Figure 1.
Peripheral blood smear and bone marrow biopsy before and after gilteritinib treatment. (A-C) Before gilteritinib treatment. (D-F) At relapse. (G-I) Two months after gilteritinib treatment. (A) Multiple monocytes and myeloblasts identified in peripheral blood smear (×40). (B) Clusters comprising blasts, monocytoid cells, and dysplastic normoblasts in bone marrow smear (×100). (C) NPM immunostain demonstrating both nuclear and cytoplasmic stains (×40). (D) A few monocytes and blasts in peripheral blood (×40). (E) Multiple monocytoid cells and blasts in clusters in bone marrow smear (×100). (F) Both nuclear and cytoplasmic stains by NPM immunostaining (×40). (G) Leukopenia without circulating blasts, polychromasia, and nucleated red blood cells in peripheral blood smear (×40). (H) Numerous erythroid precursors, dysplastic normoblasts identified in bone marrow smear (×100). (I) NPM immunostain redemonstrating abnormal staining pattern in both cytoplasms and nuclei (×40). (J) Erythroid precursors indicated by E-cadherin (×10) were within the distribution of NPM immunostain (×10) (K) at relapse. (L) Erythroid precursors indicated by CD71 (×10) that markedly increased after gilteritinib treatment were (M) a large proportion of NPM1-mutated cells in bone marrow.

Peripheral blood smear and bone marrow biopsy before and after gilteritinib treatment. (A-C) Before gilteritinib treatment. (D-F) At relapse. (G-I) Two months after gilteritinib treatment. (A) Multiple monocytes and myeloblasts identified in peripheral blood smear (×40). (B) Clusters comprising blasts, monocytoid cells, and dysplastic normoblasts in bone marrow smear (×100). (C) NPM immunostain demonstrating both nuclear and cytoplasmic stains (×40). (D) A few monocytes and blasts in peripheral blood (×40). (E) Multiple monocytoid cells and blasts in clusters in bone marrow smear (×100). (F) Both nuclear and cytoplasmic stains by NPM immunostaining (×40). (G) Leukopenia without circulating blasts, polychromasia, and nucleated red blood cells in peripheral blood smear (×40). (H) Numerous erythroid precursors, dysplastic normoblasts identified in bone marrow smear (×100). (I) NPM immunostain redemonstrating abnormal staining pattern in both cytoplasms and nuclei (×40). (J) Erythroid precursors indicated by E-cadherin (×10) were within the distribution of NPM immunostain (×10) (K) at relapse. (L) Erythroid precursors indicated by CD71 (×10) that markedly increased after gilteritinib treatment were (M) a large proportion of NPM1-mutated cells in bone marrow.

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