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Fig. 3 | Molecular Cancer

Fig. 3

From: Overexpression of wild type RRAS2, without oncogenic mutations, drives chronic lymphocytic leukemia

Fig. 3

RRAS2-driven CLL harbors a highly conserved pattern of somatic mutations. a Pie chart representation of the somatic mutation distribution from CD19 + CD5+ leukemic cells by chromosome. Spleens from seven Rosa26-RRAS2fl/flxmb1-Cre mice were included in this analysis (ages in panel e). b Ingenuity Pathway Analysis (IPA) diagram of the immunological and hematological neoplastic signature generated from the 270 mutations present in all seven different Rosa26-RRAS2fl/flxmb1-Cre mice. c Pie chart representation of the co-occurrence of gene mutations in murine CLL vs human CLL. d Summary of most frequently mutated genes in 1094 cases of human CLL also identified in Rosa26-RRAS2 murine CLL. The panel also shows each gene’s condition in MBL (monoclonal B lymphocytosis) and other human leukemias (BL:Burkitt Lymphoma; MCL: Mantle Cell Lymphoma; DLBCL: Diffuse Large B Cell Lymphoma; CTL:Cutaneous T cell lymphoma; FL: Follicular Lymphoma; MM: Multiple Myeloma; MZL; Marginal Zone Lymphoma; SS: Sezary Syndrome). e Heatmap of mutation rates of 107 mutated genes detected in CD19 + CD5+ leukemic cells from seven Rosa26-RRAS2fl/flxmb1-Cre independent mice (age of mice: Ctrl 1–3, 12 wk.; Ctrl 4–6 25 wk.; BCLL-9, 104 wk.; BCLL10–11 and BCLL16–17, 54 wk.; BCLL13–14, 32 wk). Black: homozygous; grey: heterozygous; white: unmutated. f Schematic representation of registered missense mutations in SPEN, ARID1A and AKAP13 in human CLL patients (green dots: missense mutation; black dots: truncating mutations; orange dots: splicing site mutation). Red text indicates mutations found in Rosa26-RRAS2fl/flxmb1-Cre mice which are also present in human genes

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