Kralovics R . Genetic complexity of myeloproliferative neoplasms. Leukemia 2008; 22: 1841–1848. ArticleCASPubMed Google Scholar
James C, Ugo V, Le Couedic JP, Staerk J, Delhommeau F, Lacout C et al. A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera. Nature 2005; 434: 1144–1148. ArticleCASPubMed Google Scholar
Kralovics R, Passamonti F, Buser A, Teo S, Tiedt R, Passweg J et al. A gain-of-function mutation of JAK2 in myeloproliferative disorders. N Engl J Med 2005; 352: 1779–1790. ArticleCASPubMed Google Scholar
Levine R, Wadleigh M, Cools J, Ebert B, Wernig G, Huntly B et al. Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis. Cancer Cell 2005; 7: 387–397. ArticleCASPubMed Google Scholar
Baxter EJ, Scott LM, Campbell PJ, East C, Fourouclas N, Swanton S et al. Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders. Lancet 2005; 365: 1054–1061. ArticleCASPubMed Google Scholar
Scott L, Tong W, Levine R, Scott M, Beer P, Stratton M et al. JAK2 exon 12 mutations in polycythemia vera and idiopathic erythrocytosis. N Engl J Med 2007; 356: 459–468. ArticleCASPubMedPubMed Central Google Scholar
Pietra D, Li S, Brisci A, Passamonti F, Rumi E, Theocharides A et al. Somatic mutations of JAK2 exon 12 in patients with JAK2 (V617F)-negative myeloproliferative disorders. Blood 2008; 111: 1686–1689. ArticleCASPubMed Google Scholar
Pikman Y, Lee B, Mercher T, McDowell E, Ebert B, Gozo M et al. MPLW515L is a novel somatic activating mutation in myelofibrosis with myeloid metaplasia. PLoS Med 2006; 3: e270. ArticlePubMedPubMed Central Google Scholar
Pardanani A, Levine R, Lasho T, Pikman Y, Mesa R, Wadleigh M et al. MPL515 mutations in myeloproliferative and other myeloid disorders: a study of 1182 patients. Blood 2006; 108: 3472–3476. ArticleCASPubMed Google Scholar
Grand FH, Hidalgo-Curtis CE, Ernst T, Zoi K, Zoi C, McGuire C et al. Frequent CBL mutations associated with 11q acquired uniparental disomy in myeloproliferative neoplasms. Blood 2009; 113: 6182–6192. ArticleCASPubMed Google Scholar
Delhommeau F, Dupont S, Della Valle V, James C, Trannoy S, Massé A et al. Mutation in TET2 in myeloid cancers. N Engl J Med 2009; 360: 2289–2301. ArticlePubMed Google Scholar
Wolanskyj A, Lasho T, Schwager S, McClure R, Wadleigh M, Lee S et al. JAK2 mutation in essential thrombocythaemia: clinical associations and long-term prognostic relevance. Br J Haematol 2005; 131: 208–213. ArticleCASPubMed Google Scholar
Theocharides A, Boissinot M, Girodon F, Garand R, Teo S, Lippert E et al. Leukemic blasts in transformed JAK2-V617F-positive myeloproliferative disorders are frequently negative for the JAK2-V617F mutation. Blood 2007; 110: 375–379. ArticleCASPubMed Google Scholar
Campbell PJ, Baxter EJ, Beer PA, Scott LM, Bench AJ, Huntly BJ et al. Mutation of JAK2 in the myeloproliferative disorders: timing, clonality studies, cytogenetic associations, and role in leukemic transformation. Blood 2006; 108: 3548–3555. ArticleCASPubMed Google Scholar
Abdel-Wahab O, Manshouri T, Patel J, Harris K, Yao J, Hedvat C et al. Genetic analysis of transforming events that convert chronic myeloproliferative neoplasms to leukemias. Cancer Res 2010; 70: 447–452. ArticleCASPubMedPubMed Central Google Scholar
