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A previously unidentified alternatively spliced isoform of t(8;21) transcript promotes leukemogenesis.
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The tetramer structure of the Nervy homology two domain, NHR2, is critical for AML1/ETO's activity.
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NFAT dysregulation by increased dosage of DSCR1 and DYRK1A on chromosome 21.
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Erythroid inhibition by the leukemic fusion AML1-ETO is associated with impaired acetylation of the major erythroid transcription factor GATA-1.
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Dasatinib (BMS-354825) inhibits KITD816V, an imatinib-resistant activating mutation that triggers neoplastic growth in most patients with systemic mastocytosis.
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The AML1-ETO fusion gene and the FLT3 length mutation collaborate in inducing acute leukemia in mice.
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Repression of c-kit and its downstream substrates by GATA-1 inhibits cell proliferation during erythroid maturation.
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The systemic mastocytosis-specific activating cKit mutation D816V can be inhibited by the tyrosine kinase inhibitor AMN107.
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Effect of transcription-factor concentrations on leukemic stem cells.
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Identification of Flt3+ lympho-myeloid stem cells lacking erythro-megakaryocytic potential a revised road map for adult blood lineage commitment.
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