يعرض 1 - 2 نتائج من 2 نتيجة بحث عن '"Lenfant, Françoise"', وقت الاستعلام: 0.65s تنقيح النتائج
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    دورية أكاديمية

    المساهمون: Ligue Contre le Cancer, Association pour la Recherche sur le Cancer

    المصدر: Cellular and Molecular Life Sciences ; volume 78, issue 15, page 5681-5705 ; ISSN 1420-682X 1420-9071

    الوصف: 17β-estradiol controls post-natal mammary gland development and exerts its effects through Estrogen Receptor ERα, a member of the nuclear receptor family. ERα is also critical for breast cancer progression and remains a central therapeutic target for hormone-dependent breast cancers. In this review, we summarize the current understanding of the complex ERα signaling pathways that involve either classical nuclear “genomic” or membrane “non-genomic” actions and regulate in concert with other hormones the different stages of mammary development. We describe the cellular and molecular features of the luminal cell lineage expressing ERα and provide an overview of the transgenic mouse models impacting ERα signaling, highlighting the pivotal role of ERα in mammary gland morphogenesis and function and its implication in the tumorigenic processes. Finally, we describe the main features of the ERα-positive luminal breast cancers and their modeling in mice.

  2. 2
    دورية أكاديمية

    المصدر: EMBO Molecular Medicine ; volume 6, issue 10, page 1328-1346 ; ISSN 1757-4676 1757-4684

    مصطلحات موضوعية: Molecular Medicine

    الوصف: Estetrol (E 4 ) is a natural estrogen with a long half‐life produced only by the human fetal liver during pregnancy. The crystal structures of the estrogen receptor α ( ER α) ligand‐binding domain bound to 17β‐estradiol (E 2 ) and E 4 are very similar, as well as their capacity to activate the two activation functions AF ‐1 and AF ‐2 and to recruit the coactivator SRC 3. In vivo administration of high doses of E 4 stimulated uterine gene expression, epithelial proliferation, and prevented atheroma, three recognized nuclear ER α actions. However, E 4 failed to promote endothelial NO synthase activation and acceleration of endothelial healing, two processes clearly dependent on membrane‐initiated steroid signaling ( MISS ). Furthermore, E 4 antagonized E 2 MISS ‐dependent effects in endothelium but also in MCF ‐7 breast cancer cell line. This profile of ER α activation by E 4 , uncoupling nuclear and membrane activation, characterizes E 4 as a selective ER modulator which could have medical applications that should now be considered further.