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     <dc:title xml:lang="fr">Rôle de CD95/CD95L dans les cancers du sein triple négatifs et de l’ovaire</dc:title>
     <dcterms:alternative xml:lang="en">Role of CD95/CD95L in triple negative breast cancer and ovarian cancers</dcterms:alternative>
     <dc:subject xml:lang="fr">Cancer du sein triple négatif</dc:subject><dc:subject xml:lang="fr">Organes génitaux femelles -- Cancer</dc:subject><dc:subject xml:lang="fr">Micro-environnement tumoral</dc:subject><dc:subject xml:lang="fr">Immunothérapie anticancéreuse</dc:subject><dc:subject xml:lang="fr">Antigènes CD95</dc:subject>
     <dc:subject xml:lang="en">Triple negative breast cancer</dc:subject><dc:subject xml:lang="en">Ovarian cancer</dc:subject><dc:subject xml:lang="en">CD95 antigens</dc:subject>
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						<tef:elementdEntree autoriteSource="Sudoc" autoriteExterne="256050392">Cancer du sein triple négatif</tef:elementdEntree>
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						<tef:elementdEntree autoriteSource="Sudoc" autoriteExterne="027657434">Organes génitaux femelles -- Cancer</tef:elementdEntree>
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						<tef:elementdEntree autoriteSource="Sudoc" autoriteExterne="157478920">Micro-environnement tumoral</tef:elementdEntree>
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						<tef:elementdEntree autoriteSource="Sudoc" autoriteExterne="027357155">Immunothérapie anticancéreuse</tef:elementdEntree>
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						<tef:elementdEntree autoriteSource="Sudoc" autoriteExterne="050170449">Antigènes CD95</tef:elementdEntree>
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     <dcterms:abstract xml:lang="fr">Les cancers du sein triple négatifs et les cancers de l’ovaire séreux de haut grade partagent des caractéristiques biologiques communes, et le système immunitaire joue un rôle important dans le contrôle de l’évolution tumorale dans ces 2 maladies. Initialement caractérisée par son rôle dans l’apopotose des cellules immunitaires, la signalisation activée par l’interaction CD95/CD95L et son ligand soluble sCD95L est impliquée dans de nombreux rôles biologiques au-delà de l’apoptose, notamment dans les processus d’oncogénèse. Notre équipe avait montré le rôle pronostic négatif du sCD95L, favorisant l’invasion tumorale et les métastases chez les patientes atteintes de cancer du sein triple négatif.  Dans les cancers de l’ovaire, le niveau de sCD95L est un facteur pronostic positif corrélé à l’infiltrat immunitaire, soulevant l’hypothèse d’une régulation de cet infiltrat par la signalisation CD95/CD95L. Dans les cancers du sein triple négatifs, la signalisation CD95 impacte la réponse immune anti-tumorale. Ces travaux montrent qu’une meilleure compréhension des mécanismes biologiques activés par la voie CD95/CD95L dans les cancers de l’ovaire séreux de haut grade et dans les cancers du sein triple négatif pourrait permettre de mieux sélectionner les patientes pour des traitements modulant la réponse immune. Le ciblage de cette voie pourrait permettre d’améliorer la prise en charge thérapeutiques. </dcterms:abstract>
     <dcterms:abstract xml:lang="en">Triple-negative breast cancer and high-grade serous ovarian cancer share common biological features, and the immune system plays an important role in controlling tumor progression in both diseases. Initially characterized by its role in immune cell apoptosis, the signaling activated by the CD95/CD95L interaction and its soluble ligand sCD95L is involved in many biological roles beyond apoptosis, notably in oncogenesis processes. Our team had shown the negative prognostic role of sCD95L, promoting tumor invasion and metastasis in patients with triple negative breast cancer. In ovarian cancer, the level of sCD95L is a positive prognostic factor correlated with the immune infiltrate, raising the hypothesis that this infiltrate is regulated by CD95/CD95L signaling. In triple-negative breast cancer, CD95 signaling impacts the anti-tumor immune response.  This work shows that a better understanding of the biological mechanisms activated by the CD95/CD95L pathway in high-grade serous ovarian cancer and in triple-negative breast cancer could allow better selection of patients for treatments modulating the immune response. Targeting this pathway could lead to improved therapeutic management.</dcterms:abstract>
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