ArticleMolecular and cellular biology1999
Disordered T-cell development and T-cell malignancies in SCL LMO1 double-transgenic mice: parallels with E2A-deficient mice.
Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 99 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
- MonoallelicFrontiers in immunology · 2022Article
- MutantCancer research · 2021Article
- Ldb1 is required for Lmo2 oncogene-induced thymocyte self-renewal and T-cell acute lymphoblastic leukemia.Blood · 2020Article
- Small molecule inhibits T-cell acute lymphoblastic leukaemia oncogenic interaction through conformational modulation of LMO2.Oncotarget · 2020Article
- [Study on expression of LIM domain only protein 1 in SD rat oral buccal mucosa carcinogenesis induced by 4-nitro-quinoline N-oxide].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2020Article
- A unique mutator phenotype reveals complementary oncogenic lesions leading to acute leukemia.JCI insight · 2019Article
- APOBEC signature mutation generates an oncogenic enhancer that drives LMO1 expression in T-ALL.Leukemia · 2017Article
- High-throughput screening in niche-based assay identifies compounds to target preleukemic stem cells.The Journal of clinical investigation · 2016Article
- The LMO2 oncogene regulates DNA replication in hematopoietic cells.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- SCL, LMO1 and Notch1 reprogram thymocytes into self-renewing cells.PLoS genetics · 2014Article
- NUP98-PHF23 is a chromatin-modifying oncoprotein that causes a wide array of leukemias sensitive to inhibition of PHD histone reader function.Cancer discovery · 2014Article
- Article
- A mouse model for inducible overexpression of Prdm14 results in rapid-onset and highly penetrant T-cell acute lymphoblastic leukemia (T-ALL).Disease models & mechanisms · 2013Article
- Bivalent promoter marks and a latent enhancer may prime the leukaemia oncogene LMO1 for ectopic expression in T-cell leukaemia.Leukemia · 2013Article
- Lmo2 induces hematopoietic stem cell-like features in T-cell progenitor cells prior to leukemia.Stem cells (Dayton, Ohio) · 2013Article
- Illegitimate V(D)J recombination involving nonantigen receptor loci in lymphoid malignancy.Genes, chromosomes & cancer · 2012Review
- Notch Signaling in T-Cell Development and T-ALL.ISRN hematology · 2011Article
- Enforced expression of Simian virus 40 large T-antigen leads to testicular germ cell tumors in zebrafish.Zebrafish · 2010Article
- Modeling T-cell acute lymphoblastic leukemia induced by the SCL and LMO1 oncogenes.Genes & development · 2010Article
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
Abstract
The gene most commonly activated by chromosomal rearrangements in patients with T-cell acute lymphoblastic leukemia (T-ALL) is SCL/tal. In collaboration with LMO1 or LMO2, the thymic expression of SCL/tal leads to T-ALL at a young age with a high degree of penetrance in transgenic mice. We now show that SCL LMO1 double-transgenic mice display thymocyte developmental abnormalities in terms of proliferation, apoptosis, clonality, and immunophenotype prior to the onset of a frank malignancy. At 4 weeks of age, thymocytes from SCL LMO1 mice show 70% fewer total thymocytes, with increased rates of both proliferation and apoptosis, than control thymocytes. At this age, a clonal population of thymocytes begins to populate the thymus, as evidenced by oligoclonal T-cell-receptor gene rearrangements. Also, there is a dramatic increase in immature CD44(+) CD25(-) cells, a decrease in the more mature CD4(+) CD8(+) cells, and development of an abnormal CD44(+) CD8(+) population. An identical pattern of premalignant changes is seen with either a full-length SCL protein or an amino-terminal truncated protein which lacks the SCL transactivation domain, demonstrating that the amino-terminal portion of SCL is not important for leukemogenesis. Lastly, we show that the T-ALL which develop in the SCL LMO1 mice are strikingly similar to those which develop in E2A null mice, supporting the hypothesis that SCL exerts its oncogenic action through a functional inactivation of E proteins.
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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.