Deletions of the transcription factor Ikaros in myeloproliferative neoplasms
暂无分享,去创建一个
M. Cazzola | R. Kralovics | F. Passamonti | H. Gisslinger | T. Klampfl | A. Harutyunyan | T. Berg | B. Gisslinger | D. Olcaydu | E. Rumi | D. Pietra | R. Jäger | Roland Jäger | Damla Olcaydu
[1] A. Green,et al. Somatic mutations of IDH1 and IDH2 in the leukemic transformation of myeloproliferative neoplasms. , 2010, The New England journal of medicine.
[2] O. Abdel-Wahab,et al. Genetic analysis of transforming events that convert chronic myeloproliferative neoplasms to leukemias. , 2010, Cancer research.
[3] R. Foà,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. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[4] Ken Chen,et al. Recurring mutations found by sequencing an acute myeloid leukemia genome. , 2009, The New England journal of medicine.
[5] R. Levine,et al. Mutation in TET2 in myeloid cancers. , 2009, The New England journal of medicine.
[6] R. Foà,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). , 2009, Blood.
[7] M. Loh,et al. JAK mutations in high-risk childhood acute lymphoblastic leukemia , 2009, Proceedings of the National Academy of Sciences.
[8] Ashot Harutyunyan,et al. A common JAK2 haplotype confers susceptibility to myeloproliferative neoplasms , 2009, Nature Genetics.
[9] K. Anderson,et al. Specific JAK2 mutation (JAK2R683) and multiple gene deletions in Down syndrome acute lymphoblastic leukemia. , 2009, Blood.
[10] A. Hall,et al. Frequent CBL mutations associated with 11q acquired uniparental disomy in myeloproliferative neoplasms. , 2008, Blood.
[11] R. Kralovics. Genetic complexity of myeloproliferative neoplasms , 2008, Leukemia.
[12] Christopher B. Miller,et al. BCR–ABL1 lymphoblastic leukaemia is characterized by the deletion of Ikaros , 2008, Nature.
[13] M. Cazzola,et al. Somatic mutations of JAK2 exon 12 in patients with JAK2 (V617F)-negative myeloproliferative disorders. , 2008, Blood.
[14] T. Sugimoto,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 , 2008, Leukemia & lymphoma.
[15] M. Stratton,et al. JAK2 exon 12 mutations in polycythemia vera and idiopathic erythrocytosis. , 2007, The New England journal of medicine.
[16] P. Campbell,et al. The myeloproliferative disorders. , 2006, The New England journal of medicine.
[17] Soon-Siong Teo,et al. Leukemic blasts in transformed JAK2-V617F-positive myeloproliferative disorders are frequently negative for the JAK2-V617F mutation. , 2006, Blood.
[18] D. Gilliland,et al. MPL515 mutations in myeloproliferative and other myeloid disorders: a study of 1182 patients. , 2006, Blood.
[19] P. Campbell,et al. Mutation of JAK2 in the myeloproliferative disorders: timing, clonality studies, cytogenetic associations, and role in leukemic transformation. , 2006, Blood.
[20] Sandra A. Moore,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. , 2006, Blood.
[21] R. Kralovics,et al. Acquisition of the V617F mutation of JAK2 is a late genetic event in a subset of patients with myeloproliferative disorders. , 2006, Blood.
[22] Sandra A. Moore,et al. MPLW515L Is a Novel Somatic Activating Mutation in Myelofibrosis with Myeloid Metaplasia , 2006, PLoS medicine.
[23] Anne E Carpenter,et al. A Lentiviral RNAi Library for Human and Mouse Genes Applied to an Arrayed Viral High-Content Screen , 2006, Cell.
[24] S. Bohlander,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 , 2005, Genes, chromosomes & cancer.
[25] M. Wadleigh,et al. JAK2V617F mutation in essential thrombocythaemia: clinical associations and long‐term prognostic relevance , 2005, British journal of haematology.
[26] Stefan N Constantinescu,et al. A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera. , 2005, Nature.
[27] Mario Cazzola,et al. A gain-of-function mutation of JAK2 in myeloproliferative disorders. , 2005, The New England journal of medicine.
[28] Sandra A. Moore,et al. Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis. , 2005, Cancer cell.
[29] H. F. Barker,et al. The t(8;9)(p22;p24) is a recurrent abnormality in chronic and acute leukemia that fuses PCM1 to JAK2. , 2005, Cancer research.
[30] P. Campbell,et al. Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders , 2005, The Lancet.
[31] R. Mesa,et al. Leukemic transformation in myelofibrosis with myeloid metaplasia: a single-institution experience with 91 cases. , 2005, Blood.
[32] Philippe Kastner,et al. Ikaros is critical for B cell differentiation and function , 2002, European journal of immunology.
[33] A. Bank,et al. Multiple hematopoietic defects and delayed globin switching in Ikaros null mice , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[34] K Wheatley,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. , 1998, Blood.
[35] R Berger,et al. A TEL-JAK2 fusion protein with constitutive kinase activity in human leukemia. , 1997, Science.
[36] Luigi Naldini,et al. Multiply attenuated lentiviral vector achieves efficient gene delivery in vivo , 1997, Nature Biotechnology.
[37] A. Sharpe,et al. Selective defects in the development of the fetal and adult lymphoid system in mice with an Ikaros null mutation. , 1996, Immunity.
[38] K. Georgopoulos,et al. A dominant mutation in the Ikaros gene leads to rapid development of leukemia and lymphoma , 1995, Cell.
[39] K. Shannon,et al. Childhood monosomy 7: epidemiology, biology, and mechanistic implications. , 1995, Blood.
[40] A. Sharpe,et al. The ikaros gene is required for the development of all lymphoid lineages , 1994, Cell.
[41] D. Moore,et al. Ikaros, an early lymphoid-specific transcription factor and a putative mediator for T cell commitment. , 1992, Science.
[42] R. Arceci. Deletion of IKZF1 and Prognosis in Acute Lymphoblastic Leukemia , 2010 .