Figure 3.
BM response to KIT inhibition in patients with SM. (A) At baseline, atypical (hypogranular, immature, and spindle-shaped) MCs in dense aggregates fill the BM (hematoxylin and eosin stain and CD25 immunohistochemical stain). (B) After a few months of therapy, dense aggregates are few in number, and predominantly loose clusters of MCs are present, with fewer atypical MCs (CD117 immunohistochemical stain). (C) By several months of therapy, only interstitial scattered single MCs remain, which are mostly small, round, and well granulated, with few atypical spindle-shaped MCs (tryptase immunohistochemical stain). During this same time period, MCs that express CD25 initially will lose expression of this aberrant marker, reverting to a normal MC phenotype. Serum tryptase levels similarly decline and generally correlate with MC burden in the BM. All magnification ×40.

BM response to KIT inhibition in patients with SM. (A) At baseline, atypical (hypogranular, immature, and spindle-shaped) MCs in dense aggregates fill the BM (hematoxylin and eosin stain and CD25 immunohistochemical stain). (B) After a few months of therapy, dense aggregates are few in number, and predominantly loose clusters of MCs are present, with fewer atypical MCs (CD117 immunohistochemical stain). (C) By several months of therapy, only interstitial scattered single MCs remain, which are mostly small, round, and well granulated, with few atypical spindle-shaped MCs (tryptase immunohistochemical stain). During this same time period, MCs that express CD25 initially will lose expression of this aberrant marker, reverting to a normal MC phenotype. Serum tryptase levels similarly decline and generally correlate with MC burden in the BM. All magnification ×40.

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