Figure 2.
Figure 2. Representative BM histomorphology of different myeloid neoplasms with eosinophilia. (A-B) CEL, NOS. (A) Hematoxylin and eosin (H&E). Histology of the BM shows an extremely hypercellular marrow with packed infiltrates of eosinophils. Normal blood cell precursors are absent. (B) Wright-Giemsa. Cytomorphological aspects on a BM smear also exhibit an abundance of eosinophils at all stages of maturation. Note that significant cellular atypia is absent. (C-D) KIT D816V-positive systemic mastocytosis with associated chronic eosinophilic leukemia (SM-CEL). (C) H&E. BM histology reveals a markedly hypercellular marrow with a massive increase in eosinophils. Centrally located in the marrow space, a compact infiltrate consisting of pale, mostly spindle-shaped cells is easily detected (left). (D) Higher magnification and Wright-Giemsa stain reveals that the spindle-shaped cells contain metachromatic granules, although in lesser number than normal mast cells. The presence of compact infiltrates mainly consisting of spindle-shaped cells allows prompt diagnosis of a systemic mastocytosis. (E-F) FIP1L1-PDGFRA-positive myeloid neoplasm. (E) H&E-stained BM shows massive hypercellularity with increase in eosinophils, which form narrow rows as an indirect sign of fibrosis. Normal blood cell precursors, in particular megakaryocytes, are missing. (F) ABC method. Anti-CD117 immunohistochemistry reveals an increase in spindle-shaped, mostly loosely scattered mast cells, with expression of CD117 (KIT). Note a small cohesive group of round mast cells on the right not sufficient for a diagnosis of systemic mastocytosis to be established. Mast cells display aberrant expression of CD25 (not depicted), which is seen outside the setting of mastocytosis only in FIP1L1-PDGFRA-positive myeloid neoplasms. (G-H) PCM1-JAK2-positive myeloid neoplasm. (G) H&E. (H) Wright-Giemsa. Extremely hypercellular BM with subtotal depletion of fat cells and massive increase in erythroblasts forming irregular giant erythra filling whole marrow spaces, and thus exceeding the size seen in any other myeloid neoplasm or reactive states. Images courtesy of Professor Hans-Peter Horny.

Representative BM histomorphology of different myeloid neoplasms with eosinophilia. (A-B) CEL, NOS. (A) Hematoxylin and eosin (H&E). Histology of the BM shows an extremely hypercellular marrow with packed infiltrates of eosinophils. Normal blood cell precursors are absent. (B) Wright-Giemsa. Cytomorphological aspects on a BM smear also exhibit an abundance of eosinophils at all stages of maturation. Note that significant cellular atypia is absent. (C-D) KIT D816V-positive systemic mastocytosis with associated chronic eosinophilic leukemia (SM-CEL). (C) H&E. BM histology reveals a markedly hypercellular marrow with a massive increase in eosinophils. Centrally located in the marrow space, a compact infiltrate consisting of pale, mostly spindle-shaped cells is easily detected (left). (D) Higher magnification and Wright-Giemsa stain reveals that the spindle-shaped cells contain metachromatic granules, although in lesser number than normal mast cells. The presence of compact infiltrates mainly consisting of spindle-shaped cells allows prompt diagnosis of a systemic mastocytosis. (E-F) FIP1L1-PDGFRA-positive myeloid neoplasm. (E) H&E-stained BM shows massive hypercellularity with increase in eosinophils, which form narrow rows as an indirect sign of fibrosis. Normal blood cell precursors, in particular megakaryocytes, are missing. (F) ABC method. Anti-CD117 immunohistochemistry reveals an increase in spindle-shaped, mostly loosely scattered mast cells, with expression of CD117 (KIT). Note a small cohesive group of round mast cells on the right not sufficient for a diagnosis of systemic mastocytosis to be established. Mast cells display aberrant expression of CD25 (not depicted), which is seen outside the setting of mastocytosis only in FIP1L1-PDGFRA-positive myeloid neoplasms. (G-H) PCM1-JAK2-positive myeloid neoplasm. (G) H&E. (H) Wright-Giemsa. Extremely hypercellular BM with subtotal depletion of fat cells and massive increase in erythroblasts forming irregular giant erythra filling whole marrow spaces, and thus exceeding the size seen in any other myeloid neoplasm or reactive states. Images courtesy of Professor Hans-Peter Horny.

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