ArticleOncogene2008
Atm heterozygosity does not increase tumor susceptibility to ionizing radiation alone or in a p53 heterozygous background.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Cancer Cells Haploinsufficient for ATM Are Sensitized to PARP Inhibitors byInternational journal of molecular sciences · 2022Article
- Targeting the ATM Kinase to Enhance the Efficacy of Radiotherapy and Outcomes for Cancer Patients.Seminars in radiation oncology · 2022Review
- Inflammation, a significant player of Ataxia-Telangiectasia pathogenesis?Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018Review
- Postmastectomy Radiation Therapy: Are We Ready to Individualize Radiation?International journal of breast cancer · 2018Review
- ATM mutations for surgeons.Familial cancer · 2017Review
- MEK inhibitors block growth of lung tumours with mutations in ataxia-telangiectasia mutated.Nature communications · 2016Article
- Article
- Genomic Biomarkers for Breast Cancer Risk.Advances in experimental medicine and biology · 2016Review
- Mutational Analysis of Ionizing Radiation Induced Neoplasms.Cell reports · 2015Article
- Role of DNA damage response pathways in preventing carcinogenesis caused by intrinsic replication stress.Oncogene · 2014Article
- Radiotherapy-induced malignancies: review of clinical features, pathobiology, and evolving approaches for mitigating risk.Frontiers in oncology · 2013Article
- A bioinformatics filtering strategy for identifying radiation response biomarker candidates.PloS one · 2012Article
- Loss of p53 Ser18 and Atm results in embryonic lethality without cooperation in tumorigenesis.PloS one · 2011Article
- Chromatin protein L3MBTL1 is dispensable for development and tumor suppression in mice.The Journal of biological chemistry · 2010Article
- Atm-deficient mice exhibit increased sensitivity to dextran sulfate sodium-induced colitis characterized by elevated DNA damage and persistent immune activation.Cancer research · 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
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Ataxia-Telangiectasia (A-T) is an autosomal recessive human disease characterized by genetic instability, radiosensitivity, immunodeficiency and cancer predisposition, because of mutation in both alleles of the ATM (ataxia-telangiectasia mutated) gene. The role of Atm heterozygosity in cancer susceptibility is controversial, in both human and mouse. Earlier studies identified deletions near the Atm gene on mouse chromosome 9 in radiation-induced lymphomas from p53 heterozygous mice. To determine whether Atm was the target of these deletions, Atm heterozygous as well as Atm/P53 double heterozygous mice were treated with ionizing radiation. There were no significant differences in tumor latency, progression and lifespan after gamma-radiation in Atm heterozygous mice compared with their wild-type control counterparts. Deletions were found on chromosome 9 near the Atm locus in radiation-induced tumors, but in 50% of the cases the deletion included the knockout allele, and the expression of Atm was maintained in the tumors indicating that loss of heterozygosity on chromosome 9 is not driven by Atm, but by an alternative tumor suppressor gene located near Atm on this chromosome. We conclude that Atm heterozygosity does not confer an increase in tumor susceptibility in this context.
Indexed as
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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.