Auswahl der wissenschaftlichen Literatur zum Thema „Cancer du sein – Étiologie“
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Zeitschriftenartikel zum Thema "Cancer du sein – Étiologie"
Béjar, D., S. Aouadi, H. Gharsalli, J. Hsinet, S. Laâbidi, S. Mâalej und L. Douik El Gharbi. „Les pleurésies au cours du cancer du sein : caractéristiques cliniques et principales étiologies“. Revue des Maladies Respiratoires 34 (Januar 2017): A116. http://dx.doi.org/10.1016/j.rmr.2016.10.267.
Der volle Inhalt der QuelleSarles, H., und J. P. Bernard. „Pathogenie des Pancrétites Chroniques“. Canadian Journal of Gastroenterology 2, Nr. 4 (1988): 159–64. http://dx.doi.org/10.1155/1988/286791.
Der volle Inhalt der Quellede Marneffe, Emmanuelle, und Isabelle Lambotte. „Adolescence et santé mentale, quand les réseaux sociaux s’en mêlent… Le cas du cyber-harcèlement“. Cahiers critiques de thérapie familiale et de pratiques de réseaux 71, Nr. 2 (26.10.2023): 63–79. http://dx.doi.org/10.3917/ctf.071.0063.
Der volle Inhalt der QuelleBenjelloun, H., S. Maiouak, N. Zaghba, H. Moubachir, A. Bakhatar, N. Yassine und A. Bahlaoui. „Cancer du col utérin : étiologie rare de métastases endobronchiques“. Revue des Maladies Respiratoires 32 (Januar 2015): A109. http://dx.doi.org/10.1016/j.rmr.2014.10.592.
Der volle Inhalt der QuelleLévy, C. „Cancer du sein“. Oncologie 12, Nr. 8 (22.07.2010): 479–83. http://dx.doi.org/10.1007/s10269-010-1918-3.
Der volle Inhalt der QuelleLévy, C. „Cancer du sein“. Oncologie 13, Nr. 8 (26.07.2011): 510–13. http://dx.doi.org/10.1007/s10269-011-2047-3.
Der volle Inhalt der QuelleLévy, C. „Cancer du sein“. Oncologie 14, Nr. 8 (28.07.2012): 475–77. http://dx.doi.org/10.1007/s10269-012-2187-4.
Der volle Inhalt der QuelleLévy, C. „Cancer du sein“. Oncologie 15, Nr. 7-8 (Juli 2013): 399–401. http://dx.doi.org/10.1007/s10269-013-2305-7.
Der volle Inhalt der QuelleLazard, Tristan, Guillaume Bataillon, Thomas Walter und Anne Vincent Salomon. „Cancer du sein“. médecine/sciences 39, Nr. 12 (Dezember 2023): 926–28. http://dx.doi.org/10.1051/medsci/2023169.
Der volle Inhalt der QuelleVignal, Philippe, Patrick Zemb und Danielle Juguet-Carfatan. „Cancer du sein hyperéchogène“. Imagerie de la Femme 15, Nr. 4 (Dezember 2005): 243–45. http://dx.doi.org/10.1016/s1776-9817(05)80678-9.
Der volle Inhalt der QuelleDissertationen zum Thema "Cancer du sein – Étiologie"
Perrin-Vidoz, Laure. „Étude de la dégradation des ARN messagers porteurs d'un codon de terminaison prématuré : implication dans la prédisposition génétique au cancer du sein et de l'ovaire chez les patients porteurs de mutations germinales du gène BRCA1“. Lyon 1, 2003. http://www.theses.fr/2003LYO10038.
Der volle Inhalt der QuelleAubé, Michel. „Étude des effets endocriniens produits par les organochlorés en lien avec la carcinogenèse mammaire“. Thesis, Université Laval, 2008. http://www.theses.ulaval.ca/2008/25154/25154.pdf.
Der volle Inhalt der QuelleBencheikh, Meryem. „Pertes d'hétérozygotie dans les cancers du sein : incidence et corrélations avec d'autres altérations génomiques“. Montpellier 2, 1992. http://www.theses.fr/1992MON20065.
Der volle Inhalt der QuelleCollette, Jordan. „Etude des mécanismes impliqués dans la régulation de la tumorigenèse mammaire par le long ARN non codant H19“. Electronic Thesis or Diss., Université de Lille (2018-2021), 2019. http://www.theses.fr/2019LILUS109.
