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  • 1
    Electronic Resource
    Electronic Resource
    Chemoprevention of mammary tumor virus-induced and chemical carcinogen-induced rodent mammary tumors by natural plant products (1994)
    Springer
    Breast cancer research and treatment 30 (1994), S. 233-242 
    Details
    ISSN: 1573-7217
    Keywords: animal tumor models ; β-carotene ; betel leaf extract ; catechin ; chemoprevention ; natural products
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The natural plant products turmeric, β-carotene, catechin, and betel leaf extract were evaluated for their antitumor effects on mammary tumorigenesis in murine mammary tumor expressing C3H (Jax) mice and in Wistar rats treated with the chemical carcinogen 7-12-dimethylbenz(a)anthracene (DMBA). Administration of turmeric through the diet and of β-carotene, catechin, and betel leaf extract through the drinking water to virgin female C3H mice resulted in decreased tumor incidence and tumor burden. Administering 5% turmeric in the diet from 2 months of age showed suppression of mammary tumor virus-related reverse transcriptase activity and of preneoplastic changes in the mammary glands. Furthermore, feeding turmeric from 6 months of age resulted in a 100% inhibition of mammary tumors. In the DMBA model of rat mammary tumorigenesis, administration of turmeric, catechin, and betel leaf extract resulted in decreased tumor burden and tumor incidence, and a delay in the onset of mammary tumors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00665965
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  • 2
    Electronic Resource
    Electronic Resource
    In vitro biotransformation of estradiol by explant cultures of murine mammary tissues (1989)
    Springer
    Breast cancer research and treatment 13 (1989), S. 173-181 
    Details
    ISSN: 1573-7217
    Keywords: estradiol metabolism ; mammary tissue ; explant culture
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In vivo experiments have demonstrated a correlation between the extent of 16α-hydroxylation of estradiol and incidence of mammary cancer. The ability of mammary ductal epithelium (MDE), the site for neoplastic transformation, to metabolize estradiol or to accumulate estradiol metabolites has not been unequivocally established. Using a newly developed mammary explant culture system and a radiometric assay, we have compared the site-specific metabolism of estradiol (E2) by the C-17-oxidation and C-16α-hydroxylation pathways in mouse tissues that differ in relative risk for mammary cancer. A comparison between MDE (target tissue) and liver (nontarget tissue) from NFS (low risk) and C3H/ouj (high risk) mice revealed that: a) increase in C-17-oxidation was similar in MDE and liver from the two strains, and b) while C-16α-hydroxylation was similar in liver from the two strains (p = 0.5, n.s.), it was increased 4-fold in the MDE from the high risk C3H/ouj strain relative to that from the low risk NFS strain (p = 0.001). Furthermore,in vivo administration of progesterone resulted in modulation of cell proliferation as well as of E2 metabolism in mammary explant cultures. The effect of progesterone depended upon the presence of the MtV-2 proviral gene. This study demonstrates that mammary explants can extrahepatically metabolize estradiol. The specific risk-related increase in C-16α-hydroxylation suggests that intrinsic metabolic ability of the target tissue leading to the formation of 16α-hydroxyestrone from estradiol may be a determinant in the relative risk for developing mammary cancer.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01806529
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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