We’re happy to share the publication of a study in iScience by Cell Press “Pharmacological inhibition of RAS overcomes FLT3 inhibitor resistance in FLT3-ITD+ AML through AP-1 and RUNX1”, with contribution from Dr Sophie Kellaway. In this paper, Dr Daniel Coleman et al. showed that a novel RAS inhibitor could deplete FLT3-ITD leukaemic cells, even after they had adapted to become resistant to FLT3 inhibitors gilteritinib/quizartinib. This could be an important avenue going forward to address the important problem of targeted inhibitor resistance in AML.
Read more here:
Pharmacological inhibition of RAS overcomes FLT3 inhibitor resistance in FLT3-ITD+ AML through AP-1 and RUNX1
• FLT3 inhibition in patients with AML blocks AP-1 and RUNX1 chromatin binding
• Relapse after FLT3 inhibition is caused by rewiring of MAP Kinase signaling
• Rewiring is caused by RAS-dependent alternate growth factor action
• RAS and RUNX1 inhibition block MAP Kinase rewiring
• Relapse after FLT3 inhibition is caused by rewiring of MAP Kinase signaling
• Rewiring is caused by RAS-dependent alternate growth factor action
• RAS and RUNX1 inhibition block MAP Kinase rewiring
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