ArticleThe EMBO journal1994
Generation of the AML1-EVI-1 fusion gene in the t(3;21)(q26;q22) causes blastic crisis in chronic myelocytic leukemia.
Article in The EMBO journal, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.
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Who cites it
104 citing papers in PubMed, 332 citations in OpenAlex.
- Article
- The oncogenic role of ecotropic viral integration site 1 in hematological malignancies: mechanisms of activation and leukemogenesis.Frontiers in immunology · 2026Review
- Review
- Emergence of t(3;21)(q26.2;q22) during eltrombopag treatment in a patient with relapsed aplastic anemia who received chemotherapy for angioimmunoblastic T-cell lymphoma.Leukemia research reports · 2022Article
- Identification of therapeutic targets of the hijacked super-enhancer complex in EVI1-rearranged leukemia.Leukemia · 2021Article
- RUNX1-EVI1 disrupts lineage determination and the cell cycle by interfering with RUNX1 and EVI1 driven gene regulatory networks.Haematologica · 2021Article
- Different mutant RUNX1 oncoproteins program alternate haematopoietic differentiation trajectories.Life science alliance · 2021Article
- RUNX1 and RUNX2 transcription factors function in opposing roles to regulate breast cancer stem cells.Journal of cellular physiology · 2020Article
- EVI1 in Leukemia and Solid Tumors.Cancers · 2020Review
- Coexistence of recurrent chromosomal abnormalities and the Philadelphia chromosome in acute and chronic myeloid leukemias: report of five cases and review of literature.Molecular cytogenetics · 2020Article
- Article
- RUNX family: Oncogenes or tumor suppressors (Review).Oncology reports · 2019Review
- Suppression of Breast Cancer Stem Cells and Tumor Growth by the RUNX1 Transcription Factor.Molecular cancer research : MCR · 2018Article
- C/EBPα overrides epigenetic reprogramming by oncogenic transcription factors in acute myeloid leukemia.Blood advances · 2018Article
- Regulation of Hematopoiesis and Hematological Disease by TGF-β Family Signaling Molecules.Cold Spring Harbor perspectives in biology · 2017Review
- Acute myeloid leukemia with t(3;21)(q26.2;q22) developing following low-dose methotrexate therapy for rheumatoid arthritis and expressing two AML1/MDS1/EVI1 fusion proteins: A case report.Oncology letters · 2017Article
- RUNX1-ETO and RUNX1-EVI1 Differentially Reprogram the Chromatin Landscape in t(8;21) and t(3;21) AML.Cell reports · 2017Article
- Review
- RUNX3 facilitates growth of Ewing sarcoma cells.Journal of cellular physiology · 2014Article
- Genetic events other than BCR-ABL1.Current hematologic malignancy reports · 2014Review
44 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The t(3;21)(q26;q22) translocation, which is one of the consistent chromosomal abnormalities found in blastic crisis of chronic myelocytic leukemia (CML), is thought to play an important role in the leukemic progression of CML to an acute blastic crisis phase. The AML1 gene, which is located at the translocation breakpoint of the t(8;21)(q22;q22) translocation found in acute myelocytic leukemia, was also rearranged by the t(3;21)(q26;q22) translocation. Screening of a cDNA library of the t(3;21)-carrying leukemic cell line cells (SKH1) resulted in the isolation of two potentially complete AML1-EVI-1 chimeric cDNAs of 6 kb. Two species of AML1-EVI-1 fusion transcripts of 8.2 and 7.0 kb were detected in SKH1 cells. These cells expressed the 180 kDa AML1-EVI-1 fusion protein containing an N-terminal half of AML1 including a runt homology domain which is fused to the entire zinc finger EVI-1 protein. The AML1-EVI-1 fusion transcript was consistent in all three cases of the t(3;21)-carrying leukemia examined by RNA-based PCR. These findings strongly suggest that the t(3;21) translocation results in the formation of a new class of chimeric transcription factor which could contribute to the leukemic progression of CML through interference with cell growth and differentiation.
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