Figure 3.

Summary of the various molecular mechanisms that may interact in the pathogenesis of AML t(8;21); RUNX1-RUNX1T1, and potential therapies. Fusion RUNX1-RUNX1T1 leads to aberrations in a number of intracellular pathways including downregulation of tumor suppressors, activation of oncogenes, abnormal activation of specific signaling pathways, and block of transcription factors, and often occurs with concurrent mutations. These may be amenable to therapeutic targeting. PARP, poly(ADP-ribose) polymerase.