Green A, Beer P . Somatic mutations of IDH1 and IDH2 in the leukemic transformation of myeloproliferative neoplasms. N Engl J Med 2010; 362: 369–370. ArticleCASPubMed Google Scholar
Mardis ER, Ding L, Dooling DJ, Larson DE, McLellan MD, Chen K et al. Recurring mutations found by sequencing an acute myeloid leukemia genome. N Engl J Med 2009; 361: 1058–1066. ArticleCASPubMedPubMed Central Google Scholar
Kralovics R, Teo SS, Li S, Theocharides A, Buser AS, Tichelli A et al. Acquisition of the V617F mutation of JAK2 is a late genetic event in a subset of patients with myeloproliferative disorders. Blood 2006; 108: 1377–1380. ArticleCASPubMed Google Scholar
Olcaydu D, Harutyunyan A, Jäger R, Berg T, Gisslinger B, Pabinger I et al. A common JAK2 haplotype confers susceptibility to myeloproliferative neoplasms. Nat Genet 2009; 41: 450–454. ArticleCASPubMed Google Scholar
Moffat J, Grueneberg DA, Yang X, Kim SY, Kloepfer AM, Hinkle G et al. A lentiviral RNAi library for human and mouse genes applied to an arrayed viral high-content screen. Cell 2006; 124: 1283–1298. ArticleCASPubMed Google Scholar
Zufferey R, Nagy D, Mandel RJ, Naldini L, Trono D . Multiply attenuated lentiviral vector achieves efficient gene delivery in vivo. Nat Biotechnol 1997; 15: 871–875. ArticleCASPubMed Google Scholar
Georgopoulos K, Bigby M, Wang J, Molnar A, Wu P, Winandy S et al. The Ikaros gene is required for the development of all lymphoid lineages. Cell 1994; 79: 143–156. ArticleCASPubMed Google Scholar
Winandy S, Wu P, Georgopoulos K . A dominant mutation in the Ikaros gene leads to rapid development of leukemia and lymphoma. Cell 1995; 83: 289–299. ArticleCASPubMed Google Scholar
Wang J, Nichogiannopoulou A, Wu L, Sun L, Sharpe A, Bigby M et al. Selective defects in the development of the fetal and adult lymphoid system in mice with an Ikaros null mutation. Immunity 1996; 5: 537–549. ArticleCASPubMed Google Scholar
Kano G, Morimoto A, Takanashi M, Hibi S, Sugimoto T, Inaba T et al. Ikaros dominant negative isoform (Ik6) induces IL-3-independent survival of murine pro-B lymphocytes by activating JAK-STAT and up-regulating Bcl-xl levels. Leuk Lymphoma 2008; 49: 965–973. ArticleCASPubMed Google Scholar
Georgopoulos K, Moore D, Derfler B . Ikaros, an early lymphoid-specific transcription factor and a putative mediator for T cell commitment. Science 1992; 258: 808–812. ArticleCASPubMed Google Scholar
Kirstetter P, Thomas M, Dierich A, Kastner P, Chan S . Ikaros is critical for B cell differentiation and function. Eur J Immunol 2002; 32: 720–730. ArticleCASPubMed Google Scholar
Lopez RA, Schoetz S, DeAngelis K, O’Neill D, Bank A . Multiple hematopoietic defects and delayed globin switching in Ikaros null mice. Proc Natl Acad Sci USA 2002; 99: 602–607. ArticleCASPubMedPubMed Central Google Scholar
Mullighan C, Miller C, Radtke I, Phillips L, Dalton J, Ma J et al. BCR-ABL1 lymphoblastic leukaemia is characterized by the deletion of Ikaros. Nature 2008; 453: 110–114. ArticleCASPubMed Google Scholar
