ArticlePloS one2009
Targeted deletion of p73 in mice reveals its role in T cell development and lymphomagenesis.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
The trial behind it
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- p73α1, a p73 C-terminal isoform, regulates tumor suppression and the inflammatory response via Notch1.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Identification of methylation signatures associated with CAR T cell in B-cell acute lymphoblastic leukemia and non-hodgkin's lymphoma.Frontiers in oncology · 2022Article
- Deferasirox-Dependent Iron Chelation Enhances Mitochondrial Dysfunction and Restores p53 Signaling by Stabilization of p53 Family Members in Leukemic Cells.International journal of molecular sciences · 2020Article
- Tissue-specific roles of p73 in development and homeostasis.Journal of cell science · 2019Review
- The p53 family members have distinct roles during mammalian embryonic development.Cell death and differentiation · 2017Article
- p73 and FoxJ1: Programming Multiciliated Epithelia.Trends in cell biology · 2016Article
- p53 Activity Dominates That of p73 upon Mdm4 Loss in Development and Tumorigenesis.Molecular cancer research : MCR · 2016Article
- p73 is an essential regulator of neural stem cell maintenance in embryonal and adult CNS neurogenesis.Cell death and differentiation · 2010Article
- Tracing the protectors path from the germ line to the genome.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcriptional silencing of the p73 gene through methylation has been demonstrated in human leukemias and lymphomas. However, the role of p73 in the malignant process remains to be explored. We show here that p73 acts as a T cell-specific tumor suppressor in a genetically defined mouse model, and that concomitant ablation of p53 and p73 predisposes mice to an increased incidence of thymic lymphomas compared to the loss of p53 alone. Our results demonstrate a causal role for loss of p73 in progression of T cell lymphomas to the stage of aggressive, disseminated disease. We provide evidence that tumorigenesis in mice lacking p53 and p73 proceeds through mechanisms involving altered patterns of gene expression, defects in early T cell development, impaired apoptosis, and the ensuing accumulation of chromosomal aberrations. Collectively, our data imply that tumor suppressive properties of p73 are highly dependent on cellular context, wherein p73 plays a major role in T cell development and neoplasia.
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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.