-damaging agents to improve AML treatment outcomes.