ArticleThe Journal of experimental medicine2008
Oncogenesis of T-ALL and nonmalignant consequences of overexpressing intracellular NOTCH1.
Article in The Journal of experimental medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
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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
55 citing papers in PubMed, 96 citations in OpenAlex.
- BCAT1 is a NOTCH1 target and sustains the oncogenic function of NOTCH1.Haematologica · 2025Article
- Notch signaling pathway in cancer: from mechanistic insights to targeted therapies.Signal transduction and targeted therapy · 2024Review
- RNA helicase DHX15 exemplifies a unique dependency in acute leukemia.Haematologica · 2023Article
- A double-negative thymocyte-specific enhancer augments Notch1 signaling to direct early T cell progenitor expansion, lineage restriction and β-selection.Nature immunology · 2022Article
- Review
- Inhibition of mitochondrial complex I reverses NOTCH1-driven metabolic reprogramming in T-cell acute lymphoblastic leukemia.Nature communications · 2022Article
- Cancer-associated mutations in VAV1 trigger variegated signaling outputs and T-cell lymphomagenesis.The EMBO journal · 2021Article
- Therapeutic targeting of Notch signaling and immune checkpoint blockade in a spontaneous, genetically heterogeneous mouse model of T-cell acute lymphoblastic leukemia.Disease models & mechanisms · 2019Article
- Phf6-null hematopoietic stem cells have enhanced self-renewal capacity and oncogenic potentials.Blood advances · 2019Article
- TCF-1 and HEB cooperate to establish the epigenetic and transcription profiles of CD4Nature immunology · 2018Article
- STIM1 and STIM2 Mediate Cancer-Induced Inflammation in T Cell Acute Lymphoblastic Leukemia.Cell reports · 2018Article
- The NOTCH1/CD44 axis drives pathogenesis in a T cell acute lymphoblastic leukemia model.The Journal of clinical investigation · 2018Article
- Therapeutic Targeting of mTOR in T-Cell Acute Lymphoblastic Leukemia: An Update.International journal of molecular sciences · 2018Review
- High selective pressure for Notch1 mutations that induce Myc in T-cell acute lymphoblastic leukemia.Blood · 2016Article
- Oncogenic Notch signaling in T-cell and B-cell lymphoproliferative disorders.Current opinion in hematology · 2016Review
- Trib2 Suppresses Tumor Initiation in Notch-Driven T-ALL.PloS one · 2016Article
- The PIAS-like Coactivator Zmiz1 Is a Direct and Selective Cofactor of Notch1 in T Cell Development and Leukemia.Immunity · 2015Article
- The evolution of thymic lymphomas in p53 knockout mice.Genes & development · 2014Article
- Long-range enhancer activity determines Myc sensitivity to Notch inhibitors in T cell leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Cyclin C is a haploinsufficient tumour suppressor.Nature cell biology · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Mutations resulting in overexpression of intracellular Notch1 (ICN1) are frequently observed in human T cell acute lymphoblastic leukemia (T-ALL). We have determined the consequences of ICN1 overexpression from retroviral vectors introduced into bone marrow cells. Early consequences are the generation of polyclonal nontumorigenic CD4(+)8(+) T cell receptor (TCR)-alphabeta(+) cells that do not qualify as tumor precursors despite the observation that they overexpress Notch 1 and c-Myc and degrade the tumor suppressor E2A by posttranslational modification. The first tumorigenic cells are detected among more immature CD4(-)8(+)TCR-alphabeta(-) cells that give rise to monoclonal tumors with a single, unique TCR-beta chain and diverse TCR-alpha chains, pinpointing malignant transformation to a stage after pre-TCR signaling and before completion of TCR-alpha rearrangement. In T-ALL, E2A deficiency is accompanied by further transcriptional up-regulation of c-Myc and concomitant dysregulation of the c-Myc-p53 axis at the transcriptional level. Even though the tumors consist of phenotypically heterogeneous cells, no evidence for tumor stem cells was found. As judged by array-based comparative genomic hybridization (array CGH) and spectral karyotype (SKY) analysis, none of the tumors arise because of genomic instability.
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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.