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Johanie Lépine

Researcher at Laval University

Publications -  21
Citations -  968

Johanie Lépine is an academic researcher from Laval University. The author has contributed to research in topics: Medicine & Endometrial cancer. The author has an hindex of 13, co-authored 16 publications receiving 890 citations.

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Specificity and regioselectivity of the conjugation of estradiol, estrone, and their catecholestrogen and methoxyestrogen metabolites by human uridine diphospho-glucuronosyltransferases expressed in endometrium.

TL;DR: Data show that several UGT enzymes detected in the endometrium are involved in the glucuronidation of E(2) and its 2-OH, 4- OH, and 2-MeO metabolites that exert various biological effects in the tissue.
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Metabolic inactivation of estrogens in breast tissue by UDP-glucuronosyltransferase enzymes: an overview

TL;DR: This review addresses the most recent findings on the identification of UGT enzymes that are responsible for the glucuronidation of E2 and its metabolites, and evidence regarding their potential role in breast cancer.
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Characterization of Common UGT1A8, UGT1A9, and UGT2B7 Variants with Different Capacities to Inactivate Mutagenic 4-Hydroxylated Metabolites of Estradiol and Estrone

TL;DR: Findings suggest that specific polymorphisms in UGT genes may modulate the exposure to carcinogenic metabolites of E2 and potentially lead to an altered risk of breast and endometrial cancers in women carrying the variant alleles.
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Regulation of the UGT1A1 bilirubin‐conjugating pathway: Role of a new splicing event at the UGT1A locus

TL;DR: The results indicate that this newly discovered alternative splicing mechanism at the UGT1A locus amplifies the structural diversity of human UGT proteins and describes the identification of an additional posttranscriptional regulatory mechanism of the glucuronidation pathway.
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The Functional UGT1A1 Promoter Polymorphism Decreases Endometrial Cancer Risk

TL;DR: It is suggested that lower expression of UGT1A1 decreases the risk of endometrial cancer by reducing the excretion of 2-hydroxyestradiol, the antiproliferative metabolite of E2, in the endometrium.