ArticleOncogene2007
The nonhomologous end joining factor Artemis suppresses multi-tissue tumor formation and prevents loss of heterozygosity.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- Studies of lncRNAs in DNA double strand break repair: what is new?Oncotarget · 2017Review
- Kub5-Hera, the human Rtt103 homolog, plays dual functional roles in transcription termination and DNA repair.Nucleic acids research · 2014Article
- Dystrophin and dysferlin double mutant mice: a novel model for rhabdomyosarcoma.Cancer genetics · 2012Article
- A hypomorphic Artemis human disease allele causes aberrant chromosomal rearrangements and tumorigenesis.Human molecular genetics · 2011Article
- Radiation exposure from imaging tests: is there an increased cancer risk?Expert review of cardiovascular therapy · 2011Review
- Nuclear positioning, higher-order folding, and gene expression of Mmu15 sequences are refractory to chromosomal translocation.Chromosoma · 2011Article
- ARTEMIS stabilizes the genome and modulates proliferative responses in multipotent mesenchymal cells.BMC biology · 2010Article
- Global changes in processing of mRNA 3' untranslated regions characterize clinically distinct cancer subtypes.Cancer research · 2009Article
- Colocalization of somatic and meiotic double strand breaks near the Myc oncogene on mouse chromosome 15.Genes, chromosomes & cancer · 2009Article
- Assessing cancer risks of low-dose radiation.Nature reviews. Cancer · 2009Review
- Complex oncogenic translocations with gene amplification are initiated by specific DNA breaks in lymphocytes.Cancer research · 2009Article
- DNA-PKcs and Artemis function in the end-joining phase of immunoglobulin heavy chain class switch recombination.The Journal of experimental medicine · 2008Article
- DNA-damage repair; the good, the bad, and the ugly.The EMBO journal · 2008Review
- AID-deficient Bcl-xL transgenic mice develop delayed atypical plasma cell tumors with unusual Ig/Myc chromosomal rearrangements.The Journal of experimental medicine · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Nonhomologous end joining (NHEJ) is a critical DNA repair pathway, with proposed tumor suppression functions in many tissues. Mutations in the NHEJ factor ARTEMIS cause radiation-sensitive severe combined immunodeficiency in humans and may increase susceptibility to lymphoma in some settings. We now report that deficiency for Artemis (encoded by Dclre1c/Art in mouse) accelerates tumorigenesis in several tissues in a Trp53 heterozygous setting, revealing tumor suppression roles for NHEJ in lymphoid and non-lymphoid cells. We also show that B-lineage lymphomas in these mice undergo loss of Trp53 heterozygosity by allele replacement, but arise by mechanisms distinct from those in Art Trp53 double null mice. These findings demonstrate a general tumor suppression function for NHEJ, and reveal that interplay between NHEJ and Trp53 loss of heterozygosity influences the sequence of multi-hit oncogenesis. We present a model where p53 status at the time of tumor initiation is a key determinant of subsequent oncogenic mechanisms. Because Art deficient mice represent a model for radiation-sensitive severe combined immunodeficiency, our findings suggest that these patients may be at risk for both lymphoid and non-lymphoid cancers.
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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.