ArticleThe EMBO journal1997
An scl gene product lacking the transactivation domain induces bony abnormalities and cooperates with LMO1 to generate T-cell malignancies in transgenic mice.
Article in The EMBO journal, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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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
59 citing papers in PubMed, 143 citations in OpenAlex.
- SIL-TAL1-Positive Adult T-ALL with t(11;14)(p15;q11.2): A Rare Case Report Highlighting Prognostic Challenges and Treatment Implications.Journal of inflammation research · 2025Article
- Inhibition of the NOTCH and mTOR pathways by nelfinavir as a novel treatment for T cell acute lymphoblastic leukemia.International journal of oncology · 2023Article
- Targeting Leukemia-Initiating Cells and Leukemic Niches: The Next Therapy Station for T-Cell Acute Lymphoblastic Leukemia?Cancers · 2022Review
- TAL1 cooperates with PI3K/AKT pathway activation in T-cell acute lymphoblastic leukemia.Haematologica · 2022Article
- Generation of InducibleInternational journal of molecular sciences · 2022Article
- MonoallelicFrontiers in immunology · 2022Article
- Oncogene-Induced Reprogramming in Acute Lymphoblastic Leukemia: Towards Targeted Therapy of Leukemia-Initiating Cells.Cancers · 2021Review
- Review
- Small molecule inhibition of Dynamin-dependent endocytosis targets multiple niche signals and impairs leukemia stem cells.Nature communications · 2020Article
- Small molecule inhibits T-cell acute lymphoblastic leukaemia oncogenic interaction through conformational modulation of LMO2.Oncotarget · 2020Article
- The Genetics and Mechanisms of T-Cell Acute Lymphoblastic Leukemia.Cold Spring Harbor perspectives in medicine · 2020Review
- Restricted cell cycle is essential for clonal evolution and therapeutic resistance of pre-leukemic stem cells.Nature communications · 2018Article
- Leukemia-Initiating Cells in T-Cell Acute Lymphoblastic Leukemia.Frontiers in oncology · 2017Review
- Article
- High-throughput screening in niche-based assay identifies compounds to target preleukemic stem cells.The Journal of clinical investigation · 2016Article
- Review
- The genetics and mechanisms of T cell acute lymphoblastic leukaemia.Nature reviews. Cancer · 2016Review
- Disregulated expression of the transcription factor ThPOK during T-cell development leads to high incidence of T-cell lymphomas.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- SCL, LMO1 and Notch1 reprogram thymocytes into self-renewing cells.PLoS genetics · 2014Article
- Murine models of acute leukemia: important tools in current pediatric leukemia research.Frontiers in oncology · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The product of the scl (also called tal-1 or TCL5) gene is a basic domain, helix-loop-helix (bHLH) transcription factor required for the development of hematopoietic cells. Additionally, scl gene disruption and dysregulation, by either chromosomal translocations or a site-specific interstitial deletion whereby 5' regulatory elements of the sil gene become juxtaposed to the body of the scl gene, is associated with T-cell acute lymphoblastic leukemia (ALL) and T-cell lymphoblastic lymphoma. Here we show that an inappropriately expressed scl protein, driven by sil regulatory elements, can cause aggressive T-cell malignancies in collaboration with a misexpressed LMO1 protein, thus recapitulating the situation seen in a subset of human T-cell ALL. Moreover, we show that inappropriately expressed scl can interfere with the development of other tissues derived from mesoderm. Lastly, we show that an scl construct lacking the scl transactivation domain collaborates with misexpressed LMO1, demonstrating that the scl transactivation domain is dispensable for oncogenesis, and supporting the hypothesis that the scl gene product exerts its oncogenic action through a dominant-negative mechanism.
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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.