Figure 7
Figure 7. Gene expression profiling experiments. (A) Hox genes from 4 Hox gene clusters and the Meis gene family are shown as heat maps for the 3 leukemia subtypes (MLL, B/T BAL, and pro-B ALL) after comparison with bone marrow of mock-transduced mice. (Top panel) Log2 changes. (Middle panel) Significant P values. (Bottom panel) Signal intensities in arbitrary light units. With the exception of down-regulated Hoxa9 and Meis1 in B/T BAL and pro-B ALL, none of the observed changes was calculated as significant (gray areas in middle panel). (B) Common and unique signatures of all 3 disease phenotypes. (Top panel) Commonly deregulated genes in all 3 disease phenotypes (regardless of whether only AF4·MLL or both transgenes were present). (Bottom panel) Unique signatures for each subtype. Genes were listed only if the observed log2 change was more than ± 2 (equals ± 4-fold) and arbitrary light units were > 500.

Gene expression profiling experiments. (A) Hox genes from 4 Hox gene clusters and the Meis gene family are shown as heat maps for the 3 leukemia subtypes (MLL, B/T BAL, and pro-B ALL) after comparison with bone marrow of mock-transduced mice. (Top panel) Log2 changes. (Middle panel) Significant P values. (Bottom panel) Signal intensities in arbitrary light units. With the exception of down-regulated Hoxa9 and Meis1 in B/T BAL and pro-B ALL, none of the observed changes was calculated as significant (gray areas in middle panel). (B) Common and unique signatures of all 3 disease phenotypes. (Top panel) Commonly deregulated genes in all 3 disease phenotypes (regardless of whether only AF4·MLL or both transgenes were present). (Bottom panel) Unique signatures for each subtype. Genes were listed only if the observed log2 change was more than ± 2 (equals ± 4-fold) and arbitrary light units were > 500.

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