ArticleNeoplasia (New York, N.Y.)2014
Strain background determines lymphoma incidence in Atm knockout mice.
Article in Neoplasia (New York, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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, 21 citations in OpenAlex.
- A Unique Spectrum of Spontaneous Tumors inCells · 2022Article
- A novel, ataxic mouse model of ataxia telangiectasia caused by a clinically relevant nonsense mutation.eLife · 2021Article
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- NADAging cell · 2021Article
- Growth in ataxia telangiectasia.Orphanet journal of rare diseases · 2021Article
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- Article
- Ataxia-telangiectasia mutated is required for the development of protective immune memory after influenza A virus infection.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Nbn-Mre11 interaction is required for tumor suppression and genomic integrity.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Ataxia telangiectasia and Rad3-related inhibitors and cancer therapy: where we stand.Journal of hematology & oncology · 2019Review
- The impact of glutamine supplementation on the symptoms of ataxia-telangiectasia: a preclinical assessment.Molecular neurodegeneration · 2016Article
- Article
- A novel mouse model for ataxia-telangiectasia with a N-terminal mutation displays a behavioral defect and a low incidence of lymphoma but no increased oxidative burden.Human molecular genetics · 2015Article
- Mouse Tumor Biology (MTB): a database of mouse models for human cancer.Nucleic acids research · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 6 institutions in 2 countries.
Funding
Abstract
About 10% to 30% of patients with ataxia-telangiectasia (A-T) develop leukemias or lymphomas. There is considerable interpatient variation in the age of onset and leukemia/lymphoma type. The incomplete penetrance and variable age of onset may be attributable to several factors. These include competing mortality from other A-T-associated pathologies, particularly neurodegeneration and interstitial lung disease, allele-specific effects of ataxia-telangiectasia mutated (ATM) gene mutations. There is also limited evidence from clinical observations and studies using Atm knockout mice that modifier genes may account for some variation in leukemia/lymphoma susceptibility. We have introgressed the Atm(tm1Awb) knockout allele (Atm(-)) onto several inbred murine strains and observed differences in thymic lymphoma incidence and latency between Atm(-/-) mice on the different strain backgrounds and between their F1 hybrids. The lymphomas that arose in these mice had a pattern of sequence gains and losses that were similar to those previously described by others. These results provide further evidence for the existence of modifier genes controlling lymphomagenesis in individuals carrying defective copies of Atm, at least in mice, the characterized Atm(-) congenic strain set provides a resource with which to identify these genes. In addition, we found that fewer than expected Atm(-/-) pups were weaned on two strain backgrounds and that there was no correlation between body weight of young Atm-/- mice and lymphoma incidence or latency.
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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.