Fig. 2: Analysis of mutation density dissects aberrant targeting of SHM and CSR. | Leukemia

Fig. 2: Analysis of mutation density dissects aberrant targeting of SHM and CSR.

From: Mutational mechanisms shaping the coding and noncoding genome of germinal center derived B-cell lymphomas

Fig. 2

A Patterns of nucleotide exchanges in their triplet contexts as extracted cohort wide in the switch regions (upper track) and the regions containing V, D and J genes (middle track). These patterns are not mutational signatures, instead they correspond to visualizations of mutational catalogs. Scales on the y-axes in the different tracks are not fixed, instead a horizontal line is inserted at 5% for rough orientation and comparison. B Clustering of the kataegis clusters according to their contributions from CSR-like and SHM-like mutational processes with contributions of SHM-like and CSR-like as axes. Assessment of the contributions of these two mechanisms to all kataegis clusters was performed by non-negative least squares and subsequent unsupervised k-means clustering (k = 3). Kataegis clusters dominated by a CSR-like pattern are colored in orange, clusters dominated by a SHM-like pattern are colored in green and clusters dominated by neither pattern (other) are colored in purple. C kataegis clusters and kataegis regions displayed as oncoprint. The x-axis encodes samples, the y-axis the kataegis regions, which are ordered by recurrency of affection (≥3%, note that for a better overview, the well established kataegis regions in the IG, BCL2 and BCL6 loci are excluded from the inferred oncoprint-like ordering of the samples and only shown for completeness in the lowest five rows). The oncoprint carries four layers of annotation (normalized horizontal stacked barplots): (i) the fractions of the different kataegis cluster categories (SHM-like = green, CSR-like = orange and other = purple); (ii) the mean distance to the closest TSS in bp; (iii) the fraction of variants overlapping exons (black); and (iv) the fractions of chromatin states from GC B cells annotated to the variants in the respective kataegis regions.

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