Figure 1.
Figure 1. Recurrently mutated genes in the tumor cells of cHL. (Top) Total number of nonsilent somatic mutations present in each of the 34 cHL cases, identified by their identification number and annotated based on histological subtype (ld, lymphocyte depletion; lr, lymphocyte-rich; mc, mixed cellularity; nc, not classifiable; ns, nodular sclerosis). EBV infection status, presence/absence of JAK2 copy number gains, and the status of 3 JAK-STAT pathway genes (PTPN1, STAT3, and STAT5B) that were found mutated in <3 cases are provided for individual cases (columns) in the heat map below, along with the mutation pattern of genes found mutated in ≥ 3 cases (rows). Color codes at the bottom denote the type of mutation. The bar plots on the right give the percentage and absolute number of cases showing the feature displayed in the corresponding row across all samples.

Recurrently mutated genes in the tumor cells of cHL. (Top) Total number of nonsilent somatic mutations present in each of the 34 cHL cases, identified by their identification number and annotated based on histological subtype (ld, lymphocyte depletion; lr, lymphocyte-rich; mc, mixed cellularity; nc, not classifiable; ns, nodular sclerosis). EBV infection status, presence/absence of JAK2 copy number gains, and the status of 3 JAK-STAT pathway genes (PTPN1, STAT3, and STAT5B) that were found mutated in <3 cases are provided for individual cases (columns) in the heat map below, along with the mutation pattern of genes found mutated in ≥ 3 cases (rows). Color codes at the bottom denote the type of mutation. The bar plots on the right give the percentage and absolute number of cases showing the feature displayed in the corresponding row across all samples.

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