Iacobucci I, Storlazzi C, Cilloni D, Lonetti A, Ottaviani E, Soverini S et al. Identification and molecular characterization of recurrent genomic deletions on 7p12 in the IKZF1 gene in a large cohort of BCR-ABL1-positive acute lymphoblastic leukemia patients: on behalf of Gruppo Italiano Malattie Ematologiche dell’Adulto Acute Leukemia Working Party (GIMEMA AL WP). Blood 2009; 114: 2159–2167. ArticleCASPubMed Google Scholar
Grimwade D, Walker H, Oliver F, Wheatley K, Harrison C, Harrison G et al. The importance of diagnostic cytogenetics on outcome in AML: analysis of 1,612 patients entered into the MRC AML 10 trial. The Medical Research Council Adult and Children's Leukaemia Working Parties. Blood 1998; 92: 2322–2333. CASPubMed Google Scholar
Mesa R, Li C, Ketterling R, Schroeder G, Knudson R, Tefferi A . Leukemic transformation in myelofibrosis with myeloid metaplasia: a single-institution experience with 91 cases. Blood 2005; 105: 973–977. ArticleCASPubMed Google Scholar
Mullighan C, Su X, Zhang J, Radtke I, Phillips L, Miller C et al. Deletion of IKZF1 and prognosis in acute lymphoblastic leukemia. N Engl J Med 2009; 360: 470–480. ArticleCASPubMedPubMed Central Google Scholar
Martinelli G, Iacobucci I, Storlazzi C, Vignetti M, Paoloni F, Cilloni D et al. IKZF1 (Ikaros) deletions in BCR-ABL1-positive acute lymphoblastic leukemia are associated with short disease-free survival and high rate of cumulative incidence of relapse: a GIMEMA AL WP report. J Clin Oncol 2009; 27: 5202–5207. ArticleCASPubMed Google Scholar
Luna-Fineman S, Shannon KM, Lange BJ . Childhood monosomy 7: epidemiology, biology, and mechanistic implications. Blood 1995; 85: 1985–1999. CASPubMed Google Scholar
Lacronique V, Boureux A, Valle V, Poirel H, Quang C, Mauchauffé M et al. A TEL-JAK2 fusion protein with constitutive kinase activity in human leukemia. Science 1997; 278: 1309–1312. ArticleCASPubMed Google Scholar
Reiter A, Walz C, Watmore A, Schoch C, Blau I, Schlegelberger B et al. The t(8;9)(p22;p24) is a recurrent abnormality in chronic and acute leukemia that fuses PCM1 to JAK2. Cancer Res 2005; 65: 2662–2667. ArticleCASPubMed Google Scholar
Griesinger F, Hennig H, Hillmer F, Podleschny M, Steffens R, Pies A et al. A BCR-JAK2 fusion gene as the result of a t(9;22)(p24;q11.2) translocation in a patient with a clinically typical chronic myeloid leukemia. Genes Chromosomes Cancer 2005; 44: 329–333. ArticleCASPubMed Google Scholar
Mercher T, Wernig G, Moore S, Levine R, Gu T, Fröhling S et al. JAK2T875N is a novel activating mutation that results in myeloproliferative disease with features of megakaryoblastic leukemia in a murine bone marrow transplantation model. Blood 2006; 108: 2770–2779. ArticleCASPubMedPubMed Central Google Scholar
Kearney L, Gonzalez De Castro D, Yeung J, Procter J, Horsley SW, Eguchi-Ishimae M et al. Specific JAK2 mutation (JAK2R683) and multiple gene deletions in Down syndrome acute lymphoblastic leukemia. Blood 2009; 113: 646–648. ArticleCASPubMed Google Scholar
Mullighan C, Zhang J, Harvey R, Collins-Underwood J, Schulman B, Phillips L et al. JAK mutations in high-risk childhood acute lymphoblastic leukemia. Proc Natl Acad Sci USA 2009; 106: 9414–9418. ArticleCASPubMedPubMed Central Google Scholar