The t(8;21) translocation in acute myeloid leukemia results in production of an AML1‐MTG8 fusion transcript

The t(8;21) translocation is one of the most frequent chromosome abnormalities in acute myeloid leukemia. It has been shown that the t(8;21) breakpoints on chromosome 21 cluster within a single specific intron of the AML1 gene, which is highly homologous to the Drosophila segmentation gene runt. Her...

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Bibliographic Details
Published in:The EMBO journal 1993-07, Vol.12 (7), p.2715-2721
Main Authors: Miyoshi, H., Kozu, T., Shimizu, K., Enomoto, K., Maseki, N., Kaneko, Y., Kamada, N., Ohki, M.
Format: Article
Language:English
Subjects:
Acute Disease
Amino Acid Sequence
Animals
Base Sequence
Biological and medical sciences
Cell Line
Chromosomes, Human, Pair 21
Chromosomes, Human, Pair 8
Cloning, Molecular
Core Binding Factor Alpha 2 Subunit
DNA, Neoplasm
DNA-Binding Proteins - genetics
Hematologic and hematopoietic diseases
Humans
Leukemia, Myeloid - genetics
Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis
Medical sciences
Mice
Molecular Sequence Data
Neoplasm Proteins - genetics
Proto-Oncogene Proteins
Recombinant Fusion Proteins - genetics
RUNX1 Translocation Partner 1 Protein
Sequence Homology, Amino Acid
Transcription Factors - genetics
Translocation, Genetic
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Summary:The t(8;21) translocation is one of the most frequent chromosome abnormalities in acute myeloid leukemia. It has been shown that the t(8;21) breakpoints on chromosome 21 cluster within a single specific intron of the AML1 gene, which is highly homologous to the Drosophila segmentation gene runt. Here we report that this translocation juxtaposes the AML1 gene with a novel gene, named MTG8, on chromosome 8, resulting in the synthesis of an AML1‐MTG8 fusion transcript. The fusion protein predicted by the AML1‐MTG8 transcript consists of the runt homology region of AML1 and the most part of MTG8, which contains putative zinc finger DNA binding motifs and proline‐rich regions constituting a characteristic feature of transcription factors. The MTG8 gene is not expressed in normal hematopoietic cells, whereas AML1 is expressed at high levels. Our results indicate that the production of chimeric AML1‐MTG8 protein, probably a chimeric transcription factor, may contribute to myeloid leukemogenesis.
ISSN:0261-4189
1460-2075
DOI:10.1002/j.1460-2075.1993.tb05933.x