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Methyl groups in carcinogenesis: effects on DNA methylation and gene expression.
TLDR
The results of the experiments described here lend support to the hypothesis that intake of such a diet, by causing depletion of S-adenosylmethionine pools, results in DNA hypomethylation, which in turn leads to changes in expression of genes that may have key roles in regulation of growth.
Irreversible global DNA hypomethylation as a key step in hepatocarcinogenesis induced by dietary methyl deficiency.
TLDR
The association between DNA hypomethylation and expansion of foci suggests that stableDNA hypometHylation is a promoting factor for clonal expansion of initiated cells in rodents.
The prospective role of abnormal methyl metabolism in cadmium toxicity.
TLDR
Comparing the effects on the enzyme DNA methyltransferase (MTase) of two metal ions: the essential metal Zn and the carcinogen Cd provides evidence that the carcinogenic effects of Cd may be mediated in part through abnormal DNA methylation.
Cadmium carcinogenesis in male Wistar [Crl:(WI)BR] rats: dose-response analysis of tumor induction in the prostate and testes and at the injection site.
TLDR
It is indicated that CdCl2 can induce preneoplastic lesions of the prostate that appear to develop into tumors only at doses well below those causing marked degeneration of the testes and atrophy of the prostatic atrophy.
Histone H3 lysine 9 and H4 lysine 20 trimethylation and the expression of Suv4-20h2 and Suv-39h1 histone methyltransferases in hepatocarcinogenesis induced by methyl deficiency in rats.
TLDR
Experimental support for the epigenetic hypothesis of tumorigenesis that considers stress-induced epigenetic reprogramming of the cell as an important prerequisite to succeeding mutations is provided.
Blood S-adenosylmethionine concentrations and lymphocyte methylenetetrahydrofolate reductase activity in diabetes mellitus and diabetic nephropathy.
TLDR
Evidence is provided that alterations in the blood concentrations of SAM and related compounds are abnormal in patients with diabetes, particularly in those with nephropathy and that hyperhomocysteinemia in these patients may be due to a generalized metabolic abnormality.
Breaks in genomic DNA and within the p53 gene are associated with hypomethylation in livers of folate/methyl-deficient rats.
TLDR
Evidence is provided that DNA strand breaks are induced in high molecular weight DNA and also within the p53 gene in liver tissue from methyl-deficient rats and in nuclei isolated from livers of methyl- deficient rats, which was found to be more sensitive to enzyme- and oxidant-induced DNA strand break induction.
Enzymic reduction of carcinogenic aromatic nitro compounds by rat and mouse liver fractions.
TLDR
4-nitroquinoline- N -oxide was rapidly reduced by rat liver post-mitochondrial fraction to yield high levels of the 4-hydroxylamine derivative, as well as small but significant quantities of the corresponding amine.
Hepatocarcinogenesis in rats fed methyl-deficient, amino acid-defined diets.
TLDR
All DENA-initiated rats fed the severely deficient Diet 5, died within 23 experimental weeks with livers containing hepatocytes of atypical appearance and, particularly at the 2 higher dosages, a cirrhotic pseudonodular architecture.
Are metals dietary carcinogens?
TLDR
In attempting to understand the role which dietary metals could play in human carcinogenesis, it was found that the many factors involved and the lack of specific information made it difficult to reach firm conclusions on the hazards of dietary metals.
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