Figure 1.
Panel A shows a heat map displaying patient characteristics, E B V infection status, R N A-seq performance, and somatic variants across patients P 1.1, P1.2, P 6, P 4, P 2, P 3, and P 5. The disease types include D L B C L, L P D, and H L, indicated by different colors. E B V status is marked as positive or negative, and RNA-seq is noted as performed or not. The heat map highlights somatic variants in genes such as C A R D 11, G N A 13, M E C O M, I R F 4, P 2 R Y 8, K R A S, and C C N D 3, with color intensity indicating the number of mutations (one mutation or equal or less than 2 mutations). Panel B shows a scatter plot of variant allele frequencies (V A F s) in sequential tumors from patient P 1, plotting V A F in P1.1 versus V A F in P 1.2, indicating distinct clones associated with different somatic variants. Panel C illustrates the proposed clonal evolution model of sequential tumors in patient P 1, showing divergence into distinct D L B C L clones (P 1.1 and P 1.2) associated with specific somatic alterations in the context of S A P deficiency and E B V infection.
Patient characteristics and predicted mechanisms of tumor development. (A–C) Overview of the LPD type of each patient, EBV infection, RNA-seq status, and somatic variants (A). HL, Hodgkin lymphoma. Variant allele frequencies (VAFs) of somatic variants in first and second tumors in P1 are plotted on y and x axes, respectively (B). Distinct clones arose in sequential tumors, driven by different somatic variants plus EBV (C).