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. Author manuscript; available in PMC: 2012 Jul 26.
Published in final edited form as: Oncogene. 2011 Jun 27;31(4):494–506. doi: 10.1038/onc.2011.251

Fig. 2. The absence of the clathrin-binding region of CALM alters the phenotype of CALM-AF10+ myeloid neoplasms.

Fig. 2

(A) Schematic representation of CALM, AF10 and CALM-AF10 fusion proteins. The two breakpoints in CALM, and one of the four breakpoints in AF10 are indicated by black lines and the base pair position. The two CALM-AF10 fusion proteins used in this study are shown. (B) Survival curves of mice injected with progenitor cells transduced with CALM2091AF10, CALM1926AF10 or MIGR1 (control vector). CA= CALM-AF10; 2ND = secondary recipients of primary MPD or AML cells. (C) Fluorescence-activated cell sorter analysis of cells isolated from spleen of CALM-AF10 mice. Analysis of GFP-gated cells reveals an enrichment of myeloid lineage-specific markers (CD11b+Gr-1med-hi) and decrease in erythroid cells (CD71+Ter119+) in CALM2091AF10 and CALM1926AF10 mice compared to control (MIGR1) mice. (D) Peripheral blood, bone marrow aspirates and spleen touch preparations (TP) were stained with Wright-Giemsa. Paraffin-embedded liver and spleen sections were stained with hematoxylin and eosin. Original magnification ×100 for spleen and liver; ×500 for blood, spleen-TP and bone marrow; ×1000 for spleen and insets.