Characterization of aberrant c-Myc phosphorylation and stability in acute myeloid and lymphoblastic leukemia

c-Myc is a key transcription factor regulating hematopoiesis, and its overexpression is common in leukemia. c-Myc stability is controlled by phosphorylation at serine 62 (S62) and threonine 58 (T58), influencing protein degradation. This dissertation demonstrates that elevated c-Myc levels in lymphoid and myeloid leukemia are linked to increased protein stability and altered phosphorylation at these sites. Mechanisms include constitutive activation of upstream signaling and deregulation of degradation-promoting proteins. Overexpression of AXIN1 in a mouse lymphoma model delayed tumor onset, supporting strategies to target c-Myc stability. These findings identify aberrant c-Myc stabilization as a therapeutic target in leukemia.