ArticleBlood2011
Functional interactions between Lmo2, the Arf tumor suppressor, and Notch1 in murine T-cell malignancies.
Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- Overexpression of Lmo2 initiates T-lymphoblastic leukemia via impaired thymocyte competition.The Journal of experimental medicine · 2023Article
- Non-Canonical Functions of the ARF Tumor Suppressor in Development and Tumorigenesis.Biomolecules · 2021Review
- Review
- Lmo2 expression defines tumor cell identity during T-cell leukemogenesis.The EMBO journal · 2018Article
- Evaluating the Safety of Retroviral Vectors Based on Insertional Oncogene Activation and Blocked Differentiation in Cultured Thymocytes.Molecular therapy : the journal of the American Society of Gene Therapy · 2016Article
- The LMO2 oncogene regulates DNA replication in hematopoietic cells.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Article
- Hhex regulates Kit to promote radioresistance of self-renewing thymocytes in Lmo2-transgenic mice.Leukemia · 2015Article
- Effect of a single nucleotide polymorphism in miR-146a on COX-2 protein expression and lung function in smokers with chronic obstructive pulmonary disease.International journal of chronic obstructive pulmonary disease · 2015Article
- Article
- Loss of function tp53 mutations do not accelerate the onset of myc-induced T-cell acute lymphoblastic leukaemia in the zebrafish.British journal of haematology · 2014Article
- LMO2 induces T-cell leukemia with epigenetic deregulation of CD4.Experimental hematology · 2014Article
- Interleukin-7 receptor mutants initiate early T cell precursor leukemia in murine thymocyte progenitors with multipotent potential.The Journal of experimental medicine · 2014Article
- Article
- Lmo2 induces hematopoietic stem cell-like features in T-cell progenitor cells prior to leukemia.Stem cells (Dayton, Ohio) · 2013Article
- Epigenetic regulation of the Ink4a-Arf (Cdkn2a) tumor suppressor locus in the initiation and progression of Notch1-driven T cell acute lymphoblastic leukemia.Experimental hematology · 2013Article
- LIM-domain-only proteins in cancer.Nature reviews. Cancer · 2013Review
- Mouse transplant models for evaluating the oncogenic risk of a self-inactivating XSCID lentiviral vector.PloS one · 2013Article
- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
LMO2 is a target of chromosomal translocations in T-cell tumors and was activated by retroviral vector insertions in T-cell tumors from X-SCID patients in gene therapy trials. To better understand the cooperating genetic events in LMO2-associated T-cell acute lymphoblastic leukemia (T-ALL), we investigated the roles of Arf tumor suppressor loss and Notch activation in murine models of transplantation. Lmo2 overexpression enhanced the expansion of primitive DN2 thymocytes, eventually facilitating the stochastic induction of clonal CD4(+)/CD8(+) malignancies. Inactivation of the Arf tumor suppressor further increased the self-renewal capacity of the primitive, preleukemic thymocyte pool and accelerated the development of aggressive, Lmo2-induced T-cell lympholeukemias. Notch mutations were frequently detected in these Lmo2-induced tumors. The Arf promoter was not directly engaged by Lmo2 or mutant Notch, and use of a mouse model in which activation of a mutant Notch allele depends on previous engagement of the Arf promoter revealed that Notch activation could occur as a subsequent event in T-cell tumorigenesis. Therefore, Lmo2 cooperates with Arf loss to enhance self-renewal in primitive thymocytes. Notch mutation and Arf inactivation appear to independently cooperate in no requisite order with Lmo2 overexpression in inducing T-ALL, and all 3 events remained insufficient to guarantee immediate tumor development.
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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.