ReviewCancer science2004
DNA repair and cancer: lessons from mutant mouse models.
Review in Cancer science, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
What it found
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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
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- Genetic aspects of pituitary carcinoma: A systematic review.Medicine · 2016Pooled it
- Elucidating Differences in Early-Stage Centrosome Amplification in Primary and Immortalized Mouse Cells.International journal of molecular sciences · 2023Article
- Article
- Expression of the Wnt ligands gene family and its relationship to prognosis in hepatocellular carcinoma.Cancer cell international · 2019Article
- An endogenous DNA adduct as a prognostic biomarker for hepatocarcinogenesis and its prevention by Theaphenon E in mice.Hepatology (Baltimore, Md.) · 2018Article
- High expression of ERCC5 predicts a poor prognosis in hepatocellular carcinoma.International journal of clinical and experimental pathology · 2018Article
- Genetic variants in the nucleotide excision repair pathway genes and gastric cancer susceptibility in a southern Chinese population.Cancer management and research · 2018Article
- The association of six polymorphisms of five genes involved in three steps of nucleotide excision repair pathways with hepatocellular cancer risk.Oncotarget · 2016Article
- Article
- Relationships betweenOncoTargets and therapy · 2016Article
- Knockdown of Gli1 by small-interfering RNA enhances the effects of BCNU on the proliferation and apoptosis of glioma U251 cells.International journal of clinical and experimental pathology · 2015Article
- Susceptibility of XPD and hOGG1 genetic variants to prostate cancer.Biomedical reports · 2013Article
- Variation in PAH-related DNA adduct levels among non-smokers: the role of multiple genetic polymorphisms and nucleotide excision repair phenotype.International journal of cancer · 2013Article
- Benzo[a]pyrene (BP) DNA adduct formation in DNA repair-deficient p53 haploinsufficient [Xpa(-/-)p53(+/-)] and wild-type mice fed BP and BP plus chlorophyllin for 28 days.Carcinogenesis · 2012Article
- N -ethyl- N -nitrosourea induces retinal photoreceptor damage in adult rats.Journal of toxicologic pathology · 2012Article
- Genetic variation and its role in malignancy.International journal of biomedical science : IJBS · 2011Article
- Modeling Dose-response at Low Dose: A Systems Biology Approach for Ionization Radiation.Dose-response : a publication of International Hormesis Society · 2010Article
- Response of human mammary epithelial cells to DNA damage induced by 4-hydroxyequilenin: Lack of p53-mediated G1 arrest.Chemico-biological interactions · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA damage, if the repair process, especially nucleotide excision repair (NER), is compromised or the lesion is repaired by some other error-prone mechanism, causes mutation and ultimately contributes to neoplastic transformation. Impairment of components of the DNA damage response pathway (e.g., p53) is also implicated in carcinogenesis. We currently have considerable knowledge of the role of DNA repair genes as tumor suppressors, both clinically and experimentally. The deleterious clinical consequences of inherited defects in DNA repair system are apparent from several human cancer predisposition syndromes (e.g., NER-compromised xeroderma pigmentosum [XP] and p53-deficient Li-Fraumeni syndrome). However, experimental studies to support the clinical evidence are hampered by the lack of powerful animal models. Here, we review in vivo experimental data suggesting the protective function of DNA repair machinery in chemical carcinogenesis. We specifically focus on the three DNA repair genes, O(6)-methylguanine-DNA methyltransferase gene (MGMT ), XP group A gene (XPA) and p53. First, mice overexpressing MGMT display substantial resistance to nitrosamine-induced hepatocarcinogenesis. In addition, a reduction of spontaneous liver tumors and longer survival times were evident. However, there are no known mutations in the human MGMT and therefore no associated cancer syndrome. Secondly, XPA mutant mice are indeed prone to spontaneous and carcinogen-induced tumorigenesis in internal organs (which are not exposed to sunlight). The concomitant loss of p53 resulted in accelerated onset of carcinogenesis. Finally, p53 null mice are predisposed to brain tumors upon transplacental exposure to a carcinogen. Accumulated evidence in these three mutant mouse models firmly supports the notion that the DNA repair system is vital for protection against cancer.
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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.