ArticleProceedings of the National Academy of Sciences of the United States of America2006
ATM promotes apoptosis and suppresses tumorigenesis in response to Myc.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 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.
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Who cites it
80 citing papers in PubMed, 153 citations in OpenAlex.
- IFI16 is essential to linking DNA damage and ferroptosis in acute kidney injury.Cell death & disease · 2026Article
- Transcriptional landscape of pleural mesothelioma patients in relation to NF2 gene mutational status.Journal of the Egyptian National Cancer Institute · 2025Article
- Germline-Somatic Interactions in BRCA-Associated Cancers: Unique Molecular Profiles and Clinical Outcomes Linking ATM to TP53 Synthetic Essentiality.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Article
- Phosphorylated BLM peptide acts as an agonist for DNA damage response.Nucleic acids research · 2025Article
- AHaematologica · 2024Article
- Article
- Interactions between the DNA Damage Response and the Telomere Complex in Carcinogenesis: A Hypothesis.Current issues in molecular biology · 2023Review
- Article
- Distinct clinicopathological characteristics, genomic alteration and prognosis in breast cancer with concurrent TP53 mutation and MYC amplification.Thoracic cancer · 2022Article
- Proteogenomic characterization of 2002 human cancers reveals pan-cancer molecular subtypes and associated pathways.Nature communications · 2022Article
- Cyclin-Dependent Kinase Synthetic Lethality Partners in DNA Damage Response.International journal of molecular sciences · 2022Review
- Identifying tumor immunity-associated molecular features in liver hepatocellular carcinoma by multi-omics analysis.Frontiers in molecular biosciences · 2022Article
- Development of an AAV DNA-based synthetic vector for the potential gene therapy of hemophilia in children.Frontiers in microbiology · 2022Article
- Tilting MYC toward cancer cell death.Trends in cancer · 2021Review
- MYC: a multipurpose oncogene with prognostic and therapeutic implications in blood malignancies.Journal of hematology & oncology · 2021Review
- Evolving Mechanisms in the Pathophysiology of Pemphigus Vulgaris: A Review Emphasizing the Role of Desmoglein 3 in Regulating p53 and the Yes-Associated Protein.Life (Basel, Switzerland) · 2021Review
- Demethylase-independent function of JMJD2D as a novel antagonist of p53 to promote Liver Cancer initiation and progression.Theranostics · 2020Article
- Rap1 regulates hematopoietic stem cell survival and affects oncogenesis and response to chemotherapy.Nature communications · 2019Article
- Clinicopathological significance of ataxia telangiectasia-mutated (ATM) kinase and ataxia telangiectasia-mutated and Rad3-related (ATR) kinase in MYC overexpressed breast cancers.Breast cancer research and treatment · 2019Article
- GSK3 suppression upregulates β-catenin and c-Myc to abrogate KRas-dependent tumors.Nature communications · 2018Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Overexpression of the c-myc oncogene contributes to the development of a significant number of human cancers. In response to deregulated Myc activity, the p53 tumor suppressor is activated to promote apoptosis and inhibit tumor formation. Here we demonstrate that p53 induction in response to Myc overexpression requires the ataxia-telangiectasia mutated (ATM) kinase, a major regulator of the cellular response to DNA double-strand breaks. In a transgenic mouse model overexpressing Myc in squamous epithelial tissues, inactivation of Atm suppresses apoptosis and accelerates tumorigenesis. Deregulated Myc expression induces DNA damage in primary transgenic keratinocytes and the formation of gammaH2AX and phospho-SMC1 foci in transgenic tissue. These findings suggest that Myc overexpression causes DNA damage in vivo and that the ATM-dependent response to this damage is critical for p53 activation, apoptosis, and the suppression of tumor development.
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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.