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1) Thien CB, Langdon WY. Cbl: Many adaptations to regulate protein tyrosine kinases. Nat Rev Mol Cell Biol. 2001; 2: 294-307
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2) Schmidt MHH, Dikic I. The cbl interactome and its functions. Nat Rev Mol Cell Biol. 2005; 6: 907-18
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3) Sanada M, Suzuki T, Shih LY, et al. Gain-of-function of mutated C-CBL tumour suppressor in myeloid neoplasms. Nature. 2009; 460: 904-8
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4) Dunbar AJ, Gondek LP, OʼKeefe CL, et al. 250K single nucleotide polymorphism array karyotyping identifies acquired uniparental disomy and homozygous mutations, including novel missense substitutions of c-Cbl, in myeloid malignancies. Cancer Res. 2008; 68: 10349-57
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5) Sargin B, Choudhary C, Crosetto N, et al. Flt3-dependent transformation by inactivating c-Cbl mutations in AML. Blood. 2007; 110: 1004-12
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6) Caligiuri MA, Briesewitz R, Yu J, et al. Novel c-CBL and CBL-b ubiquitin ligase mutations in human acute myeloid leukemia. Blood. 2007; 110: 1022-4
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7) Abbas S, Rotmans G, Löwenberg B, et al. Exon 8 splice site mutations in the gene encoding the E3-ligase CBL are associated with core binding factor acute myeloid leukemias. Haematologica. 2008; 93: 1595-7
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8) Reindl C, Quentmeier H, Petropoulos K, et al. CBL exon 8/9 mutants activate the FLT3 pathway and cluster in core binding factor/11q deletion acute myeloid leukemia/myelodysplastic syndrome subtypes. Clin Cancer Res. 2009; 15: 2238-47
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9) Grand FH, Hidalgo-Curtis CE, Ernst T, et al. Frequent CBL mutations associated with 11q acquired uniparental disomy in myeloproliferative neoplasms. Blood. 2009; 113: 6182-92
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10) Vardiman JW, Thiele J, Arber DA, et al. The 2008 revision of the World Health Organization (WHO) classification of myeloid neoplasms and acute leukemia: rational and important changes. Blood. 2009; 114: 937-51
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11) Loh ML, Sakai DS, Flotho C, et al. Mutations in CBL occur frequently in juvenile myelomonocytic leukemia. Blood. 2009; 114: 1859-63
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12) Muramatsu H, Makishima H, Jankowska AM, et al. Mutations of E3 ubiquitin ligase Cbl family members but not TET2 mutations are pathogenic in juvenile myelomonocytic leukemia. Blood. 2010; 115: 1969-75
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13) Kohlmann A, Grossmann V, Klein HU, et al. Next-generation sequencing technology reveals a characteristic pattern of molecular mutations in 72. 8% of chronic myelomonocytic leukemia by detecting frequent alterations in TET2, CBL, RAS, and RUNX1. J Clin Oncol. 2010 Jul 19. [Epub ahead of print]
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14) Martinelli S, De Luca A, Stellacci E, et al. Heterozygous germline mutations in the CBL tumor-suppressor gene cause a Noonan syndrome-like phenotype. Am J Hum Genet. 2010 Jul 7. [Epub ahead of print]
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15) Lang GA, Iwakuma T, Suh YA, et al. Gain of function of a p53 hot spot mutation in a mouse model of Li-Fraumeni syndrome. Cell. 2004; 119: 861-72
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16) Olive KP, Tuveson DA, Ruhe ZH, et al. Mutant p53 gain of function in two mouse models of Li-Fraumeni syndrome. Cell. 2004; 119: 847-60
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17) Naramura M, Jang IK, Kole H, et al. c-Cbl and Cbl-b regulate T cell responsiveness by promoting ligand-induced TCR down-modulation. Nat Immunol. 2002; 3: 1192-9
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