Figure 4.
Genome-wide multiomics biology phenotype of CIMP subgroups in the NOPHO ALL2008 cohort. Unsupervised principal component analysis of (A) genome-wide DNA methylation (740 067 CpGs, n = 128 EPICv.1-analyzed T-ALL), (B) genomic alterations (294 unique CNVs, n = 128 T-ALL), and (C) whole-genome RNA expression (19 043 protein-coding genes, n = 108 T-ALL). (D) Average β-values of the array CpGs (740 067 CpGs, n = 128 EPIC-analyzed T-ALL) separated into CIMP subgroups and controls. (E) Average number of CNVs in CIMP-low (n = 51) vs CIMP-high (n = 77) T-ALL. (F) Common fusions in T-ALL and a relevant CNV in T-ALL (chr9) and 3 significantly different CNVs between CIMP low and CIMP high in 108 T-ALLs. The control cells in panels A, C, and D consisted of CD34+, CD3+, and lymph node, respectively.

Genome-wide multiomics biology phenotype of CIMP subgroups in the NOPHO ALL2008 cohort. Unsupervised principal component analysis of (A) genome-wide DNA methylation (740 067 CpGs, n = 128 EPICv.1-analyzed T-ALL), (B) genomic alterations (294 unique CNVs, n = 128 T-ALL), and (C) whole-genome RNA expression (19 043 protein-coding genes, n = 108 T-ALL). (D) Average β-values of the array CpGs (740 067 CpGs, n = 128 EPIC-analyzed T-ALL) separated into CIMP subgroups and controls. (E) Average number of CNVs in CIMP-low (n = 51) vs CIMP-high (n = 77) T-ALL. (F) Common fusions in T-ALL and a relevant CNV in T-ALL (chr9) and 3 significantly different CNVs between CIMP low and CIMP high in 108 T-ALLs. The control cells in panels A, C, and D consisted of CD34+, CD3+, and lymph node, respectively.

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