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. Author manuscript; available in PMC: 2018 Aug 1.
Published in final edited form as: Leuk Res. 2017 Jun 1;59:105–109. doi: 10.1016/j.leukres.2017.05.018

Figure 1. Clinical, histopathologic and molecular profile of patients with mast cell leukemia (aMCL).

Figure 1

A) Survival in patients with aMCL was not significantly different according to the presence or the absence of associated hematologic neoplasm (AHN) B) Survival of patients with aMCL was significantly inferior when compared with aggressive (ASM) and indolent systemic mastocytosis (ISM). (C–H) Bone marrow features of aMCL (with/without) AHN. Bone marrow biopsies (Hematoxylin and Eosin, original magnification ×400) show a mast cell infiltrate replacing the BM medullary space, comprising spindle shaped mast cells (C) or anaplastic large mast cells (D). BM aspirate smear (E) illustrates the cellular details of anaplastic mast cells from case D (Wright- Giemsa, original magnification ×1000). F–H are examples of aMCL-AHN cases. BM aspirate smear (F) shows a case of aMCL with chronic myelomonocytic leukemia. Mast cells are heavily granulated as indicated by arrows. There are increased monocytes as indicated by arrow heads. Also seen in picture F are easily identified blasts, dysplastic erythroid precursors and dysgranulopoiesis. G–H shows a case of aMCL with refractory anemia with ring sideroblasts. BM biopsy (G) shows sheets of mast cells, and dysplastic megakaryocytes (indicated by arrows); Iron stain reveals numerous ring sideroblasts (H) (original magnification ×1000). I) Summary of targeted next generation sequencing using a 49 gene panel for 8 patients with aMCL. Each column represents an individual patient and each row represents mutated genes in alphabetical order. KIT and TET2 gene mutations were most frequently observed. The amino acid changes resulting from the mutations are represented in different colors.