Figure 2.
Prednisolone response genes are differentially regulated between MLL-Af4 and -AF9 ALL. (A) GSEA to assess enrichment of prednisolone-resistant and -sensitive signatures in MLL-Af4 compared with MLL-AF9 cells. (B) Heat map of resistant and sensitive signature genes from the leading-edge subsets of GSEA analysis in panel A. The genes with MLL-Af4 or -AF9 binding peaks were designated with red and black squares, respectively. (C) ChIP-seq tracks at GSPT1 loci as an example of resistant genes upregulated in MLL-Af4 ALL. (D) Unsupervised hierarchical clustering of MLL fusion ALL patient samples based on the expression of prednisolone response genes shown in panel B. Samples were clustered into 3 groups according to the expression pattern. Patient sample data was from the Andersson data set.8 (E) Distribution of MLL-AF4 and other MLL fusion patient samples in 3 clustering groups described in panel D. P value was calculated by χ2 test. NES, normalized enrichment score.

Prednisolone response genes are differentially regulated between MLL-Af4 and -AF9 ALL. (A) GSEA to assess enrichment of prednisolone-resistant and -sensitive signatures in MLL-Af4 compared with MLL-AF9 cells. (B) Heat map of resistant and sensitive signature genes from the leading-edge subsets of GSEA analysis in panel A. The genes with MLL-Af4 or -AF9 binding peaks were designated with red and black squares, respectively. (C) ChIP-seq tracks at GSPT1 loci as an example of resistant genes upregulated in MLL-Af4 ALL. (D) Unsupervised hierarchical clustering of MLL fusion ALL patient samples based on the expression of prednisolone response genes shown in panel B. Samples were clustered into 3 groups according to the expression pattern. Patient sample data was from the Andersson data set.8 (E) Distribution of MLL-AF4 and other MLL fusion patient samples in 3 clustering groups described in panel D. P value was calculated by χ2 test. NES, normalized enrichment score.

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