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Tea Lanisnik Rizner

Researcher at University of Ljubljana

Publications -  26
Citations -  1077

Tea Lanisnik Rizner is an academic researcher from University of Ljubljana. The author has contributed to research in topics: Cochliobolus lunatus & Hydroxysteroid dehydrogenase. The author has an hindex of 16, co-authored 26 publications receiving 990 citations. Previous affiliations of Tea Lanisnik Rizner include University of Pennsylvania.

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AKR1C1 and AKR1C3 may determine progesterone and estrogen ratios in endometrial cancer.

TL;DR: It is suggested that the expression of AKR 1C1 and AKR1C3 in endometrial cancer will govern the ratio of P:E2, which may contribute to diminished protection by P and enhanced estrogen action.
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Human Type 3 3α-Hydroxysteroid Dehydrogenase (Aldo-Keto Reductase 1C2) and Androgen Metabolism in Prostate Cells

TL;DR: In prostate cells AKR1C2 acts as a 3-ketosteroid reductase to eliminate 5alpha-DHT and prevents activation of the androgen receptor, and does not act as an oxidase due to either potent product inhibition by NADPH or because it cannot surmount the oxidative 17beta-HSD present.
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Estrogen metabolism and action in endometriosis.

TL;DR: The potential role of aberrant expression of individual estrogen-metabolizing enzymes is discussed, and a model mechanism for increased formation of estradiol is presented separately for different types of endometriosis.
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Disturbed Estrogen and Progesterone Action in Ovarian Endometriosis

TL;DR: The authors' data indicate that several enzymes of estrogen and progesterone metabolism are aberrantly expressed in endometriosis, which can lead to increased local levels of mitogenic estradiol and decreased levels of protective progestersone.
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Aberrant pre-receptor regulation of estrogen and progesterone action in endometrial cancer.

TL;DR: Examination of expression of the pre-receptor regulatory enzymes aromatase, 17beta-hydroxysteroid dehydrogenases, 20alpha-HSDs, sulfatase and sulfotransferase, and estrogen (ERs) and progesterone (PRs) receptors in samples of endometrial cancer and adjacent normal endometrium found no significant gene up-regulation was seen.