ArticleProceedings of the National Academy of Sciences of the United States of America2006
XRCC4 suppresses medulloblastomas with recurrent translocations in p53-deficient mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 118 citations in OpenAlex.
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- A gene dosage-dependent effect unveils NBS1 as both a haploinsufficient tumour suppressor and an essential gene for SHH-medulloblastoma.Neuropathology and applied neurobiology · 2022Article
- Transcription-associated DNA DSBs activate p53 during hiPSC-based neurogenesis.Scientific reports · 2022Article
- SHLD1 is dispensable for 53BP1-dependent V(D)J recombination but critical for productive class switch recombination.Nature communications · 2022Article
- The origin of unwanted editing byproducts in gene editing.Acta biochimica et biophysica Sinica · 2022Article
- The recent advances in non-homologous end-joining through the lens of lymphocyte development.DNA repair · 2020Review
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- Induction of recurrent break cluster genes in neural progenitor cells differentiated from embryonic stem cells in culture.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Modeling pediatric medulloblastoma.Brain pathology (Zurich, Switzerland) · 2020Review
- Loss of H3K36 Methyltransferase SETD2 Impairs V(D)J Recombination during Lymphoid Development.iScience · 2020Article
- DNA damage in aging, the stem cell perspective.Human genetics · 2020Review
- Differential expression of DNA-dependent protein kinase catalytic subunit in the brain of neonatal mice and young adult mice.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2020Article
- Mediator of DNA Damage Checkpoint Protein 1 Facilitates V(D)J Recombination in Cells Lacking DNA Repair Factor XLF.Biomolecules · 2019Article
- The nucleoskeleton protein IFFO1 immobilizes broken DNA and suppresses chromosome translocation during tumorigenesis.Nature cell biology · 2019Article
- Article
- Defective DNA damage repair leads to frequent catastrophic genomic events in murine and human tumors.Nature communications · 2018Article
5 more citing papers are in PubMed but not listed here.
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Authors and funding
20 authors at 5 institutions in 1 country.
Funding
Abstract
Inactivation of the XRCC4 nonhomologous end-joining factor in the mouse germ line leads to embryonic lethality, in association with apoptosis of newly generated, postmitotic neurons. We now show that conditional inactivation of the XRCC4 in nestin-expressing neuronal progenitor cells, although leading to no obvious phenotype in a WT background, leads to early onset of neuronally differentiated medulloblastomas (MBs) in a p53-deficient background. A substantial proportion of the XRCC4/p53-deficient MBs have high-level N-myc gene amplification, often intrachromosomally in the context of complex translocations or other alterations of chromosome 12, on which N-myc resides, or extrachromosomally within double minutes. In addition, most XRCC4/p53-deficient MBs harbor clonal translocations of chromosome 13, which frequently involve chromosome 6 as a partner. One copy of the patched gene (Ptc), which lies on chromosome 13, was deleted in all tested XRCC4/p53-deficient MBs in the context of translocations or interstitial deletions. In addition, Cyclin D2, a chromosome 6 gene, was amplified in a subset of tumors. Notably, amplification of Myc-family or Cyclin D2 genes and deletion of Ptc also have been observed in human MBs. We therefore conclude that, in neuronal cells of mice, the nonhomologous end-joining pathway plays a critical role in suppressing genomic instability that, in a p53-deficient background, routinely contributes to genesis of MBs with recurrent chromosomal alterations.
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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.