ReviewNature reviews. Cancer2016
DNA damage and the balance between survival and death in cancer biology.
Review in Nature reviews. Cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 606 papers, 4 of them syntheses that pooled it.
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
606 citing papers in PubMed, 4 syntheses or guidelines pooled it, 1,184 citations in OpenAlex.
- Comprehensive analysis of regulated cell death pathways: intrinsic disorder, protein-protein interactions, and cross-pathway communication.Apoptosis : an international journal on programmed cell death · 2025Pooled it
- Mechanistic investigation and the optimal dose based on baicalin in the treatment of ulcerative colitis-A preclinical systematic review and meta-analysis.BMC gastroenterology · 2025Pooled it
- Mechanisms of traditional Chinese medicine overcoming of radiotherapy resistance in breast cancer.Frontiers in oncology · 2024Pooled it
- Efficacy and safety of veliparib plus chemotherapy for the treatment of lung cancer: A systematic review of clinical trials.PloS one · 2023Pooled it
- Benzo[a]pyrene vs. Tapinarof: unraveling ligand-specific AHR transcriptional responses in immortalized keratinocytes.Archives of toxicology · 2026Article
- Article
- A Toxoplasma gondii-derived ROP38 protein engages Ser15/Thr18-linked p53 activation and DNA damage-associated apoptotic signaling in human cancer cells.Cell communication and signaling : CCS · 2026Article
- BKJournal of neuro-oncology · 2026Article
- Urolithin A mitigates doxorubicin-induced myocardial injury via suppression of ROS-driven apoptotic signaling.Histology and histopathology · 2026Article
- Identification of Key Indicators in the Adverse Outcome Pathway for Genetic Damage Induced by Chromate Exposure: A Machine Learning-Based Cross-Sectional Study.Environment & health (Washington, D.C.) · 2026Article
- The Oligomeric State of Rad6-Rad18 and Its Interactions with Translesion Synthesis Proteins.Biomolecules · 2026Article
- Review
- FAL1 facilitates cisplatin resistance of lung adenocarcinoma via BMI1/BIM-mediated apoptosis-autophagy interaction.Molecular and cellular biochemistry · 2026Article
- Assessment of cytotoxicity and genomic instability induced by coal-derived nanoparticles in V79 and HaCaT Cells.Archives of toxicology · 2026Article
- DEPACE-seq enables high-fidelity, single-nucleotide-resolution mapping of abasic sites and characterization of dynamic and long-lived AP landscapes in mammalian genomes.Nucleic acids research · 2026Article
- Beyond apoptosis: nanomedicine enabled reprogramming of tumor cell death for next-generation radiosensitization.Journal of nanobiotechnology · 2026Review
- Reply to Trela, B.A.; Guffroy, M.R. Comment on "AlAsmari et al. Venetoclax Induces Cardiotoxicity Through Modulation of Oxidative-Stress-Mediated Cardiac Inflammation and Apoptosis via NF-κB and BCL-2 Pathway.International journal of molecular sciences · 2026Article
- RNA-triggered cell killing with CRISPR-Cas12a2.Nature · 2026Article
- Association of SIRT1 rs12778366 (T > C) polymorphism with reduced esophageal cancer risk: a case-control study from North India".Molecular biology reports · 2026Article
- Tilting the balance of life and death: navigating DNA replication stress in cancer therapy.Experimental & molecular medicine · 2026Review
546 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
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA is vulnerable to damage resulting from endogenous metabolites, environmental and dietary carcinogens, some anti-inflammatory drugs, and genotoxic cancer therapeutics. Cells respond to DNA damage by activating complex signalling networks that decide cell fate, promoting not only DNA repair and survival but also cell death. The decision between cell survival and death following DNA damage rests on factors that are involved in DNA damage recognition, and DNA repair and damage tolerance, as well as on factors involved in the activation of apoptosis, necrosis, autophagy and senescence. The pathways that dictate cell fate are entwined and have key roles in cancer initiation and progression. Furthermore, they determine the outcome of cancer therapy with genotoxic drugs. Understanding the molecular basis of these pathways is important not only for gaining insight into carcinogenesis, but also in promoting successful cancer therapy. In this Review, we describe key decision-making nodes in the complex interplay between cell survival and death following DNA damage.
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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.