Mice expressing mutant NFE2 acquire chromosomal aberrations and Trp53 mutations similar to those observed in human AML. (A-E) Array-comparative genomic hybridization of leukemic mice to wild-type controls. Genomic DNA of BM, spleen, or granulocytic sarcoma tissue from individual leukemic mice was hybridized to a pool of n = 10 wild-type controls. Detection of an equal amount of fluorescence in both DNAs results in a plot along the axis in the middle of the graph. Loss of DNA is depicted as signals below the axis; a gain of genetic material as signals above the axis. (A) Mouse #524, (top) BM and (bottom) granulocytic sarcoma. (B) Mouse #540, (top) spleen and (bottom) granulocytic sarcoma. (Bottom insert) Detailed view of the aberrations in the granulocytic sarcoma of mouse #540. (Top) amplification of band 15qD1; (bottom) higher magnification of the probes amplified in band 15qD1. (C) Mouse #539, (top) BM and (middle) granulocytic sarcoma, (insert) detailed view of the amplified region on chromosome 18. (D) Mouse #556, (top) granulocytic sarcoma, (bottom) detailed view of the amplified region on chromosome 9. (E) Commute plot of the chromosomal aberrations identified. BM, bone marrow; MyS, myelosarcoma; PDGFD, platelet-derived growth factor D; Sp, spleen; T, tumor; WT, wild-type NFE2 overexpression. *Region spanning 1.9 Mb containing Myc. (F) Acquired mutations in Trp53.