ArticleCancer research2008
ATM acts downstream of ATR in the DNA damage response signaling of bystander cells.
Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
48 citing papers in PubMed, 123 citations in OpenAlex.
- Computational advances in the design and discovery of artemis inhibitors for radiosensitization in cancer therapy.Frontiers in chemistry · 2025Article
- Nonrepair functions of DNA mismatch repair proteins: new avenues for precision oncology.Trends in cancer · 2025Review
- ATR signaling controls the bystander responses of human chondrosarcoma cells by promoting RAD51-dependent DNA repair.International journal of radiation biology · 2024Article
- Low-Dose Non-Targeted Effects and Mitochondrial Control.International journal of molecular sciences · 2023Review
- The intercellular communications mediating radiation-induced bystander effects and their relevance to environmental, occupational, and therapeutic exposures.International journal of radiation biology · 2023Review
- Radiation-induced bystander effect and its clinical implications.Frontiers in oncology · 2023Review
- Role of Mitochondria in Radiation Responses: Epigenetic, Metabolic, and Signaling Impacts.International journal of molecular sciences · 2021Review
- Review
- The Radiobiology of Radiopharmaceuticals.Seminars in radiation oncology · 2021Review
- Bisdemethoxycurcumin Enhances the Sensitivity of Non-small Cell Lung Cancer Cells to Icotinib via Dual Induction of Autophagy and Apoptosis.International journal of biological sciences · 2020Article
- ATM controls DNA repair and mitochondria transfer between neighboring cells.Cell communication and signaling : CCS · 2019Article
- Enhancing the Bystander and Abscopal Effects to Improve Radiotherapy Outcomes.Frontiers in oncology · 2019Review
- Radiation, inflammation and the immune response in cancer.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- Targeted and Off-Target (Bystander and Abscopal) Effects of Radiation Therapy: Redox Mechanisms and Risk/Benefit Analysis.Antioxidants & redox signaling · 2018Review
- Extracellular vesicles transfer nuclear Abl-dependent and radiation-induced miR-34c into unirradiated cells to cause bystander effects.Molecular biology of the cell · 2018Article
- The influence of non-DNA-targeted effects on carbon ion-induced low-dose hyper-radiosensitivity in MRC-5 cells.Journal of radiation research · 2016Article
- Oxidative Stress and Carbonyl Lesions in Ulcerative Colitis and Associated Colorectal Cancer.Oxidative medicine and cellular longevity · 2016Review
- Radioprotection of targeted and bystander cells by methylproamine.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2015Article
- BRCA1, FANCD2 and Chk1 are potential molecular targets for the modulation of a radiation-induced DNA damage response in bystander cells.Cancer letters · 2015Article
- Introduction to radiobiology of targeted radionuclide therapy.Frontiers in medicine · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
This study identifies ataxia-telangiectasia mutated (ATM) as a further component of the complex signaling network of radiation-induced DNA damage in nontargeted bystander cells downstream of ataxia-telangiectasia and Rad3-related (ATR) and provides a rationale for molecular targeted modulation of these effects. In directly irradiated cells, ATR, ATM, and DNA-dependent protein kinase (DNA-PK) deficiency resulted in reduced cell survival as predicted by the known important role of these proteins in sensing DNA damage. A decrease in clonogenic survival was also observed in ATR/ATM/DNA-PK-proficient, nonirradiated bystander cells, but this effect was completely abrogated in ATR and ATM but not DNA-PK-deficient bystander cells. ATM activation in bystander cells was found to be dependent on ATR function. Furthermore, the induction and colocalization of ATR, 53BP1, ATM-S1981P, p21, and BRCA1 foci in nontargeted cells was shown, suggesting their involvement in bystander DNA damage signaling and providing additional potential targets for its modulation. 53BP1 bystander foci were induced in an ATR-dependent manner predominantly in S-phase cells, similar to gammaH2AX foci induction. In conclusion, these results provide a rationale for the differential modulation of targeted and nontargeted effects of radiation.
Indexed as
Identifiers
What OpenQuestion holds
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.