ArticleRadiation oncology (London, England)2010
Hemizygosity for Atm and Brca1 influence the balance between cell transformation and apoptosis.
Article in Radiation oncology (London, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Multi-locus inherited neoplasia alleles syndromes in cancer: implications for clinical practice.European journal of human genetics : EJHG · 2025Pooled it
- Trp53 Deficiency Increases the Frequency of Hprt Mutant T Lymphocytes Following High-LET Iron Particle Irradiation of Mice.Environmental and molecular mutagenesis · 2026Article
- FLASH Radiotherapy: Benefits, Mechanisms, and Obstacles to Its Clinical Application.International journal of molecular sciences · 2024Review
- A novelFrontiers in oncology · 2023Article
- NRF2 Mediates Cellular Resistance to Transformation, Radiation, and Inflammation in Mice.Antioxidants (Basel, Switzerland) · 2022Article
- Double heterozygous pathogenic variants prevalence in a cohort of patients with hereditary breast cancer.Frontiers in oncology · 2022Article
- Double Heterozygous Mutations in theBreast care (Basel, Switzerland) · 2021Article
- Haploinsufficiency in mouse models of DNA repair deficiency: modifiers of penetrance.Cellular and molecular life sciences : CMLS · 2012Review
- Mechanisms of increased risk of tumorigenesis in Atm and Brca1 double heterozygosity.Radiation oncology (London, England) · 2011Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn recent years data from both mouse models and human tumors suggest that loss of one allele of genes involved in DNA repair pathways may play a central role in genomic instability and carcinogenesis. Additionally several examples in mouse models confirmed that loss of one allele of two functionally related genes may have an additive effect on tumor development. To understand some of the mechanisms involved, we examined the role of monoallelic loss or Atm and Brca1 on cell transformation and apoptosis induced by radiation.
methodsCell transformation and apoptosis were measured in mouse embryo fibroblasts (MEF) and thymocytes respectively. Combinations of wild type and hemizygous genotypes for ATM and BRCA1 were tested in various comparisons.
resultsHaploinsufficiency of either ATM or BRCA1 resulted in an increase in the incidence of radiation-induced transformation of MEF and a corresponding decrease in the proportion of thymocytes dying an apoptotic death, compared with cells from wild-type animals. Combined haploinsufficiency for both genes resulted in an even larger effect on apoptosis.
conclusionsUnder stress, the efficiency and capacity for DNA repair mediated by the ATM/BRCA1 cell signalling network depends on the expression levels of both proteins.
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Registered trials
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