ArticleOncogene2004
Both AML1 and EVI1 oncogenic components are required for the cooperation of AML1/MDS1/EVI1 with BCR/ABL in the induction of acute myelogenous leukemia in mice.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 46 citations in OpenAlex.
- Chronic Myeloid Leukemia: Modern therapies, current challenges and future directions.Blood reviews · 2021Review
- 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
- EVI1 overexpression reprograms hematopoiesis via upregulation of Spi1 transcription.Nature communications · 2018Article
- RUNX1-Evi-1 fusion gene inhibited differentiation and apoptosis in myelopoiesis: an in vivo study.BMC cancer · 2015Article
- -7/7q- syndrome in myeloid-lineage hematopoietic malignancies: attempts to understand this complex disease entity.Oncogene · 2015Review
- Evi1 defines leukemia-initiating capacity and tyrosine kinase inhibitor resistance in chronic myeloid leukemia.Oncogene · 2014Article
- Stem cell maintenance and disease progression in chronic myeloid leukemia.International journal of hematology · 2013Review
- Selection for Evi1 activation in myelomonocytic leukemia induced by hyperactive signaling through wild-type NRas.Oncogene · 2013Article
- Article
- Zinc finger transcription factor ecotropic viral integration site 1 is induced by all-trans retinoic acid (ATRA) and acts as a dual modulator of the ATRA response.The FEBS journal · 2009Article
- Inducible expression of EVI1 in human myeloid cells causes phenotypes consistent with its role in myelodysplastic syndromes.Journal of leukocyte biology · 2009Article
- Pathogenetic significance of ecotropic viral integration site-1 in hematological malignancies.Cancer science · 2009Review
- Role of the RUNX1-EVI1 fusion gene in leukemogenesis.Cancer science · 2008Review
- Article
- AML1-Evi-1 specifically transforms hematopoietic stem cells through fusion of the entire Evi-1 sequence to AML1.Leukemia · 2008Article
- Sox4 cooperates with Evi1 in AKXD-23 myeloid tumors via transactivation of proviral LTR.Blood · 2006Article
- Review
- The leukemic fusion gene AML1-MDS1-EVI1 suppresses CEBPA in acute myeloid leukemia by activation of Calreticulin.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
We have previously shown that BCR/ABL, a fusion protein generated by the t(9;22)(q34;q11) translocation found in the vast majority of chronic myelogenous leukemia (CML), cooperates with AML1/MDS1/EVI1 (AME), a fusion transcription factor generated by a t(3;21)(q26;q22) translocation identified as a secondary mutation in some cases of CML during the blast phase (CML-BC), in the rapid induction of an acute myelogenous leukemia (AML) in mice. In this study, we evaluated the leukemogenic potential of EVI1-, MDS1/EVI1- and AML1-related oncoproteins (AML1Delta, AML1/MDS1). We found that ectopic expression of either EVI1 or MDS1/EVI1 impaired hematopoiesis. However, neither EVI1 nor MDS1/EVI1 was sufficient for inducing AML in mice, although EVI1 did induce some hematologic neoplasia other than AML with a low efficiency. In addition, unlike AME, none of the EVI1- or AML1-related oncoproteins examined were capable of fully cooperating with BCR/ABL in the induction of AML. The results indicate that both the AML1 and EVI1 oncogenic components are required for the leukemogenic potential of AME and for the cooperation of AME and BCR/ABL in the induction of AML.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.