Der volle Inhalt der QuelleThe H19 gene is subject to genomic imprinting and does not encode protein. The product of this gene, the long non coding RNA (lncRNA) H19, act as an RNA and is involved in development and the tumorigenesis. The H19 RNA is the precursor of miR-675. My thesis work identified new mechanism involved in the regulation of breast tumorigenesis by H19. We have demonstrated that the lncRNA H19 negatively regulates the p53 protein in breast cancer cell lines. My work revealed that H19 interacts with p53 and MDM2 to induce the degradation of p53 and impedes its nuclear localization. This new mechanism of H19 in breast cancer could explain the lack of clinical relevance of the p53 mutational state measured by immunohistochemistry in breast cancer. My work also revealed that not only the lncRNA H19 is involved in the regulation of breast cancer stem cells but also the miR-675-5p. Indeed, we have shown a correlation between overexpression of H19 and expression of a cancer stem cell phenotype in patient tumors. Furthermore, the modulation of H19 or miR-675 expression regulates the functional capacities associated with breast cancer stem cells. I also initiated a project that will allow the identification of H19 and miR-675 target genes in breast cancer cell lines. To conclude, I highlighted the implication of the lncRNA H19 and miR-675 in different process involved in breast cancer tumorigenesis
Morisset-Malzac, Muriel. „Régulation intracellulaire et activité protéolytique d'une protéine régulée par les oestrogènes dans les cancers du sein“. Montpellier 2, 1987. http://www.theses.fr/1987MON20258.
Der volle Inhalt der QuelleFreiss, Gilles. „Oestrogènes, antioestrogènes et cancer du sein : 1/ anticorps monoclonaux et dosage de la pro-cathepsine D : 2/ antioestrogènes et facteurs de croissance“. Montpellier 2, 1990. http://www.theses.fr/1990MON20191.
Der volle Inhalt der QuelleTomellini, Elisa. „Etude des effets du NGF et du proNGF sur les cellules souches du cancer du sein“. Thesis, Lille 1, 2013. http://www.theses.fr/2013LIL10077/document.
Der volle Inhalt der QuelleDespite significant advances in cancer research and treatment, breast cancer remains one of the leading causes of cancer-related death in women. NGF (Nerve Growth Factor) and its precursor (proNGF) are overexpressed in breast cancer cells, where they exert a mitotic, anti-apoptotic and pro-invasive effects through an autocrine loop. In the last few years, a raising number of experimental data indicate the importance of “cancer stem cells” (CSC) in tumour development, metastasis and resistance to therapies.The objective of my thesis was to evaluate the influence of NGF and proNGF on breast CSC biology and to determine their consequences on tumour development. We demonstrated that NGF and proNGF are able to enrich for CSC in several breast cancer cell lines. This enrichment is connected to the overexpression of several transcription factors essential for stem cells self-renewal and pluripotency. Tumorigenicity assays in SCID mice proved that cells from MCF-7 cell line cultured with NGF or proNGF are more tumorigenic than the control condition. Nevertheless, only cells pre-treated with NGF were able to develop metastases in brain, lung and liver and to go through an epithelial-to-mesenchymal transition, demonstrating that NGF and proNGF induce their effects through different signaling pathways. Taken together, our results have shown that NGF and proNGF contribute to the regulation of stem cells’ plasticity in vitro and in vivo. Future perspectives concern the comprehension of involved molecular mechanisms in order to better understand their implication in breast cancer development
Joimel, Ulrich. „Étude de la contribution des monocytes/ macrophages dans la promotion tumorale : leurs rôles dans l'angiogenèse et les thromboses- essais de stratégies thérapeutiques“. Rouen, 2012. http://www.theses.fr/2010ROUER012.
