ReviewThe American journal of pathology1998
Warner-Lambert/Parke-Davis Award Lecture. Pathological and physiological double-strand breaks: roles in cancer, aging, and the immune system.
Review in The American journal of pathology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 121 citations in OpenAlex.
- Gold Nanoparticle-Mediated DNA Damage Under FLASH Electron-Beam Irradiation: A Monte Carlo Study.Nanomaterials (Basel, Switzerland) · 2026Article
- Human‑made electromagnetic fields: Ion forced‑oscillation and voltage‑gated ion channel dysfunction, oxidative stress and DNA damage (Review).International journal of oncology · 2021Review
- spn-A/rad51 mutant exhibits enhanced genomic damage, cell death and low temperature sensitivity in somatic tissues.Chromosoma · 2021Article
- Targeted Cancer Therapy: Vital Oncogenes and a New Molecular Genetic Paradigm for Cancer Initiation Progression and Treatment.International journal of molecular sciences · 2016Review
- Cell type-specific properties and environment shape tissue specificity of cancer genes.Scientific reports · 2016Article
- Dynamics of double strand breaks and chromosomal translocations.Molecular cancer · 2014Review
- Article
- Nonhomologous DNA end joining (NHEJ) and chromosomal translocations in humans.Sub-cellular biochemistry · 2010Review
- Adenovirus-mediated expression of UHRF1 reduces the radiosensitivity of cervical cancer HeLa cells to gamma-irradiation.Acta pharmacologica Sinica · 2009Article
- Altered kinetics of nonhomologous end joining and class switch recombination in ligase IV-deficient B cells.The Journal of experimental medicine · 2008Article
- Deletion of Ku70, Ku80, or both causes early aging without substantially increased cancer.Molecular and cellular biology · 2007Article
- In vivo mutagenic effect of very low dose radiation.Dose-response : a publication of International Hormesis Society · 2006Article
- Heterogeneity of humoral immune abnormalities in children with Nijmegen breakage syndrome: an 8-year follow-up study in a single centre.Clinical and experimental immunology · 2002Article
- Displacement of DNA-PKcs from DNA ends by the Werner syndrome protein.Nucleic acids research · 2002Article
- Short inverted repeats initiate gene amplification through the formation of a large DNA palindrome in mammalian cells.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- V(D)J-mediated translocations in lymphoid neoplasms: a functional assessment of genomic instability by cryptic sites.The Journal of experimental medicine · 2002Article
- Homologous Recombination and Its Role in Carcinogenesis.Journal of biomedicine & biotechnology · 2002Article
- Role of the non-homologous DNA end joining pathway in the early steps of retroviral infection.The EMBO journal · 2001Article
- Crystal structure of the Xrcc4 DNA repair protein and implications for end joining.The EMBO journal · 2000Article
- The nicking step in V(D)J recombination is independent of synapsis: implications for the immune repertoire.Molecular and cellular biology · 2000Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Pathological agents such as ionizing radiation and oxidative free radicals can cause breaks in both strands of the DNA at a given site (double-strand break). This is the most serious type of DNA damage because neither strand is able to provide physical integrity or information content, as would be the case for single-strand DNA damage where one strand of the duplex remains intact. The repair of such breaks usually results in an irreversible alteration of the DNA. Two physiological forms of intentional double-strand (ds) DNA breakage and rejoining occur during lymphoid differentiation. One is V(D)J recombination occurring during early B and T cell development, and the other is class switch recombination, occurring exclusively in mature B cells. The manner in which physiological and most pathological double-strand DNA breaks are rejoined to restore chromosomal integrity are the same. Defects during the phases in which pathological or physiological breaks are generated or in which they are joined can result in chromosomal translocations or loss of genetic information at the site of breakage. Such events are the first step in some cancers and may be a key contributor to changes in DNA with age. Inherited defects in this process can result in severe combined immune deficiency. Hence, pathological and physiological DNA double-strand breaks are related to immune defects and cancer and may be one of the key ways in which DNA is damaged during aging.
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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.