ArticleProceedings of the National Academy of Sciences of the United States of America1993
The 3;21 translocation in myelodysplasia results in a fusion transcript between the AML1 gene and the gene for EAP, a highly conserved protein associated with the Epstein-Barr virus small RNA EBER 1.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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57 citing papers in PubMed, 177 citations in OpenAlex.
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- RUNX1 truncation resulting from a cryptic and novel t(6;21)(q25;q22) chromosome translocation in acute myeloid leukemia: A case report.Oncology reports · 2016Article
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- Acute myeloid leukemia with t(7;21)(q11.2;q22) expresses a novel, reversed-sequence RUNX1-DTX2 chimera.International journal of hematology · 2012Article
- Deregulated transcription factors in leukemia.International journal of hematology · 2011Review
- Modulation of innate immunity system by Epstein-Barr virus-encoded non-coding RNA and oncogenesis.Cancer science · 2010Review
- Chromatin regulation by AML1 complex.International journal of hematology · 2008Article
- Mutations of the HIPK2 gene in acute myeloid leukemia and myelodysplastic syndrome impair AML1- and p53-mediated transcription.Oncogene · 2007Article
- Drosophila ribosomal proteins are associated with linker histone H1 and suppress gene transcription.Genes & development · 2006Article
- Oncogenic potential of the RUNX gene family: 'overview'.Oncogene · 2004Review
- Cooperativity between mutations in tyrosine kinases and in hematopoietic transcription factors in AML.Leukemia · 2002Article
- Dichotomy of AML1-ETO functions: growth arrest versus block of differentiation.Molecular and cellular biology · 2001Article
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5 authors at 1 institution in 1 country.
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Abstract
In the 8;21 translocation, the AML1 gene, located at chromosome band 21q22, is translocated to chromosome 8 (q22), where it is fused to the ETO gene and transcribed as a chimeric gene. AML1 is the human homolog of the recently cloned mouse gene pebp2 alpha B, homologous to the DNA binding alpha subunit of the polyoma enhancer factor pebp2. AML1 is also involved in a translocation with chromosome 3 that is seen in patients with therapy-related acute myeloid leukemia and myelodysplastic syndrome and in chronic myelogenous leukemia in blast crisis. We have isolated a fusion cDNA clone from a t(3;21) library derived from a patient with therapy-related myelodysplastic syndrome; this clone contains sequences from AML1 and from EAP, which we have now localized to band 3q26. EAP has previously been characterized as a highly expressed small nuclear protein of 128 residues (EBER 1) associated with Epstein-Barr virus small RNA. The fusion clone contains the DNA binding 5' part of AML1 that is fused to ETO in the t(8;21) and, in addition, at least one other exon. The translocation replaces the last nine codons of AML1 with the last 96 codons of EAP. The fusion does not maintain the correct reading frame of EAP and may not lead to a functional chimeric protein.
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