ReviewCancers2022
Cancer and Radiosensitivity Syndromes: Is Impaired Nuclear ATM Kinase Activity the Primum Movens?
Review in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 15 citations in OpenAlex.
- NATURAL VARIATION IN RADIOTOLERANCE IS ASSOCIATED WITH DIFFERENCES IN INNATE IMMUNE ACTIVITY AND S-PHASE TRANSCRIPTION IN DROSOPHILA MELANOGASTER.bioRxiv : the preprint server for biology · 2026Article
- Adjuvant Radiation Therapy in Breast Cancer Patients With Neurofibromatosis Type 1: Safety and Long-Term Outcomes.Advances in radiation oncology · 2026Article
- Caffeine May Delay the Radiation-Induced Nucleoshuttling of the ATM Kinase and Reduce the Recognition of the DNA Double-Strand Breaks in Human Cells.Biomolecules · 2025Article
- Long-Term Tumor Control After Carbon Ion Radiation Therapy Boost in Locally Advanced Cervical Clear Cell Adenocarcinoma.International journal of particle therapy · 2025Article
- Skin Fibroblasts from Individuals Self-Diagnosed as Electrosensitive Reveal Two Distinct Subsets with Delayed Nucleoshuttling of the ATM Protein in Common.International journal of molecular sciences · 2025Article
- Radiosensitivity in individuals with tuberous sclerosis complex.Discover oncology · 2024Article
- Prediction of Cancer Proneness under Influence of X-rays with Four DNA Mutability and/or Three Cellular Proliferation Assays.Cancers · 2024Article
- When DNA Mutations Interplay with Cellular Proliferation: A Narrative History of Theories of Carcinogenesis.Cancers · 2024Review
- The Chromosome Passenger Complex (CPC) Components and Its Associated Pathways Are Promising Candidates to Differentiate Between Normosensitive and Radiosensitive ATM-Mutated Cells.Biomarker insights · 2024Article
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Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
There are a number of genetic syndromes associated with both high cancer risk and clinical radiosensitivity. However, the link between these two notions remains unknown. Particularly, some cancer syndromes are caused by mutations in genes involved in DNA damage signaling and repair. How are the DNA sequence errors propagated and amplified to cause cell transformation? Conversely, some cancer syndromes are caused by mutations in genes involved in cell cycle checkpoint control. How is misrepaired DNA damage produced? Lastly, certain genes, considered as tumor suppressors, are not involved in DNA damage signaling and repair or in cell cycle checkpoint control. The mechanistic model based on radiation-induced nucleoshuttling of the ATM kinase (RIANS), a major actor of the response to ionizing radiation, may help in providing a unified explanation of the link between cancer proneness and radiosensitivity. In the frame of this model, a given protein may ensure its own specific function but may also play additional biological role(s) as an ATM phosphorylation substrate in cytoplasm. It appears that the mutated proteins that cause the major cancer and radiosensitivity syndromes are all ATM phosphorylation substrates, and they generally localize in the cytoplasm when mutated. The relevance of the RIANS model is discussed by considering different categories of the cancer syndromes.
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.