Figure 4.
Combined mutations and copy number loss separated into the 2 EBV-tissue positive PCNSL subtypes and EBV−HIV−PCNSL. Mutations and/or CN loss were categorized into pathway categories. CN loss is shown for HLA class I/II. For antigen presentation/processing mutations were combined with CN loss. Mutations for immune function, BCR-NF-κB signaling, epigenetic regulation, cell cycle/adhesion and B-cell differentiation. Percentages are shown for each PCNSL subtype, with P values for paired subtypes: *P ≤ .05; **P ≤ .01; ***P ≤ .001; ****P ≤ .0001. There were 42, 20, and 16 cases of EBV− HIV−, EBV+ HIV+, and EBV+ HIV− PCNSL, respectively (data for the single EBV− HIV− PCNSL tissue is not shown).

Combined mutations and copy number loss separated into the 2 EBV-tissue positive PCNSL subtypes and EBVHIVPCNSL. Mutations and/or CN loss were categorized into pathway categories. CN loss is shown for HLA class I/II. For antigen presentation/processing mutations were combined with CN loss. Mutations for immune function, BCR-NF-κB signaling, epigenetic regulation, cell cycle/adhesion and B-cell differentiation. Percentages are shown for each PCNSL subtype, with P values for paired subtypes: *P ≤ .05; **P ≤ .01; ***P ≤ .001; ****P ≤ .0001. There were 42, 20, and 16 cases of EBV HIV, EBV+ HIV+, and EBV+ HIV PCNSL, respectively (data for the single EBV HIV PCNSL tissue is not shown).

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