Figure 3
Figure 3. Identification of deregulated gene expression programs in AK-AML. (A) Median gene expression fold change of selected MsigDB gene signatures that overlap significantly (P < 1e-5, median, subclass-wise) with patient-specific AK-AML signatures. (B-C) Cell cycle analysis of CD34+ cells from healthy subjects (n = 3) and t(8;21) AML patients (n = 3). (D) Median gene expression fold-change (vs normal GMPs) in cell cycle-related gene signatures for purified normal BM populations together with the experimentally determined cell cycle status (cell cycle profiles were presented in Mora-Jensen et al48). The correlation coefficient between “percentage of cells in SG2M” and the average median fold change for the 6 cell cycle signatures was r2=0.8. The following populations are depicted: early promyelocytes (ePM), late promyelocytes (lPM), MY, MM, band cells (BC) and polymorphonuclear neutrophilic granulocytes (PMN).

Identification of deregulated gene expression programs in AK-AML. (A) Median gene expression fold change of selected MsigDB gene signatures that overlap significantly (P < 1e-5, median, subclass-wise) with patient-specific AK-AML signatures. (B-C) Cell cycle analysis of CD34+ cells from healthy subjects (n = 3) and t(8;21) AML patients (n = 3). (D) Median gene expression fold-change (vs normal GMPs) in cell cycle-related gene signatures for purified normal BM populations together with the experimentally determined cell cycle status (cell cycle profiles were presented in Mora-Jensen et al48 ). The correlation coefficient between “percentage of cells in SG2M” and the average median fold change for the 6 cell cycle signatures was r2=0.8. The following populations are depicted: early promyelocytes (ePM), late promyelocytes (lPM), MY, MM, band cells (BC) and polymorphonuclear neutrophilic granulocytes (PMN).

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