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Fig. 2 | Journal of Translational Medicine

Fig. 2

From: Mitochondrial dysfunction fuels drug resistance in adult T-cell acute lymphoblastic leukemia

Fig. 2

Biological features of mitochondria are depleted in adult T-ALL tumours. A: Results of the GSEA analysis for the gene set of fatty acid β-oxidation from the database MSigDB and for the gene set of lipid metabolism from the database MitoPathways, calculated in the T-ALL group “MT+” versus the group “MT-” of our pooled adult T-ALL dataset. The GSEA results were considered significant if the calculated p-values < 0.05 and false discovery rates (FDR) < 0.25. Mitochondria-depleted T-ALL tumours “MT-” are significantly depleted for lipid metabolism and β-oxidation. B: Results of the GSEA analysis for three gene sets of glycolysis from the database MSigDB. These gene sets are significantly enriched in the group “MT+” compared to the group “MT-”. C: Results of the GSEA analysis for the gene set “GOBP POSITIVE REGULATION OF AUTOPHAGY” which is significantly depleted in the in the group “MT+” versus the group “MT-”. D: Results of the GSEA analysis for the gene set of ABC transporters, calculated in the T-ALL group “MT+” versus the group “MT-”. Mitochondria-depleted T-ALL tumours “MT-” are significantly enriched for genes expressing the ABC transporter family. E: Comparative expression levels of the gene ABCB1 in the groups “MT+” and “MT-”. The expression levels of ABCB1 are significantly higher in mitochondria-depleted T-ALL tumours. The p-value corresponds to the two-sided statistical t-test. Additionally, the figure indicates the corresponding effect size (Cohen’s d) and 95% confidence interval

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