Fig. 7: Relapsed bHLH/LMO human L-ICs are depleted for cell cycle genes and enriched for ETP-ALL, TAL1 and therapy resistance genes.
From: The role of quiescent thymic progenitors in TAL/LMO2-induced T-ALL chemotolerance
A GSEA analysis showing depletion of KEGG cell cycle genes in hL-IC (CD7+CD1a−) compared to DP blasts (CD7+CD1a+) in REL-14 (above) and REL-13 (below). B GSEA analysis showing enrichment of of ETP-ALL genes (Zhang et al. Nature, 2012) in hL-IC (CD7+CD1a−) compared to DP blasts in REL-14 (above) and REL-13 (below). C GSEA analysis showing enrichment of de novo Prednisone Resistance genes (Paugh et al. Nature Genetics, 2015) in hL-IC compared to DP blasts in REL-14 (above) and REL-13 (below). D Overlap of shared leading edge de novo Prednisone Resistance Genes between REL-13 and REL-14. E GSEA analysis showing enrichment of TAL1 target genes (Sanda et al. Cancer Cell, 2012) in REL-14 (above) and REL-13 (below) hL-IC compared to DP blasts. F DepMap analysis showing TAL1 expression is inversely correlated with KEGG cell cycle pathway scores in human T-ALL cells (r = −0.7089; p = 0.0031). Red circles indicate cell lines annotated as TAL1 positive. G Overlap of leukemic dDN3, MRD, and LRC (Ebinger et al. Cancer Cell, 2016), TAL1 (Sanda et al. Cancer Cell, 2012) and LMO2 (McCormack et al. Science, 2010) signatures.
