Figure 2.
Innate immune signaling in primitive cells promotes advantage of clonal competition and predicts poor prognosis at diagnosis. (A) Box plot showing gene score of innate immune gene set (n = 334) in patients with pAML vs HDs among each cell type. N.S., not significant; ∗∗∗P < .001, Wilcoxon rank-sum test. (B) Violin plot (top) and heat map (bottom) showing gene score of innate immune gene set (n = 334) in primitive cells across distinct pAML subtypes and HDs. ∗∗∗P < .001, Wilcoxon rank-sum test. (C) Scatter plot showing the Spearman correlation (with a 95% confidence interval for the regression line) between the gene score of innate immune gene set (n = 334) and the clone size in pAML2 at diagnosis. The upper left corner displays the Spearman correlation coefficient (R) and the P value. (D) Gene score of innate immune gene set (n = 334) in each cell type compared between relapse and nonrelapse groups in different pAML subtypes. ∗P < .05; ∗∗P < .01, Wilcoxon rank-sum test. (E) Forest plot showing significant prognostic value of inScore genes (n = 31) by analyzing RNA-sequencing data from TARGET pediatric AML cohort. Lines represent confidence intervals (95%). The dotted vertical line indicates hazard ratio of 1. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001, Wilcoxon rank-sum test. (F) Kaplan-Meier analysis of overall survival for pediatric patients with AML in the TARGET cohort based on the inScore signature (high inScore, n = 224; low inScore, n = 225). Log-rank test. (G) inScore of patients with pAML estimated by using microarray data from the TARGET cohort according to clinical risk categories: low risk (n = 99), intermediate risk (n = 144), and high risk (n = 52). ∗∗∗P < .001, Wilcoxon rank-sum test. (H) inScore in distinct pAML molecular subtypes estimated using microarray data from the TARGET cohort. (I) Forest plot showing hazard ratios from multivariate Cox regression analysis assessing the prognostic significance of the inScore as an independent metric for overall survival in the pediatric AML TARGET cohort. The median value of the inScore was used to define high and low groups. Hazard ratios with 95% confidence intervals are presented. CDP, common dendritic cell progenitor; COG, children's oncology group; EBM, eosinophil/basophil/mast cell; FCGR, Fc gamma receptor; GMP, granulocyte/macrophage progenitor; LMPP, lymphoid-primed multipotential progenitor; MDP, monocyte-dendritic cell progenitor; MEP, megakaryocyte/erythroid progenitor; MLP, multilymphoid progenitor; NeP, neutrophil progenitor; NK, natural killer cell; NLR, NOD-like receptors; Pre-B, precursor B cell; Pro-B, progenitor B cell; RNA-seq, RNA sequencing; RNS, reactive nitrogen species; ROS, reactive oxygen species.

Innate immune signaling in primitive cells promotes advantage of clonal competition and predicts poor prognosis at diagnosis. (A) Box plot showing gene score of innate immune gene set (n = 334) in patients with pAML vs HDs among each cell type. N.S., not significant; ∗∗∗P < .001, Wilcoxon rank-sum test. (B) Violin plot (top) and heat map (bottom) showing gene score of innate immune gene set (n = 334) in primitive cells across distinct pAML subtypes and HDs. ∗∗∗P < .001, Wilcoxon rank-sum test. (C) Scatter plot showing the Spearman correlation (with a 95% confidence interval for the regression line) between the gene score of innate immune gene set (n = 334) and the clone size in pAML2 at diagnosis. The upper left corner displays the Spearman correlation coefficient (R) and the P value. (D) Gene score of innate immune gene set (n = 334) in each cell type compared between relapse and nonrelapse groups in different pAML subtypes. ∗P < .05; ∗∗P < .01, Wilcoxon rank-sum test. (E) Forest plot showing significant prognostic value of inScore genes (n = 31) by analyzing RNA-sequencing data from TARGET pediatric AML cohort. Lines represent confidence intervals (95%). The dotted vertical line indicates hazard ratio of 1. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001, Wilcoxon rank-sum test. (F) Kaplan-Meier analysis of overall survival for pediatric patients with AML in the TARGET cohort based on the inScore signature (high inScore, n = 224; low inScore, n = 225). Log-rank test. (G) inScore of patients with pAML estimated by using microarray data from the TARGET cohort according to clinical risk categories: low risk (n = 99), intermediate risk (n = 144), and high risk (n = 52). ∗∗∗P < .001, Wilcoxon rank-sum test. (H) inScore in distinct pAML molecular subtypes estimated using microarray data from the TARGET cohort. (I) Forest plot showing hazard ratios from multivariate Cox regression analysis assessing the prognostic significance of the inScore as an independent metric for overall survival in the pediatric AML TARGET cohort. The median value of the inScore was used to define high and low groups. Hazard ratios with 95% confidence intervals are presented. CDP, common dendritic cell progenitor; COG, children's oncology group; EBM, eosinophil/basophil/mast cell; FCGR, Fc gamma receptor; GMP, granulocyte/macrophage progenitor; LMPP, lymphoid-primed multipotential progenitor; MDP, monocyte-dendritic cell progenitor; MEP, megakaryocyte/erythroid progenitor; MLP, multilymphoid progenitor; NeP, neutrophil progenitor; NK, natural killer cell; NLR, NOD-like receptors; Pre-B, precursor B cell; Pro-B, progenitor B cell; RNA-seq, RNA sequencing; RNS, reactive nitrogen species; ROS, reactive oxygen species.

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