RUNX1R174* mutation in OCI-AML2 cells alters expression of CD86, CD14, and CD117 (c-Kit) and reduces DMSO-induced morphologic differentiation. (A-B) Representative immunoblot analysis of OCI-AML2, OCI-AML2 RUNX1^R174*/wt, HL-60, and HL-60 RUNX1^R174*/R174*. The expression levels of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) in the cell lysates served as the loading control. (C) Cell cycle status of OCI-AML2 and OCI-AML2 RUNX1^R174*/wt cells as determined by flow cytometry. Mean of 3 independent experiments. (D) Expression of CD86, CD14, and CD117 (c-Kit) in OCI-AML2 and OCI-AML2 RUNX1^R174*/wt cells as determined by flow cytometry. Columns; mean of 3 experiments + standard error of the mean (SEM). * = expression values significantly different (*P < .05; **P < .005, by 2-tailed, unpaired t-test) in OCI-AML2 RUNX1^R174*/wt compared with OCI-AML2 control cells. (E-G) Percent CD11b-positive and percent differentiated (metamyelocytes and myelocytes) OCI-AML2 and OCI-AML2 RUNX1^R174*/wt cells following 96 hours treatment with 1.2% DMSO. In panels E and F, columns; mean of 3 experiments + (SEM). * = values significantly less (*P < .05; ***P < .0001, by 2-tailed, unpaired t-test) in OCI-AML2 RUNX1^R174*/wt compared with OCI-AML2 cells. Representative cells shown in panel G.