Figure 1
Figure 1. FP-positive CEL with concomitant KIT D816V mutation. (A) Hypercellular BM biopsy with a marked increase in eosinophils (Giemsa stain). (B-E) Phenotypically aberrant MCs are arranged in loose clusters and as interstial infiltrates (B) tryptase, (C) CD117, (D) CD2, and (E) CD25. (F-I) fluorescence in situ hybridization with a 4q12 tri-color rearrangement probe (F) alone or (G-H) combined with tryptase IH (fiction) (note nuclei with green/aqua fusion signals [arrows] as a surrogate for CHIC2 deletion). Normal tricolor green/orange/aqua fusion signals are marked by an arrowhead. (J) c-kit antisense sequence of microdissected MCs from FIP1L1-PDGFRA–positive CEL showing a KIT D816V mutation. (A-E) Photomicrographs by Horn Imaging Camera (Aalen, Germany) adopted to a Zeiss Imager.M1 (Carl Zeiss, Oberkochen, Germany) microscope. (F-I) Imaging system ApoTome.2 (Carl Zeiss).

FP-positive CEL with concomitant KIT D816V mutation. (A) Hypercellular BM biopsy with a marked increase in eosinophils (Giemsa stain). (B-E) Phenotypically aberrant MCs are arranged in loose clusters and as interstial infiltrates (B) tryptase, (C) CD117, (D) CD2, and (E) CD25. (F-I) fluorescence in situ hybridization with a 4q12 tri-color rearrangement probe (F) alone or (G-H) combined with tryptase IH (fiction) (note nuclei with green/aqua fusion signals [arrows] as a surrogate for CHIC2 deletion). Normal tricolor green/orange/aqua fusion signals are marked by an arrowhead. (J) c-kit antisense sequence of microdissected MCs from FIP1L1-PDGFRA–positive CEL showing a KIT D816V mutation. (A-E) Photomicrographs by Horn Imaging Camera (Aalen, Germany) adopted to a Zeiss Imager.M1 (Carl Zeiss, Oberkochen, Germany) microscope. (F-I) Imaging system ApoTome.2 (Carl Zeiss).

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