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Article

The t(3;21) Fusion Product, AML1/Evi-1, Interacts With Smad3 and Blocks Transforming Growth Factor-β–Mediated Growth Inhibition of Myeloid Cells

1 Dec 1998

Abstract excerpt

The t(3;21)(q26;q22) chromosomal translocation associated with blastic crisis of chronic myelogenous leukemia results in the formation of the AML1/Evi-1 chimeric protein, which is thought to play a causative role in leukemic transformation of hematopoietic cells. Here we show that AML1/Evi-1 represses growth-inhibitory signaling by transforming growth factor-beta (TGF-beta) in 32Dcl3 myeloid cells. The activity...

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Identifiers

PMID: 9834202
DOI: 10.1182/blood.v92.11.4003

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Related research

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Research trail→

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The t(3;21) Fusion Product, AML1/Evi-1, Interacts With Smad3 and Blocks Transforming Growth Factor-β–Mediated Growth Inhibition of Myeloid CellsPMID 9834202Read ↗

AML1-Evi-1 specifically transforms hematopoietic stem cells through fusion of the entire Evi-1 sequence to AML1.Semantic proximity Read ↗

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RUNX1-ETO and RUNX1-EVI1 Differentially Reprogram the Chromatin Landscape in t(8;21) and t(3;21) AML.Semantic proximity Read ↗

A novel gene, MEL1, mapped to 1p36.3 is highly homologous to the MDS1/EVI1 gene and is transcriptionally activated in t(1;3)(p36;q21)-positive leukemia cellsSemantic proximity Read ↗

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The oncoprotein Evi-1 represses TGF-β signalling by inhibiting Smad3Semantic proximity Read ↗

Expression of EVI1 in myelodysplastic syndromes and other hematologic malignancies without 3q26 translocationsSemantic proximity Read ↗

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