Der volle Inhalt der QuelleThis PhD research investigated the development of experimental strategies whose aim was the attenuation of the pro-tumoral role of monocytes/macrophages. Macrophages can be classified into two subcategories, classically activated macrophages (or M1) and alternatively activated macrophages (or M2). M1 exibit anti-tumoral proprieties while M2 are involved in pro-tumoral activity. NF-KB was identified as a key regulator to switch from M1 macrophage towards M2 but the mechanisms of action remain not clearly understood. We showed that 1) the coculture supernatant from macrophages and cancer cells induced an increased angiogenesis in the chicken chorioallantoic membrane that could be associated with the increased expression of CXC/ELR+ chemokines; 2) coculture induced a M2 phenotype; 3) tetrathiomolybdate (TM), an anti-angiogenic agent and an NF-KB inhibitor inhibited the coculture-induced increase in angiogenic activity, but without altering macrophages phenotype. Cooperation between macrophages and cancer cells induces a reciprocal increase of tissue factor (TF) expression. Now, TF is involved in the folination of micro-thrombi by activating factor X (FX) and it's known that micro-thrombi protect cancer cells in the bloodstream. The effects of an indirect (fondaparinux) and a direct (rivaroxaban) activated FX inhibitor in pro-coagulant activity and cytokine release from activated monocytes were then compared. We showed that 1) only rivaroxaban reduced the pro-coagulant activity, 2) the two inhibitors decreased secretion of cytokines
Julien, Sylvain. „L'antigène sialyl-Tn dans le cancer du sein : étude de la O-glycosylation et de son influence sur la croissance de lignées cellulaires sialyl-Tn positives“. Lille 1, 2004. https://pepite-depot.univ-lille.fr/LIBRE/Th_Num/2004/50376-2004-221-222.pdf.
Der volle Inhalt der QuelleCardoso, Bueno de Camargo Lívia. „Le rôle des vésicules extracellulaires dans la capacité invasive du cancer du sein : les fonctions de la famille des facteurs de transcription NFAT“. Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCC093.
Der volle Inhalt der QuelleExtracellular vesicles (EVs) represent an important means of cell communication, through which cells can exchange functional mRNAs, microRNAs and proteins, amongst other molecules. During the past few years, the understanding of their role in cancer onset and progression has been largely developed. In this work, we approach the role of EVs in changing the invasive profiles of breast cancer cell lines. We were specifically interested in studying whether the opposite effects of the members NFAT1/NFAT5 and NFAT3 (members of the Nuclear Factor of Activated T cells family of transcription factors) in breast cancer cell motility could be linked to EV function in modulating cell invasiveness. While NFAT1 and NFAT5 are expressed by more invasive breast cancer cell lines that do not express the estrogen receptor alpha (ER alpha -), NFAT3 is expressed by cell lines with less aggressive profile, that are ER alpha +. To study the possible transfer of these opposite effects of NFAT factors through EVs, highly invasive (MDA-MB 231) and poorly-invasive (T47D) breast cancer cell lines were treated with each other's EVs. We have observed that an increase of invasion is induced through EVs secreted by MDA-MB 231. EVs secreted by T47D, on the other hand reduce invasiveness. Moreover, NFAT3 expression in T47D is an essentiel aspect in this second type of response, since when its expression is inhibited in these cells their EVs no longer have the power to reduce MDA-MB 231 invasiveness. We also show that EVs originated from T47D induce the active transcription of TGFbetal ir the recipient MDA-MB 231 to blunt cell nnotility. These results were extended in vivo, where we have demonstrated that T47D EVs are able to reduce primary tumour size and decrease metastasis formation in nude mice injected with human MDA-MB 231 D3H2LN cells in the mammary fat pad. Similarly to our in vitro results, NFAT3 expression in the EV producing cells was shown to be key for their EVs to present these effects. Furthermore, we could also observe TGFbetal sera levels increased in the mice where the treatment was effective, making this molecule a potentiel candidate for following treatment efficiency. Our findings suggest that EVs could represent a possible means of inhibiting the invasion of aggressive cancer cells, and therefore may be an attractive option to decrease tumor progression and metastasis in patients
Bücher zum Thema "Cancer du sein – Étiologie"
1956-, Aldaz C. Marcelo, Hrsg. Etiology of breast and gynecological cancers: Proceedings of the Ninth International Conference on Carcinogenesis and Risk Assessment, held in Austin, Texas, November 29-December 2, 1995. New York: Wiley-Liss, 1997.
Den vollen Inhalt der Quelle findenNamer, Moïse, Michel Héry, Daniel Serin, Marc Spielmann und Joseph Gligorov. Cancer du sein. Paris: Springer Paris, 2007. http://dx.doi.org/10.1007/978-2-287-71478-8.
Der volle Inhalt der QuelleGros, Dominique. Cancer du sein. Paris: Springer Paris, 2009. http://dx.doi.org/10.1007/978-2-287-79503-9.
Der volle Inhalt der QuelleNamer, Moïse, Michel Héry, Daniel Serin und Marc Spielmann. Cancer du sein. Paris: Springer Paris, 2006. http://dx.doi.org/10.1007/2-287-31109-2.
