References
- Kindler T, Cornejo MG, Scholl C et al. K-RasG12D-induced T-cell lymphoblastic lymphoma/leukemias harbor Notch-1 mutations and are sensitive to γ-secretase inhibitors. Blood112(8), 3373–3382 (2008).
- Weng AP, Millholland JM, Yashiro-Ohtani Y et al. c-Myc is an important direct target of Notch1 in T-cell acute lymphoblastic leukemia/lymphoma. Genes Dev.20(15), 2096–2109 (2006).
- Mansour MR, Linch DC, L Foroni, Goldstone AH, Gale RE. High incidence of NOTCH1 mutations in adult patients with T-cell acute lymphoblastic leukemia. Leukemia20, 537–539 (2006).
- Maser RS, Choudhury B, Campbell PJ et al. Chromosomally unstable mouse tumours have genomic alterations similar to diverse human cancers. Nature447(7147), 966–971 (2007).
- Flex E, Petrangeli V, Stella L, Chiaretti S et al. Somatically acquired JAK1 mutations in adult acute lymphoblastic leukemia. Exp. Med.205(4), 751–758 (2008).
- Palomero T, Sulis ML, Cortina M et al. Mutational loss of PTEN induces resistance to NOTCH1 inhibition in T-cell leukemia. Nat. Med.13(10), 1203–1210 (2007).
- Ferrando AA, Neuberg DS, Staunton J et al. Gene expression signatures define novel oncogenic pathways in T cell acute lymphoblastic leukemia. Cancer Cell1(1), 75–87 (2002).
- Chervinsky DS, Zhao XF, Lam DH, Ellsworth M, Gross KW, Aplan PD. Disordered T-cell development and T-cell malignancies in SCL LMO1 double-transgenic mice: parallels with E2A-deficient mice. Mol. Cell. Biol.19, 5025–5035 (1999).
- Yan W, Young AZ, Soares VC, Kelley R, Benezra R, Zhuang Y. High incidence of T-cell tumors in E2A-null mice and E2A/Id1 double-knockout mice. Mol. Cell. Biol.17, 7317–7327 (1997).
- O’Neil J, Calvo J, McKenna K et al. Activating Notch-1 mutations in mouse models of T-ALL. Blood107, 781–785 (2006).
- Shank-Calvo JA, Draheim K, Bhasin M, Kelliher MA. p16Ink4a or p19Arf loss contributes to Tal1-induced leukemogenesis in mice. Oncogene25, 3023–3031 (2006).
- Bourne HR, Sanders DA, McCormick F. The GTPase superfamily: conserved structure and molecular mechanism. Nature349, 117–127 (1991).
- Boguski MS, McCormick F. Proteins regulating Ras and its relatives. Nature366, 643–654 (1993).
- Rodriguez-Viciana P, Warne PH, Dhand R et al. Phosphatidylinositol-3-OH kinase as a direct target of Ras. Nature370, 527–532 (1994).
- Schubbert S, Shannon K, Bollag G. Hyperactive Ras in developmental disorders and cancer. Nat. Rev. Cancer7, 295–308 (2007).
- Perentesis JP, Bhatia S, Boyle E et al.RAS oncogene mutations and outcome of therapy for childhood acute lymphoblastic leukemia. Leukemia18, 685–692 (2004).
- von Lintig FC, Huvar I, Law P, Diccianni MB, Yu AL, Boss GR. Ras activation in normal white blood cells and childhood acute lymphoblastic leukemia. Clin. Cancer Res.6, 1804–1810 (2000).
- Chan IT, Kutok JL, Williams IR et al. Conditional expression of oncogenic K-ras from its endogenous promoter induces a myeloproliferative disease. J. Clin. Invest.113, 528–538 (2004).
- Braun BS, Tuveson DA, Kong N et al. Somatic activation of oncogenic Krasin hematopoietic cells initiates a rapidly fatal myeloproliferative disorder. Proc. Natl Acad. Sci. USA101, 597–602 (2004).
- Nam CH, Rabbitts TH. The role of LMO2 in development and in T cell leukemia after chromosomal translocation or retroviral insertion. Mol. Ther.13(1), 15–25 (2006).
- Larson RC, Lavenir I, Larson TA et al. Protein dimerization between Lmo2 (Rbtn2) and Tal1 alters thymocyte development and potentiates T cell tumorigenesis in transgenic mice. EMBO J.15(5), 1021–1027 (1996).
- Kelliher MA, Seldin DC, Leder P. Tal-1 induces T cell acute lymphoblastic leukemia accelerated by casein kinase IIα. EMBO J.15, 5160–5166 (1996).
- Zhang J, Wang J, Liu Y et al. Oncogenic Kras-induced leukemogeneis: hematopoietic stem cells as the initial target and lineage-specific progenitors as the potential targets for final leukemic transformation. Blood113(6), 1304–1314 (2009).
- Robey EA, Bluestone JA. Notch signaling in lymphocyte development and function. Curr. Opin. Immunol.16(3), 360–366 (2004).
- Malecki MJ, Sanchez-Irizarry C, Mitchell JL et al. Leukemia-associated mutations within the NOTCH1 heterodimerization domain fall into at least two distinct mechanistic classes. Mol. Cell. Biol.26, 4642–4651 (2006).
- Eguchi-Ishimae M, Eguchi M, Kempski H, Greaves M. NOTCH1 mutation can be an early, prenatal genetic event in T-ALL. Blood111(1), 376–378 (2008).
- Pear WS, Aster JC, Scott ML et al. Exclusive development of T cell neoplasms in mice transplanted with bone marrow expressing activated Notch alleles. J. Exp. Med.183, 2283–2291 (1996).
- Chiang MY, Xu L, Shestova O et al. Leukemia-associated NOTCH1 alleles are weak tumor initiators but accelerate K-ras-initiated leukemia. J. Clin. Invest.118(9), 3181–3194 (2008).
- Lin YW, Nichols RA, Letterio JJ, Aplan PD. Notch-1 mutations are important for leukemic transformation in murine models of precursor-T leukemia/lymphoma. Blood107, 2540–2543 (2006).
- Mansour MR, Duke V, Foroni L, Patel B et al. NOTCH1 mutations are secondary events in some patients with T-cell acute lymphoblastic leukemia. Clin. Cancer Res.13(23), 6964–6969 (2007).
- Howe SJ, Mansour MR, Schwarzwaelder K et al. Insertional mutagenesis combined with acquired somatic mutations causes leukemogenesis following gene therapy of SCID-X1 patients. J. Clin. Invest.118(9), 3143–3150 (2008).
- Gordon WR, Roy M, Vardar-Ulu D et al. Structure of the Notch1 negative regulatory region: implications for normal activation and pathogenic signaling in T-ALL. Blood (2008) (Epub ahead of print).
- Sulis ML, Williams O, Palomero T et al. NOTCH1 extracellular juxtamembrane expansion mutations in T-ALL. Blood112(3), 733–740 (2008).
- Weijzen S, Rizzo P, Braid M et al. Activation of Notch-1 signaling maintains the neoplastic phenotype in human Ras-transformed cells. Nat. Med.8, 979–986 (2002).