ArticleMechanisms of ageing and development
Clinical implications of the basic defects in Cockayne syndrome and xeroderma pigmentosum and the DNA lesions responsible for cancer, neurodegeneration and aging.
Article in Mechanisms of ageing and development. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 27 citations in OpenAlex.
- Targeting Aging and Diseases Associated with Ferroptosis and Senescence Through Modulation of Iron, Oxidative Stress and Lipid Peroxidation.Antioxidants (Basel, Switzerland) · 2025Review
- Elf1 promotes Rad26's interaction with lesion-arrested Pol II for transcription-coupled repair.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The Multifaceted Syndromic Primary Immunodeficiencies in Children.Journal of clinical medicine · 2023Article
- The French Cohort of DNA Repair-Deficient Xeroderma Pigmentosum Patients: Risk of Hematological Malignancies.Cancers · 2023Article
- Increased risk of internal tumors in DNA repair-deficient xeroderma pigmentosum patients: analysis of four international cohorts.Orphanet journal of rare diseases · 2022Article
- UV Protection in the Cornea: Failure and Rescue.Biology · 2022Review
- Current and emerging roles of Cockayne syndrome group B (CSB) protein.Nucleic acids research · 2021Review
- Tumour predisposition and cancer syndromes as models to study gene-environment interactions.Nature reviews. Cancer · 2020Review
- Lack of XPC leads to a shift between respiratory complexes I and II but sensitizes cells to mitochondrial stress.Scientific reports · 2017Article
- Single-stranded DNA Binding by the Helix-Hairpin-Helix Domain of XPF Protein Contributes to the Substrate Specificity of the ERCC1-XPF Protein Complex.The Journal of biological chemistry · 2017Article
- Sirt1 suppresses RNA synthesis after UV irradiation in combined xeroderma pigmentosum group D/Cockayne syndrome (XP-D/CS) cells.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- E2F1 and p53 transcription factors as accessory factors for nucleotide excision repair.International journal of molecular sciences · 2012Review
- Rad26p regulates the occupancy of histone H2A-H2B dimer at the active genes in vivo.Nucleic acids research · 2012Article
- Haploinsufficiency in mouse models of DNA repair deficiency: modifiers of penetrance.Cellular and molecular life sciences : CMLS · 2012Review
- Disorders of nucleotide excision repair: the genetic and molecular basis of heterogeneity.Nature reviews. Genetics · 2009Review
- Diagnosis of Xeroderma Pigmentosum and Related DNA Repair-Deficient Cutaneous Diseases.Current medical literature. Dermatology · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cancer, aging, and neurodegeneration are all associated with DNA damage and repair in complex fashions. Aging appears to be a cell and tissue-wide process linked to the insulin-dependent pathway in several DNA repair deficient disorders, especially in mice. Cancer and neurodegeneration appear to have complementary relationships to DNA damage and repair. Cancer arises from surviving cells, or even stem cells, that have down-regulated many pathways, including apoptosis, that regulate genomic stability in a multi-step process. Neurodegeneration however occurs in nondividing neurons in which the persistence of apoptosis in response to reactive oxygen species is, itself, pathological. Questions that remain open concern: sources and chemical nature of naturally occurring DNA damaging agents, especially whether mitochondria are the true source; the target tissues for DNA damage and repair; do the human DNA repair deficient diseases delineate specific pathways of DNA damage relevant to clinical outcomes; if naturally occurring reactive oxygen species are pathological in human repair deficient disease, would anti-oxidants or anti-apoptotic agents be feasible therapeutic agent?
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.