ReviewInternational journal of molecular sciences2019
DNA Damage Stress: Cui Prodest?
Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed.
- Review
- Circadian clock control of breast cancer hallmarks: molecular mechanisms and therapeutic implications.Cancer metastasis reviews · 2026Review
- Protective Role of Adenosine Triphosphate Against Tamoxifen-Induced Retinal Toxicity in a Rat Model.Medicina (Kaunas, Lithuania) · 2026Article
- Mitochondria-targeted strategies in cancer radiotherapy: from ROS regulation to immunogenic cell death.Frontiers in cell and developmental biology · 2026Review
- Targeting MAD2L2-dependent translesion synthesis impairs DNA damage tolerance and enhances cellular response to cisplatin.Frontiers in cell and developmental biology · 2026Article
- Hypoxic adaptation theory of cancer.Frontiers in cell and developmental biology · 2026Article
- The glioblastoma ecosystem: clonal evolution, heterogeneity, and therapeutic resistance.Frontiers in cell and developmental biology · 2026Review
- Relationship Between Facial Melasma and Ocular Photoaging Diseases.Medical sciences (Basel, Switzerland) · 2025Article
- The leading role of MYC in DNA damage response: exploring opportunities for therapeutic inhibition.Frontiers in cell and developmental biology · 2025Review
- Venetoclax triggers sublethal apoptotic signaling in venetoclax-resistant acute myeloid leukemia cells and induces vulnerability to PARP inhibition and azacitidine.Cell death & disease · 2024Article
- Targeting the DNA Damage Response for Cancer Therapy by Inhibiting the Kinase Wee1.Frontiers in oncology · 2022Review
- DNA damage checkpoint execution and the rules of its disengagement.Frontiers in cell and developmental biology · 2022Review
- Dual targeting of higher-order DNA structures by azacryptands induces DNA junction-mediated DNA damage in cancer cells.Nucleic acids research · 2021Article
- Turner's syndrome mosaicism in girls with neurodevelopmental disorders: a cohort study and hypothesis.Molecular cytogenetics · 2021Article
- Disulfiram Alone Functions as a Radiosensitizer for Pancreatic Cancer BothFrontiers in oncology · 2021Article
- Article
- Sml1 Inhibits the DNA Repair Activity of Rev1 in Saccharomyces cerevisiae during Oxidative Stress.Applied and environmental microbiology · 2020Article
- PLK1 targets NOTCH1 during DNA damage and mitotic progression.The Journal of biological chemistry · 2019Article
- Special Issue on DNA Replication Stress: Summary of Topics Covered.International journal of molecular sciences · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
DNA is an entity shielded by mechanisms that maintain genomic stability and are essential for living cells; however, DNA is constantly subject to assaults from the environment throughout the cellular life span, making the genome susceptible to mutation and irreparable damage. Cells are prepared to mend such events through cell death as an extrema ratio to solve those threats from a multicellular perspective. However, in cells under various stress conditions, checkpoint mechanisms are activated to allow cells to have enough time to repair the damaged DNA. In yeast, entry into the cell cycle when damage is not completely repaired represents an adaptive mechanism to cope with stressful conditions. In multicellular organisms, entry into cell cycle with damaged DNA is strictly forbidden. However, in cancer development, individual cells undergo checkpoint adaptation, in which most cells die, but some survive acquiring advantageous mutations and selfishly evolve a conflictual behavior. In this review, we focus on how, in cancer development, cells rely on checkpoint adaptation to escape DNA stress and ultimately to cell death.
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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.