Figure 2.
Correlation of STAT3/STAT5B variants with neoplastic cells identified by flow cytometry and genetic features in STAT3/STAT5B-mutant LGLLs and MNs. (A) VAFs of STAT3/STAT5B variants correlated with their corresponding percentage of atypical T or NK cells detected by flow cytometry (R2 = 0.92) in LGLLs whereas there seemed to be no such a correlation in those in (B) MNs (R2 = 0.12). (C) In patients with LGLLs, 35% had concomitant somatic pathogenic and likely pathogenic variants, whereas in patients with MNs, 92% (P < .0001) had at least 1 concomitant variant beyond STAT3/STAT5B variants. (D) The average number of somatic variants was significantly lower in patients with LGLLs (median, 1.7 per patient; range, 1-4 per patient) than in patients with MNs (median, 4.2 per patient; range, 1-8 per patient; ∗∗∗∗P < .0001). (E) The VAFs of the leading concomitant (beyond STAT3/STAT5B) variant in LGLLs (mean, 11.9, range 1 to 32) seemed to be significantly smaller than that in MNs (mean, 37.5, range 2 to 98; ∗∗∗ P = .0003). (F) In LGLLs, there seemed to be a significant correlation (R2= 0.90) between the VAFs of STAT3/STAT5B variants to the VAF of the leading non- STAT3/STAT5B variants, suggesting that STAT3/STAT5B variants are the leading variants in all patients with LGLLs (100% in panel H, blue). (G) This correlation did not exist in MNs (R2 = 0.20), and indeed the data suggested that 48% of all STAT3/STAT5B variants (above the dashed line in panel G) were a subclone (panel H; red; P < .0001).

Correlation of STAT3/STAT5B variants with neoplastic cells identified by flow cytometry and genetic features in STAT3/STAT5B-mutant LGLLs and MNs. (A) VAFs of STAT3/STAT5B variants correlated with their corresponding percentage of atypical T or NK cells detected by flow cytometry (R2 = 0.92) in LGLLs whereas there seemed to be no such a correlation in those in (B) MNs (R2 = 0.12). (C) In patients with LGLLs, 35% had concomitant somatic pathogenic and likely pathogenic variants, whereas in patients with MNs, 92% (P < .0001) had at least 1 concomitant variant beyond STAT3/STAT5B variants. (D) The average number of somatic variants was significantly lower in patients with LGLLs (median, 1.7 per patient; range, 1-4 per patient) than in patients with MNs (median, 4.2 per patient; range, 1-8 per patient; ∗∗∗∗P < .0001). (E) The VAFs of the leading concomitant (beyond STAT3/STAT5B) variant in LGLLs (mean, 11.9, range 1 to 32) seemed to be significantly smaller than that in MNs (mean, 37.5, range 2 to 98; ∗∗∗ P = .0003). (F) In LGLLs, there seemed to be a significant correlation (R2= 0.90) between the VAFs of STAT3/STAT5B variants to the VAF of the leading non- STAT3/STAT5B variants, suggesting that STAT3/STAT5B variants are the leading variants in all patients with LGLLs (100% in panel H, blue). (G) This correlation did not exist in MNs (R2 = 0.20), and indeed the data suggested that 48% of all STAT3/STAT5B variants (above the dashed line in panel G) were a subclone (panel H; red; P < .0001).

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