Our analysis showed dramatic differences in the genetic landscapes of these cooperating mutations for CBF-AML with rearrangements involving RUNX1 compared to those that involve CBFB
Acute myeloid leukemia with t(8; 21) and inv(16) are collectively referred to as core-binding factor (CBF) AML because RUNX1 (rearranged in t[8; 21]) and CBFB
(rearranged in inv) are both subunits of the CBF transcription complex, which is critical for myeloid differentiation.
A study of mutations across breast cancer subtypes identified recurrent aberrations in the CBFB
 (core-binding factor, beta subunit) gene, deletions in its partner RUNX1 (runt-related transcription factor 1), and fusion of the MAGI3 (membrane associated guanylate kinase, WW and PDZ domain containing 3) gene with the AKT3 [v-akt murine thymoma viral oncogene homolog 3 (protein kinase B, gamma)] gene (i.
178-180) In addition, recurrent mutations in the CBFB
transcription factor gene and deletions of RUNX1 have also been identified.
Both inv(16) and t(16;16) result in fusion of CBFB
and MYH11, (54) either by inversion within a single chromosome 16 or by translocation between homologs.