ArticleLeukemia research2013
Non-homologous end joining mediated DNA repair is impaired in the NUP98-HOXD13 mouse model for myelodysplastic syndrome.
Article in Leukemia research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 13 citations in OpenAlex.
- DNA double-strand break-capturing nuclear envelope tubules drive DNA repair.Nature structural & molecular biology · 2024Article
- Article
- Mechanistic insights and potential therapeutic approaches for NUP98-rearranged hematologic malignancies.Blood · 2020Review
- Cytotoxicity and Differentiating Effect of the Poly(ADP-Ribose) Polymerase Inhibitor Olaparib in Myelodysplastic Syndromes.Cancers · 2019Article
- Nucleoporin genes in human diseases.European journal of human genetics : EJHG · 2016Review
- Oropharyngeal squamous cell carcinoma in the veteran population: Association with traditional carcinogen exposure and poor clinical outcomes.Head & neck · 2015Article
- Progressive genomic instability in the Nup98-HoxD13 model of MDS correlates with loss of the PIG-A gene product.Neoplasia (New York, N.Y.) · 2014Article
- Article
- Oxidative stress leads to increased mutation frequency in a murine model of myelodysplastic syndrome.Leukemia research · 2014Article
- Myelodysplastic syndrome: an inability to appropriately respond to damaged DNA?Experimental hematology · 2013Review
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
Abstract
Chromosomal translocations typically impair cell differentiation and often require secondary mutations for malignant transformation. However, the role of a primary translocation in the development of collaborating mutations is debatable. To delineate the role of leukemic translocation NUP98-HOXD13 (NHD13) in secondary mutagenesis, DNA break and repair mechanisms in stimulated mouse B lymphocytes expressing NHD13 were analyzed. Our results showed significantly reduced expression of non-homologous end joining (NHEJ)-mediated DNA repair genes, DNA Pkcs, DNA ligase4, and Xrcc4 leading to cell cycle arrest at G2/M phase. Our results showed that expression of NHD13 fusion gene resulted in impaired NHEJ-mediated DNA break repair.
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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.