Figure 3.
Figure 3. Correlation analysis and the robust prognostic effect of CD37 expression in patients with DLBCL. (A) A distribution plot showing that CD37− GCB-DLBCL (denoted by the yellow bar) more frequently had TP53 mutations (highlighted in red) or high levels of nuclear p50 (yellow), Myc (green), p-STAT3 (orange), and p65 (lighter red) expression compared with CD37+ GCB-DLBCL (denoted by the blue bar). (B) A distribution plot showing that CD37− ABC-DLBCL more frequently had high nuclear p50 (yellow) and survivin (pink) expression and BCL6 translocation (green), whereas CD37+ ABC-DLBCL more frequently had PI3K (blue) and CXCR4 (purple) overexpression. Each column in panels A and B represents 1 patient; cases without indicated abnormalities detected are shown in light blue (negative) or white (unknown). (C) In GCB-DLBCL, CD37 positivity predicted significantly improved survival, regardless of presence of TP53 mutations, p50high, Mychigh, p-STAT3high, GCET1high, and to a lesser extent, MYC translocations. Conversely, the adverse effect of CD37 negativity was independent of all these biomarkers. Particularly, CD37− patients without TP53 mutations and p50/Myc overexpression remained to have significantly worse survival than patients with CD37+ GCB-DLBCL. (D) In GCB-DLBCL, CD37 positivity predicted significantly better survival even when the patients had high IPI scores. (E) In ABC-DLBCL, the adverse prognostic effect of CD37 negativity was independent of p50, survivin, p63, PI3K, and CXCR4 expression and BCL6 translocations. In particular, CD37− patients without p50 and survivin overexpression remained to have significantly worse survival than patients with CD37+ ABC-DLBCL. (F) In ABC-DLBCL, CD37 and IPI had independent prognostic impact. The cutoffs for high/positive expression as indicated by p50+, Myc+, p-STAT3+, GCET1+, survivin+, p63+, PI3K+, and CXCR4+ in the figures were ≥20%, ≥70%, ≥50%, ≥50%, >25%, >5%, ≥70%, and ≥20%, respectively.

Correlation analysis and the robust prognostic effect of CD37 expression in patients with DLBCL. (A) A distribution plot showing that CD37 GCB-DLBCL (denoted by the yellow bar) more frequently had TP53 mutations (highlighted in red) or high levels of nuclear p50 (yellow), Myc (green), p-STAT3 (orange), and p65 (lighter red) expression compared with CD37+ GCB-DLBCL (denoted by the blue bar). (B) A distribution plot showing that CD37 ABC-DLBCL more frequently had high nuclear p50 (yellow) and survivin (pink) expression and BCL6 translocation (green), whereas CD37+ ABC-DLBCL more frequently had PI3K (blue) and CXCR4 (purple) overexpression. Each column in panels A and B represents 1 patient; cases without indicated abnormalities detected are shown in light blue (negative) or white (unknown). (C) In GCB-DLBCL, CD37 positivity predicted significantly improved survival, regardless of presence of TP53 mutations, p50high, Mychigh, p-STAT3high, GCET1high, and to a lesser extent, MYC translocations. Conversely, the adverse effect of CD37 negativity was independent of all these biomarkers. Particularly, CD37 patients without TP53 mutations and p50/Myc overexpression remained to have significantly worse survival than patients with CD37+ GCB-DLBCL. (D) In GCB-DLBCL, CD37 positivity predicted significantly better survival even when the patients had high IPI scores. (E) In ABC-DLBCL, the adverse prognostic effect of CD37 negativity was independent of p50, survivin, p63, PI3K, and CXCR4 expression and BCL6 translocations. In particular, CD37 patients without p50 and survivin overexpression remained to have significantly worse survival than patients with CD37+ ABC-DLBCL. (F) In ABC-DLBCL, CD37 and IPI had independent prognostic impact. The cutoffs for high/positive expression as indicated by p50+, Myc+, p-STAT3+, GCET1+, survivin+, p63+, PI3K+, and CXCR4+ in the figures were ≥20%, ≥70%, ≥50%, ≥50%, >25%, >5%, ≥70%, and ≥20%, respectively.

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