Figure 3.
pSTAT3 and H3K4me3 immunostaining in BI-ALCL. Representative STAT3 wild-type (A) and STAT3-mutated (B) BI-ALCL cases showing nuclear expression of phospho-STAT3 in tumor cells regardless of the mutational status (A, hematoxylin and eosin stain, original magnification ×200; B, hematoxylin and eosin stain, original magnification ×200). Representative cases of KMT2C/2D wild-type BI-ALCLs showing strong nuclear expression of H3K4me3 (C, original magnification ×400) and H3K4me1 (D, original magnification ×400) with similar intensities in lymphoma cells and reactive surrounding cells. By contrast, the nuclear H3K4me3 staining in a representative case of KMT2C mutated BI-ALCL was weaker in tumoral cells than in reactive cells such as neutrophils (E, original magnification ×200). Similarly, nuclear H3K4me1 staining was lost in most neoplastic cells of a KMT2D-mutated BI-ALCL case (F, original magnification ×200).

pSTAT3 and H3K4me3 immunostaining in BI-ALCL. Representative STAT3 wild-type (A) and STAT3-mutated (B) BI-ALCL cases showing nuclear expression of phospho-STAT3 in tumor cells regardless of the mutational status (A, hematoxylin and eosin stain, original magnification ×200; B, hematoxylin and eosin stain, original magnification ×200). Representative cases of KMT2C/2D wild-type BI-ALCLs showing strong nuclear expression of H3K4me3 (C, original magnification ×400) and H3K4me1 (D, original magnification ×400) with similar intensities in lymphoma cells and reactive surrounding cells. By contrast, the nuclear H3K4me3 staining in a representative case of KMT2C mutated BI-ALCL was weaker in tumoral cells than in reactive cells such as neutrophils (E, original magnification ×200). Similarly, nuclear H3K4me1 staining was lost in most neoplastic cells of a KMT2D-mutated BI-ALCL case (F, original magnification ×200).

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