ArticleOncogene2005
Defining the oncogenic function of the TEL/AML1 (ETV6/RUNX1) fusion protein in a mouse model.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
45 citing papers in PubMed, 95 citations in OpenAlex.
- The gastrointestinal microbiome and constituent short-chain fatty acids: a narrative review of an underexplored axis in acute lymphoblastic leukemia.Gut pathogens · 2026Review
- Azanucleoside treatment leads to B-cell precursor acute lymphoblastic leukemia.Blood neoplasia · 2025Article
- The Diverse Roles of ETV6 Alterations in B-Lymphoblastic Leukemia and Other Hematopoietic Cancers.Advances in experimental medicine and biology · 2024Review
- RNA binding protein IGF2BP1 synergizes with ETV6-RUNX1 to drive oncogenic signaling in B-cell Acute Lymphoblastic Leukemia.Journal of experimental & clinical cancer research : CR · 2023Article
- ETV6 Deficiency Unlocks ERG-Dependent Microsatellite Enhancers to Drive Aberrant Gene Activation in B-Lymphoblastic Leukemia.Blood cancer discovery · 2023Article
- First Case ofAnnals of laboratory medicine · 2023Article
- Lessons from mouse models in the impact of risk factors on the genesis of childhood B-cell leukemia.Frontiers in immunology · 2023Review
- Childhood B-Cell Preleukemia Mouse Modeling.International journal of molecular sciences · 2022Review
- Interactions Networks for Primary Heart Sarcomas.Cancers · 2021Article
- Fusion genes as biomarkers in pediatric cancers: A review of the current state and applicability in diagnostics and personalized therapy.Cancer letters · 2021Review
- Article
- RUNX1 and RUNX2 transcription factors function in opposing roles to regulate breast cancer stem cells.Journal of cellular physiology · 2020Article
- The correction of ETV6/RUNX1 translocation in acute lymphocytic leukemia cells: a new gene targeting system by homologous recombination mechanism.Journal of applied genetics · 2020Article
- Suppression of Breast Cancer Stem Cells and Tumor Growth by the RUNX1 Transcription Factor.Molecular cancer research : MCR · 2018Article
- Translocations involving ETS family proteins in human cancer.Integrative cancer science and therapeutics · 2018Article
- A causal mechanism for childhood acute lymphoblastic leukaemia.Nature reviews. Cancer · 2018Review
- Molecular processes involved in B cell acute lymphoblastic leukaemia.Cellular and molecular life sciences : CMLS · 2018Review
- Modeling the process of childhoodOncotarget · 2017Review
- SOX7 promotes the maintenance and proliferation of B cell precursor acute lymphoblastic cells.Oncotarget · 2017Article
- Dysregulation of BCL-2 family proteins by leukemia fusion genes.The Journal of biological chemistry · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The t(12;21) translocation, generating the TEL/AML1 fusion protein, is the most common genetic lesion in childhood cancer. Using a bone marrow transplantation model, we demonstrate that TEL/AML1 expression impinges on normal hematopoietic differentiation, leading to the in vivo accumulation and persistence of an early progenitor compartment with a Sca1(+)/Kit(hi)/CD11b(+) phenotype and an increased self-renewal capacity, as documented by replating assays in vitro. Differentiation of these cells is not blocked, but the frequency of mature blood cells arising from TEL/AML1-transduced progenitors is low. Impaired differentiation is prominently observed in the pro-B-cell compartment, resulting in an proportional increase in early progenitors in vivo, consistent with the t(12;21) ALL phenotype. Despite the accumulation of both multipotent and B-cell progenitors in vivo, no leukemia induction was observed during an observation period of over 1 year. These results are consistent with findings in twins with concordant ALL, showing that TEL/AML1 generates a preleukemic clone in utero that persists for several years in a clinically covert fashion. Furthermore, our studies showed that the pointed domain of TEL/AML1, which recruits transcriptional repressors and directs oligomerization with either TEL/AML1 or wild-type TEL, was essential for the observed differentiation impairment and could not be replaced with another oligomerization domain.
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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.