The function of leukemic stem cells (LSC), which play a key role in acute myeloid leukemia (AML), is critically dependent on their micro-environmental niche and on signaling by the CXCL12-CXCR4 axis. The present project will determine whether improved derivatives of the endogenous CXCR4 antagonist EPI-X4 will suppress LSC growth and may thus have prospects for the treatment of AML. In addition, it will be examined whether GPR15 signaling also affects LSC proliferation or migration. Finally, comprehensive peptide libraries generated from human blood or bone marrow will be examined for other endogenous peptides modulating LSC growth or function.

 

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