Proteome discovers GFI1-36N leukemic cells deregulate DNA repair protein MGMT. Proteomic analysis of primary murine and human GFI1-36S and GFI1-36N leukemic cells (A) Schematic representation of the experimental setup of murine GFI1-36S (n = 4) vs GFI1-36N (n = 4) leukemic BM cells proteome experiment, principle component analysis of measured samples, and evaluation of the results (left). Volcano plot displays significantly regulated proteins (permutation-based FDR < 0.05) is shown (right). (B) Network analysis of significantly regulated proteins between the 2 genotypes using Cytoscape. The network displays enriched Gene Ontology Biological Processes terms (P < .01). (C) Dot plot showing the significantly enriched GFI1-36N and GFI1-36S specific gene set enrichment terms based on proteomic analysis (D) Rank plot displaying the total number of DNA damage and repair proteins (highlighted with red dots) of all significantly regulated proteins in the data set. (E) Significantly regulated DNA damage and repair proteins grouped according to their specific pathways (selected from panel D). Rank plot displaying all significantly regulated proteins in GFI1 36N and 36S leukemia cells. The protein that participates in DNA damage repair are highlighted in red dots. The GFI1 36N upregulated proteins are marked in red, and downregulated proteins are marked in blue. The x-axis denotes the protein rank and y-axis denotes the –log10 P value. (F) Venn diagram showing the unique and shared number of differentially expressed proteins in murine and human AML samples (also see supplemental Figure 4H). MGMT is 1 of the shared and significantly altered proteins in both mouse and human samples. (G) Violin plot showing the log2 intensity of MGMT protein level in primary GFI1-36S (n = 4) vs GFI1-36N (n = 4) murine leukemic BM cells. (H) Violin plot showing the log2 intensity of MGMT protein level in human GFI1-36S (n = 11) vs GFI1-36N (n = 9) cells from patients with AML patient.