ReviewCarcinogenesis2020
DNA damage and mitochondria in cancer and aging.
Review in Carcinogenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis 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
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.
- Adherence to the Mediterranean diet and its protective effects against colorectal cancer: a meta-analysis of 26 studies with 2,217,404 participants.GeroScience · 2025Pooled it
- Second primary malignancy risk after thymic epithelial tumors: a Surveillance, Epidemiology, and End Results analysis integrating multiple primary-standardized incidence ratio and competing-risk models.Journal of thoracic disease · 2026Article
- The micronucleus assay in exfoliated buccal cells for occupational exposure studies: an overview.Mutagenesis · 2026Review
- Age- and Treatment-Related Patterns in Fatigue, Coping/Resilience, and Skeletal Muscle Bioenergetics (Biomedicines · 2026Article
- Mitochondrial-targeted therapeutics in oral squamous cell carcinoma: molecular and therapeutic implications.Frontiers in medicine · 2026Review
- Computationally-designed aptamers targeting RAD51-BRCA2 interaction impair homologous recombination and induce synthetic lethality.Nature communications · 2025Article
- Article
- 1,8-Cineole ameliorates vascular endothelial senescence in diabetes mellitus by directly targeting and deubiquitinating PPAR-γJournal of pharmaceutical analysis · 2025Article
- Tipping the PARylation scale: Dysregulation of PAR signaling in Huntington and neurodegenerative diseases.Journal of Huntington's disease · 2025Review
- Assessing CometChip technology for DNA damage studies in non-model species: distinct UV-induced responses in turtles and mammals.BMC research notes · 2025Article
- Mitochondrial Dysfunction as a Pathogenesis and Therapeutic Strategy for Metabolic-Dysfunction-Associated Steatotic Liver Disease.International journal of molecular sciences · 2025Review
- Review
- Nicotinamide: A Multifaceted Molecule in Skin Health and Beyond.Medicina (Kaunas, Lithuania) · 2025Review
- Exploring the Link Between Telomeres and Mitochondria: Mechanisms and Implications in Different Cell Types.International journal of molecular sciences · 2025Review
- Immunometabolism in the Aging Heart.Journal of the American Heart Association · 2025Review
- Mitochondrial Unfolded Protein Response (mtUPR) and Diseases.Current medicinal chemistry · 2025Review
- Progression of brain injuries associated with methotrexate chemotherapy in childhood acute lymphoblastic leukemia.Pediatric research · 2025Article
- Aging Lung: Molecular Drivers and Impact on Respiratory Diseases-A Narrative Clinical Review.Antioxidants (Basel, Switzerland) · 2024Review
- Metabolism: an important player in glioma survival and development.Discover oncology · 2024Review
- LPS-related muscle loss is associated with the alteration of Bacteroidetes abundance, systemic inflammation, and mitochondrial morphology in a weaned piglet model.Science China. Life sciences · 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
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Age and DNA repair deficiencies are strong risk factors for developing cancer. This is reflected in the comorbidity of cancer with premature aging diseases associated with DNA damage repair deficiencies. Recent research has suggested that DNA damage accumulation, telomere dysfunction and the accompanying mitochondrial dysfunction exacerbate the aging process and may increase the risk of cancer development. Thus, an area of interest in both cancer and aging research is the elucidation of the dynamic crosstalk between the nucleus and the mitochondria. In this review, we discuss current research on aging and cancer with specific focus on the role of mitochondrial dysfunction in cancer and aging as well as how nuclear to mitochondrial DNA damage signaling may be a driving factor in the increased cancer incidence with aging. We suggest that therapeutic interventions aimed at the induction of autophagy and mediation of nuclear to mitochondrial signaling may provide a mechanism for healthier aging and reduced tumorigenesis.
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.