ArticleMolecular and cellular biology2008
Beta-catenin expression results in p53-independent DNA damage and oncogene-induced senescence in prelymphomagenic thymocytes in vivo.
Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 72 citations in OpenAlex.
- Potential Indicators for the Development of Hepatocellular Carcinoma: A Diagnostic Strategy.Current topics in medicinal chemistry · 2026Review
- Oncogene-Induced Senescence Transcriptomes Signify Premalignant Colorectal Adenomas.Current issues in molecular biology · 2025Article
- TRIP13 protects pancreatic cancer cells against intrinsic and therapy-induced DNA replication stress.NAR cancer · 2025Article
- Targeting sphingosine kinase 1 in p53KO thymic lymphoma.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Molecular mechanisms of alveolar epithelial cell senescence and idiopathic pulmonary fibrosis: a narrative review.Journal of thoracic disease · 2023Review
- Crosstalk between Wnt/β-catenin signaling pathway and DNA damage response in cancer: a new direction for overcoming therapy resistance.Frontiers in pharmacology · 2023Review
- High Canonical Wnt/β-Catenin Activity Sensitizes Murine Hematopoietic Stem and Progenitor Cells to DNA Damage.Stem cell reviews and reports · 2020Article
- LncRNAs Regulatory Networks in Cellular Senescence.International journal of molecular sciences · 2019Review
- Mechanisms of Oncogene-Induced Replication Stress: Jigsaw Falling into Place.Cancer discovery · 2018Review
- Nuclear α-catenin mediates the DNA damage response via β-catenin and nuclear actin.Journal of cell science · 2017Article
- Prolonged inflammatory microenvironment is crucial for pro-neoplastic growth and genome instability: a detailed review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017Review
- The Immortal Senescence.Methods in molecular biology (Clifton, N.J.) · 2017Review
- Evasion of cell senescence in SHH medulloblastoma.Cell cycle (Georgetown, Tex.) · 2016Review
- Wnt activity and basal niche position sensitize intestinal stem and progenitor cells to DNA damage.The EMBO journal · 2015Article
- Review
- From inception to output, Tcf1 and Lef1 safeguard development of T cells and innate immune cells.Immunologic research · 2014Review
- MicroRNA-29 induces cellular senescence in aging muscle through multiple signaling pathways.Aging · 2014Article
- Article
- Wnt/β-catenin signaling mediates the senescence of bone marrow-mesenchymal stem cells from systemic lupus erythematosus patients through the p53/p21 pathway.Molecular and cellular biochemistry · 2014Article
- β-Catenin induces T-cell transformation by promoting genomic instability.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The expression of beta-catenin, a potent oncogene, is causally linked to tumorigenesis. Therefore, it was surprising that the transgenic expression of oncogenic beta-catenin in thymocytes resulted in thymic involution instead of lymphomagenesis. In this report, we demonstrate that this is because the expression of oncogenic beta-catenin induces DNA damage, growth arrest, oncogene-induced senescence (OIS), and apoptosis of immature thymocytes. In p53-deficient mice, the expression of oncogenic beta-catenin still results in DNA damage and OIS, but the thymocytes survive and eventually progress to thymic lymphoma. beta-Catenin-induced thymic lymphomas are distinct from lymphomas that arise in p53(-/-) mice. They are CD4(-) CD8(-), while p53-dependent lymphomas are largely CD4(+) CD8(+), and they develop at an earlier age and in the absence of c-Myc expression or Notch1 signaling. Thus, we report that oncogenic beta-catenin-induced, p53-independent growth arrest and OIS and p53-dependent apoptosis protect developing thymocytes from transformation by oncogenic beta-catenin.
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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.