ReviewThe Journal of pathology2018
Integrating the DNA damage and protein stress responses during cancer development and treatment.
Review in The Journal of pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 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
60 citing papers in PubMed, 109 citations in OpenAlex.
- Crocin I delays cellular senescence potentially via modulating SIRT1/PKM2 expression to improve lactate homeostasisExperimental and therapeutic medicine · 2026Article
- ERKed by too much signaling: from oncogenic driver to therapeutic vulnerability.Cellular and molecular life sciences : CMLS · 2026Review
- Replication Stress in Cancer: Mechanistic Insights and Therapeutic Opportunities for Radiosensitization.Current issues in molecular biology · 2026Review
- Immune cell senescence drives responsiveness to immunotherapy in melanoma.Molecular cancer · 2025Article
- The Constrained Disorder Principle: A Paradigm Shift for Accurate Interactome Mapping and Information Analysis in Complex Biological Systems.Bioengineering (Basel, Switzerland) · 2025Review
- Unveiling the molecular nexus: Long non-coding RNAs, RNA-binding proteins, and DNA damage in ovarian ischemia-reperfusion injury: A narrative review.International journal of reproductive biomedicine · 2025Review
- Reprogramming cellular senescence and aging clocks for advanced cancer immunotherapy.Molecular cancer · 2025Review
- Poly(ADP-ribose) polymerase-1 in breast cancers: expression level and its association in various molecular subtypes with a focus in Africa.Discover oncology · 2025Review
- Targeting Cellular Senescence: Pathophysiology in Multisystem Age-Related Diseases.Biomedicines · 2025Review
- Impact of glycolysis enzymes and metabolites in regulating DNA damage repair in tumorigenesis and therapy.Cell communication and signaling : CCS · 2025Review
- Current Methodologies to Assess Cellular Senescence in Cancer.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Combined In Situ Transcriptomic and Immunofluorescence to Assess the Effects on DNA Damage and Innate Immune Responses Induced by Bacterial Genotoxin in In Vivo Models.Methods in molecular biology (Clifton, N.J.) · 2025Article
- The DNA damage response and autophagy during cancer development: an antagonistic pleiotropy entanglement.Autophagy · 2024Article
- The Role of Endoplasmic Reticulum Stress on Reducing Recombinant Protein Production in Mammalian Cells.Biochemical engineering journal · 2024Article
- Machine Learning-Enhanced Estimation of Cellular Protein Levels from Bright-Field Images.Bioengineering (Basel, Switzerland) · 2024Article
- Cellular Senescence in Germ Cell Neoplasia In Situ (GCNIS) and Other Histological Types of Testicular Cancer.Medicina (Kaunas, Lithuania) · 2024Article
- Modeling Radiation-Induced Epithelial Cell Injury in Murine Three-Dimensional Esophageal Organoids.Biomolecules · 2024Article
- Article
- Mitochondrial injury induced by a Salmonella genotoxin triggers the proinflammatory senescence-associated secretory phenotype.Nature communications · 2024Article
- KDM7A-DT induces genotoxic stress, tumorigenesis, and progression of p53 missense mutation-associated invasive breast cancer.Frontiers in oncology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During evolution, cells have developed a wide spectrum of stress response modules to ensure homeostasis. The genome and proteome damage response pathways constitute the pillars of this interwoven 'defensive' network. Consequently, the deregulation of these pathways correlates with ageing and various pathophysiological states, including cancer. In the present review, we highlight: (1) the structure of the genome and proteome damage response pathways; (2) their functional crosstalk; and (3) the conditions under which they predispose to cancer. Within this context, we emphasize the role of oncogene-induced DNA damage as a driving force that shapes the cellular landscape for the emergence of the various hallmarks of cancer. We also discuss potential means to exploit key cancer-related alterations of the genome and proteome damage response pathways in order to develop novel efficient therapeutic modalities. © 2018 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.
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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.