ArticleProceedings of the National Academy of Sciences of the United States of America2001
Spontaneous hepatocellular carcinoma is reduced in transgenic mice overexpressing human O6- methylguanine-DNA methyltransferase.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- Pooled it
- Epigenetic downregulation of OEnvironmental pollution (Barking, Essex : 1987) · 2024Article
- An insertion variant of MGMT disrupts a STAT1 binding site and confers susceptibility to glioma.Cancer cell international · 2021Article
- An intronic genetic variation ofCancer management and research · 2018Article
- Overexpression of AGT promotes bronchopulmonary dysplasis via the JAK/STAT signal pathway.Oncotarget · 2017Article
- DNA Alkylating Agent Protects Against Spontaneous Hepatocellular Carcinoma Regardless of O6-Methylguanine-DNA Methyltransferase Status.Cancer prevention research (Philadelphia, Pa.) · 2016Article
- Manipulation of DNA Repair Proficiency in Mouse Models of Colorectal Cancer.BioMed research international · 2016Review
- Repair of endogenous DNA base lesions modulate lifespan in mice.DNA repair · 2014Article
- S-nitrosoglutathione reductase deficiency increases mutagenesis from alkylation in mouse liver.Carcinogenesis · 2013Article
- TGF-β signaling is often attenuated during hepatotumorigenesis, but is retained for the malignancy of hepatocellular carcinoma cells.PloS one · 2013Article
- Balancing repair and tolerance of DNA damage caused by alkylating agents.Nature reviews. Cancer · 2012Review
- Age-related instability in spermatogenic cell nuclear and mitochondrial DNA obtained from Apex1 heterozygous mice.Molecular reproduction and development · 2011Article
- BAX and tumor suppressor TRP53 are important in regulating mutagenesis in spermatogenic cells in mice.Biology of reproduction · 2010Article
- S-nitrosylation from GSNOR deficiency impairs DNA repair and promotes hepatocarcinogenesis.Science translational medicine · 2010Article
- Article
- Marked inactivation of O6-alkylguanine-DNA alkyltransferase activity with protracted temozolomide schedules.British journal of cancer · 2003Article
- Prevention of liver cancer.Current oncology reports · 2002Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
O(6)-methylguanine (O(6)mG) is a potent mutagenic and procarcinogenic DNA lesion. Organisms have evolved with a DNA repair mechanism that largely ameliorates the deleterious effects of O(6)mG through a direct reversal mechanism by a protein termed O(6)-methylguanine-DNA methyltransferase (MGMT). However, the contribution of O(6)mG to carcinogenesis, in the absence of known exposure to agents that produce it, has not been defined. Nontransgenic C3HeB male mice have a high frequency of spontaneous liver tumors. Transgenic CeHeB/FeJ mice expressing human MGMT (hMGMT) were generated that had elevated hepatic MGMT activity. The spontaneous development of hepatocellular carcinoma was significantly reduced in those mice expressing hMGMT compared with nontransgenic C3HeB/FeJ male mice. No differences were detected in spontaneous mutant frequencies in lacI transgenes in mice carrying hMGMT compared with that without hMGMT but the proportion of GC to AT transition mutations was lower in the transgenic mice carrying hMGMT as well as lacI. Tumors that arose in C3HeB/FeJ transgenic mice were largely deficient in hMGMT protein as determined by immunohistochemistry with a monoclonal antibody directed against hMGMT. Together these data indicate that spontaneous O(6)mG lesions induced hepatocellular carcinogenesis in C3HeB/FeJ male mice. These transgenic mice represent a rare example of reduced spontaneous carcinogenesis.
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Registered trials
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