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. Author manuscript; available in PMC: 2016 May 1.
Published in final edited form as: Br J Haematol. 2015 Jan 22;169(3):344–351. doi: 10.1111/bjh.13299

Figure 3.

Figure 3

RUNX3 promoter DNA methylation in clinical samples. (A) DNA methylation density of the RUNX3 promoter in 8 control individuals (4 normal bone marrow [BM] and 4 CD34+ BM), 69 acute myeloid leukemia (AML), 6 acute lymphocytic leukemia (ALL), and 19 myelodysplastic syndromes (MDS) patient samples. (B) Differential frequency of RUNX3 promoter DNA hypermethylation in inv(16) versus non-inv(16) AML subtypes. The inv(16) AML group had a 2-fold higher frequency of RUNX3 hypermethylation compared to other AML subtypes. (C) RUNX3 methylation in the RUNX1-RUNX1T1 [t(8;21)] subtype. The letter “a” after the patient number indicates sample collection at admission, and “b” and “c” are post-treatment samples. RUNX3 methylation is infrequent in this group, and it is decreased after treatment. Additional inv(16) samples were evaluated (CBFb-MyH11), and RUNX3 was hypermethylated in half of cases.