ArticleCancer science2003
Parp-1 deficiency implicated in colon and liver tumorigenesis induced by azoxymethane.
Article in Cancer science, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
25 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Two DNA repair gene polymorphisms on the risk of gastrointestinal cancers: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Pooled it
- Association between PARP-1 V762A polymorphism and cancer susceptibility: a meta-analysis.Genetic epidemiology · 2012Pooled it
- PARP‑1 in liver diseases: Molecular mechanisms, therapeutic potential and emerging clinical applications (Review).Molecular medicine reports · 2025Review
- DNA Alkylation Damage by Nitrosamines and Relevant DNA Repair Pathways.International journal of molecular sciences · 2023Review
- Genomic Instability and Cancer Risk Associated with Erroneous DNA Repair.International journal of molecular sciences · 2021Review
- PARP1 Gene Polymorphisms and the Prognosis of Esophageal Cancer Patients from Cixian High-Incidence Region in Northern China.Asian Pacific journal of cancer prevention : APJCP · 2020Article
- The role of ADP-ribose metabolism in metabolic regulation, adipose tissue differentiation, and metabolism.Genes & development · 2020Review
- Review
- Article
- PARP-1 protects against colorectal tumor induction, but promotes inflammation-driven colorectal tumor progression.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Opportunities for the repurposing of PARP inhibitors for the therapy of non-oncological diseases.British journal of pharmacology · 2018Review
- Trial watch - inhibiting PARP enzymes for anticancer therapy.Molecular & cellular oncology · 2016Review
- New facets in the regulation of gene expression by ADP-ribosylation and poly(ADP-ribose) polymerases.Chemical reviews · 2015Review
- Involvement of PARP-1 Val762Ala polymorphism in the onset of cervical cancer in caucasian women.Molecular diagnosis & therapy · 2013Article
- Loss of PIDD limits NF-κB activation and cytokine production but not cell survival or transformation after DNA damage.Cell death and differentiation · 2013Article
- Pleiotropic cellular functions of PARP1 in longevity and aging: genome maintenance meets inflammation.Oxidative medicine and cellular longevity · 2012Review
- Role of nicotinamide in DNA damage, mutagenesis, and DNA repair.Journal of nucleic acids · 2010Article
- PARP-1 Val762Ala polymorphism is associated with reduced risk of non-Hodgkin lymphoma in Korean males.BMC medical genetics · 2010Article
- Adiponectin deficiency enhances colorectal carcinogenesis and liver tumor formation induced by azoxymethane in mice.World journal of gastroenterology · 2008Article
- Increased susceptibility of Sf1(+/-) mice to azoxymethane-induced colon tumorigenesis.Cancer science · 2007Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Poly(ADP-ribose) polymerase-1 (Parp-1) is activated by DNA strand breaks and functions in the maintenance of genomic integrity and cell death control. On the other hand, Parp-1 is also involved in transcriptional regulation of various genes, and the relationship between Parp-1 deficiency and susceptibility to tumorigenesis has not been fully elucidated. In the present study, Parp-1(-/-) mice, harboring exon 1 disruption in Parp-1, and Parp-1(+/+) animals were administered azoxymethane (AOM) at a dose of 10 mg/kg body weight once a week for 6 weeks. At 30 weeks after the first carcinogen treatment, mice were sacrificed. The incidence of animals bearing either adenomas or adenocarcinomas in the colon and the average number of colon tumors per mouse were significantly higher in Parp-1(-/-) mice than in Parp-1(+/+) animals. beta-Catenin accumulation was observed in 43/44 of Parp-1 (-/-) tumors and 19/21 of the Parp-1(+/+) tumors and was not statistically different between the genotypes. This suggests that most tumors developed through a pathway involving the alteration of Wnt-beta-catenin signaling in both Parp-1(-/-) and Parp-1(+/+) mice. In the liver, where AOM is primarily activated, the incidence of animals bearing nodules and the average number of nodules per section were significantly increased in Parp-1(-/-) mice compared with Parp-1(+/+) mice. Therefore, the results indicate that susceptibility to AOM-induced tumorigenesis in the colon and also in the liver is enhanced in Parp-1(-/-) mice, and Parp-1 could have a substantial role in colon and liver tumorigenesis.
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