Project Summary
This project investigates how c-MYC and FLT3-ITD via TAK1 contribute to immune escape in AML after allogeneic stem cell transplantation. Preliminary data show that TAK1 activation upregulates immunosuppressive proteins like arginase-1 and galectin-3. Aim 1 examines in vivo how these two axes influence the graft-versus-leukaemia responses. Aim 2 analyzes the underlying signalling and transcriptional networks. In Aim 3, we validate our findings in patient samples using single-cell sequencing, cytometry and humanized mouse models to establish novel immunotherapeutic approaches for patients with AML relapse.
