4-hydroxyestradiol has been researched along with Carcinogenesis* in 4 studies
4 other study(ies) available for 4-hydroxyestradiol and Carcinogenesis
Article | Year |
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Oroxylin A, a methylated metabolite of baicalein, exhibits a stronger inhibitory effect than baicalein on the CYP1B1-mediated carcinogenic estradiol metabolite formation.
Topics: Breast Neoplasms; Carcinogenesis; Carcinogens; Cytochrome P-450 CYP1B1; Down-Regulation; Estradiol; Estrogens, Catechol; Female; Flavanones; Flavonoids; Gene Expression Regulation, Enzymologic; Gene Expression Regulation, Neoplastic; Humans; MCF-7 Cells | 2019 |
Role of Estrogen in Androgen-Induced Prostate Carcinogenesis in NBL Rats.
Androgens are thought to cause prostate cancer, but the underlying mechanisms are unclear. Data from animal studies suggest that for androgens to cause prostate cancer, they must be aromatized to estrogen and act in concert with estrogen metabolites. We tested the hypothesis that androgen-receptor and estrogen receptor-mediated effects of androgen and estrogen are necessary, as well as genotoxicity of estrogen metabolites. NBL rats were treated with androgenic and estrogenic compounds for 16-75 weeks through slow-release silastic implants or pellets. Testosterone alone induced cancer in the prostate of 37% of rats. 5α-Dihydrotestosterone, which cannot be converted to estradiol or testosterone, did not cause a significant prostate cancer incidence (4%). Addition of estradiol to 5α-dihydrotestosterone treatment did not markedly enhance prostate cancer incidence (14%), unlike adding estradiol to testosterone treatment which induced a 100% tumor incidence. Testosterone plus estradiol treatment induced a DNA adduct detectable by Topics: Androgens; Animals; Carcinogenesis; Carcinoma; Dihydrotestosterone; DNA Adducts; DNA Damage; Estradiol; Estrogens; Estrogens, Catechol; Guanosine; Humans; Incidence; Male; Prostate; Prostatic Neoplasms; Rats; Receptors, Estrogen; Testosterone | 2019 |
Long-term exposure of 4-hydroxyestradiol induces the cancer cell characteristics
Life-long estrogen exposure is one of the major risk factors in the development and progression of breast cancer. However, little is known about the molecular mechanisms, by which chronic exposure to estrogen contributes to breast carcinogenesis. The aim of the present study was to investigate the effects of long-term exposure with 4-hydroxyestradiol (4-OHE Topics: Carcinogenesis; Cell Culture Techniques; Cell Line; Cell Movement; Cell Proliferation; Cytochrome P-450 CYP1B1; Dose-Response Relationship, Drug; Epithelial Cells; Epithelial-Mesenchymal Transition; Estrogens, Catechol; Female; Humans; Mammary Glands, Human; Up-Regulation | 2019 |
Lack of Cell Proliferative and Tumorigenic Effects of 4-Hydroxyestradiol in the Anterior Pituitary of Rats: Role of Ultrarapid O-Methylation Catalyzed by Pituitary Membrane-Bound Catechol-O-Methyltransferase.
In animal models, estrogens are complete carcinogens in certain target sites. 4-Hydroxyestradiol (4-OH-E Topics: Animals; Biocatalysis; Carcinogenesis; Catechol O-Methyltransferase; Cell Proliferation; Estrogens, Catechol; Female; Humans; Methylation; Pituitary Gland, Anterior; Rats; Rats, Inbred ACI; Tumor Cells, Cultured | 2017 |