Figure 8. The genetic profile of RS differs from that of de novo DLBCL. Percentage of de novo DLBCL and RS cases carrying genetic lesions typically associated with de novo DLBCL and/or RS. The RS panel was composed of 27 cases characterized by WES and CN data (black bars). The de novo DLBCL panel was composed of 71 newly diagnosed and previously untreated DLBCL cases (ABC, n = 40, red; GCB, n = 31, blue), with available CN data and targeted resequencing data of genes commonly mutated in de novo DLBCL. For genes for which we lacked mutational analysis data, we used a recently published WES-dataset of 49 primary DLBCL cases as reported in Lohr et al. (2012; gray bars). Asterisks indicate genes differentially mutated between RS and de novo DLBCL (two-tailed Fisher’s exact test; *, P < 0.05; **, P < 0.01). CNAs, CN aberrations; D, deletion; G, gain; AMP, amplification; Tx, translocation. Biallelic disruption includes M/M, M/D, and D/D events.
Figure 8.

The genetic profile of RS differs from that of de novo DLBCL. Percentage of de novo DLBCL and RS cases carrying genetic lesions typically associated with de novo DLBCL and/or RS. The RS panel was composed of 27 cases characterized by WES and CN data (black bars). The de novo DLBCL panel was composed of 71 newly diagnosed and previously untreated DLBCL cases (ABC, n = 40, red; GCB, n = 31, blue), with available CN data and targeted resequencing data of genes commonly mutated in de novo DLBCL. For genes for which we lacked mutational analysis data, we used a recently published WES-dataset of 49 primary DLBCL cases as reported in Lohr et al. (2012; gray bars). Asterisks indicate genes differentially mutated between RS and de novo DLBCL (two-tailed Fisher’s exact test; *, P < 0.05; **, P < 0.01). CNAs, CN aberrations; D, deletion; G, gain; AMP, amplification; Tx, translocation. Biallelic disruption includes M/M, M/D, and D/D events.

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