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. 2015 Feb 17;43(5):2590–2602. doi: 10.1093/nar/gkv103

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© The Author(s) 2015. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 6. — Pathway and upstream regulators dysregulated in different clusters. (A) Pathway enrichment analysis for differentially expressed genes (DEGs) compared to pre-B-I and pre-B-II cells were done using the Ingenuity database. Values in boxes indicate -log(FDR-corrected P). B-cell development pathway is more enriched for methylation cluster III, cell cycle and mismatch repair for clusters II and IV, and glucocorticoid receptor signaling for clusters I and II. (B) Upstream regulators significantly dysregulated. Values in boxes display activation z scores calculated from the expression patterns of their downstream target genes. Chromatin modifiers including NUPR1, SMARCB1 and EP400 and cell cycle controllers including CCND1 and TBX2 are significantly dysregulated as well as MYC, RB1, CDKN2A and TP53. Among chemicals, doxorubicin and other investigative drugs for B-ALLs ranked at the top, with different degrees according to methylation clusters.