ArticleBreast cancer research : BCR2005
Atm heterozygous deficiency enhances development of mammary carcinomas in p53 heterozygous knockout mice.
Article in Breast cancer research : BCR, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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20 citing papers in PubMed, 32 citations in OpenAlex.
- Trans-Scale Insights into Variability in Radiation Cancer Risk Across Tissues, Individuals, and Species.Biology · 2025Review
- Interstitial deletion of the Apc locus in β-catenin-overexpressing cells is a signature of radiation-induced intestinal tumors in C3B6F1 ApcMin/+ mice†.Journal of radiation research · 2023Article
- Genomic and Clinicopathologic Characterization ofClinical cancer research : an official journal of the American Association for Cancer Research · 2020Article
- Adverse outcome pathways for ionizing radiation and breast cancer involve direct and indirect DNA damage, oxidative stress, inflammation, genomic instability, and interaction with hormonal regulation of the breast.Archives of toxicology · 2020Review
- The p53 inhibitor Mdm4 cooperates with multiple genetic lesions in tumourigenesis.The Journal of pathology · 2017Article
- Genomic analysis of exceptional responders to radiotherapy reveals somatic mutations in ATM.Oncotarget · 2017Article
- ATM signalling and cancer.Oncogene · 2014Review
- Tug of war between survival and death: exploring ATM function in cancer.International journal of molecular sciences · 2014Review
- Combined haploinsufficiency and genetic control of the G2/M checkpoint in irradiated cells.Radiation research · 2012Article
- Haploinsufficiency of Tumor Suppressor Genes is Driven by the Cumulative Effect of microRNAs, microRNA Binding Site Polymorphisms and microRNA Polymorphisms: An In silico Approach.Cancer informatics · 2012Article
- Mechanisms of increased risk of tumorigenesis in Atm and Brca1 double heterozygosity.Radiation oncology (London, England) · 2011Article
- Map making in the 21st century: charting breast cancer susceptibility pathways in rodent models.Journal of mammary gland biology and neoplasia · 2011Article
- RMI1 attenuates tumor development and is essential for early embryonic survival.Molecular carcinogenesis · 2011Article
- RADIOSENSITIVITY TO HIGH ENERGY IRON IONS IS INFLUENCED BY HETEROZYGOSITY forAdvances in space research : the official journal of the Committee on Space Research (COSPAR) · 2010Article
- Defining the ATM-mediated barrier to tumorigenesis in somatic mammary cells following ErbB2 activation.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Hemizygosity for Atm and Brca1 influence the balance between cell transformation and apoptosis.Radiation oncology (London, England) · 2010Article
- Limited role of murine ATM in oncogene-induced senescence and p53-dependent tumor suppression.PloS one · 2009Article
- Atm heterozygosity does not increase tumor susceptibility to ionizing radiation alone or in a p53 heterozygous background.Oncogene · 2008Article
- Linkage disequilibrium pattern of the ATM gene in breast cancer patients and controls; association of SNPs and haplotypes to radio-sensitivity and post-lumpectomy local recurrence.Radiation oncology (London, England) · 2007Article
- Trial Watch: Targeting ATM-CHK2 and ATR-CHK1 pathways for anticancer therapy.Molecular & cellular oncologyReview
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionAtaxia-telangiectasia is an autosomal-recessive disease that affects neuro-immunological functions, associated with increased susceptibility to malignancy, chromosomal instability and hypersensitivity to ionizing radiation. Although ataxia-telangiectasia mutated (ATM) heterozygous deficiency has been proposed to increase susceptibility to breast cancer, some studies have not found excess risk. In experimental animals, increased susceptibility to breast cancer is not observed in the Atm heterozygous deficient mice (Atm+/-) carrying a knockout null allele. In order to determine the effect of Atm heterozygous deficiency on mammary tumourigenesis, we generated a series of Atm+/- mice on the p53+/- background with a certain predisposition to spontaneous development of mammary carcinomas, and we examined the development of the tumours after X-irradiation.
methodsBALB/cHeA-p53+/- mice were crossed with MSM/Ms-Atm+/- mice, and females of the F1 progeny ([BALB/cHeA x MSM/Ms]F1) with four genotypes were used in the experiments. The mice were exposed to X-rays (5 Gy; 0.5 Gy/min) at age 5 weeks.
resultsWe tested the effect of haploinsufficiency of the Atm gene on mammary tumourigenesis after X-irradiation in the p53+/- mice of the BALB/cHeA x MSM/Ms background. The singly heterozygous p53+/- mice subjected to X-irradiation developed mammary carcinomas at around 25 weeks of age, and the final incidence of mammary carcinomas at 39 weeks was 31% (19 out of 61). The introduction of the heterozygous Atm knockout alleles into the background of the p53+/- genotype significantly increased the incidence of mammary carcinoma to 58% (32 out of 55) and increased the average number of mammary carcinomas per mouse. However, introduction of Atm alleles did not change the latency of development of mammary carcinoma.
conclusionOur results indicate a strong enhancement in mammary carcinogenesis by Atm heterozygous deficiency in p53+/- mice. Thus, doubly heterozygous mice represent a useful model system with which to analyze the interaction of heterozygous genotypes for p53, Atm and other genes, and their effects on mammary carcinogenesis.
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