Der volle Inhalt der QuelleNamer, Moïse, Michel Héry, Marc Spielmann, Joseph Gligorov und Frédérique Penault-Llorca. Cancer du sein. Paris: Springer Paris, 2012. http://dx.doi.org/10.1007/978-2-8178-0245-9.
Der volle Inhalt der QuelleDixon, J. M. (J. Michael), Hrsg. Cancer du sein. Montréal, Québec: Modus vivendi, 2014.
Den vollen Inhalt der Quelle findenHirshaut, Yashar. Cancer du sein. Paris: Marabout, 2004.
Den vollen Inhalt der Quelle findenes, Socie te franc ʹaise de se nologie et de pathologie mammaire Journe. Cancer du sein avance. Paris: Springer, 2007.
Den vollen Inhalt der Quelle findenSerin, Daniel, und Gaëtan de Rauglaudre. Cancer du sein avancé. Paris: Springer Paris, 2007. http://dx.doi.org/10.1007/978-2-287-72615-6.
Der volle Inhalt der QuellePhilippe, Pierre. Les familles à cancer. Montréal, Qué: Presses de l'Université de Montréal, 1989.
Den vollen Inhalt der Quelle findenBuchteile zum Thema "Cancer du sein – Étiologie"
Klein, H., L. Leufflen und A. Lesur. „Interruption de l’aménorrhée chimio-induite sous inhibiteur de l’aromatase. Étiologies et conséquences thérapeutiques dans le cancer du sein“. In Acquis et limites en sénologie / Assets and limits in breast diseases, 509–10. Paris: Springer Paris, 2013. http://dx.doi.org/10.1007/978-2-8178-0396-8_123.
Der volle Inhalt der QuelleSauvage, M., B. Trétarre, P. Grosclaude, F. Molinié, A. M. Aude, A. Danzon, A. V. Guizard und P. Arveux. „Sein“. In Survie des patients atteints de cancer en France, 225–32. Paris: Springer Paris, 2007. http://dx.doi.org/10.1007/978-2-287-39310-5_30.
Der volle Inhalt der QuelleJaffré, I., V. Bordes, M. Dejode, F. Dravet und J. M. Classe. „État de l’art des recommandations actuelles sur les marges de sécurité nécessaires lors de l’exérèse conservatrice d’un cancer du sein“. In Cancer du sein, 1–13. Paris: Springer Paris, 2012. http://dx.doi.org/10.1007/978-2-8178-0245-9_1.
Der volle Inhalt der QuelleAlran, S. „Quelle place pour le ganglion sentinelle après chimiothérapie néo-adjuvante? Place d’un score clinico-biologique d’aide à la décision de ganglion sentinelle après chimiothérapie néo-adjuvante chez les patientes ayant un cancer du sein“. In Cancer du sein, 127–33. Paris: Springer Paris, 2012. http://dx.doi.org/10.1007/978-2-8178-0245-9_10.
Der volle Inhalt der QuelleBarreau, B., F. Ettore, S. Giard, J. M. Hannoun-Levi, K. Kerrou und O. Tredan. „Prise en charge de la récidive homolatérale d’un cancer du sein après traitement conservateur initial“. In Cancer du sein, 135–64. Paris: Springer Paris, 2012. http://dx.doi.org/10.1007/978-2-8178-0245-9_11.
Der volle Inhalt der QuelleBouée, S., und F. Fagnani. „Projection de l’épidémiologie du cancer du sein en 2018 en France“. In Cancer du sein, 165–81. Paris: Springer Paris, 2012. http://dx.doi.org/10.1007/978-2-8178-0245-9_12.
Der volle Inhalt der QuelleEspié, M., A. S. Hamy und S. Frank. „Contraception orale, traitement hormonal de la ménopause, inducteurs de l’ovulation et risque de cancer du sein“. In Cancer du sein, 183–90. Paris: Springer Paris, 2012. http://dx.doi.org/10.1007/978-2-8178-0245-9_13.
Der volle Inhalt der QuelleZelek, L., und T. Bouillet. „Mode de vie et cancer du sein: Les facteurs de risque non hormonaux“. In Cancer du sein, 191–95. Paris: Springer Paris, 2012. http://dx.doi.org/10.1007/978-2-8178-0245-9_14.
Der volle Inhalt der QuelleAncelle-Park, R. „Le dépistage organisé des cancers du sein, 20 ans après: Bénéfices et controverses“. In Cancer du sein, 197–202. Paris: Springer Paris, 2012. http://dx.doi.org/10.1007/978-2-8178-0245-9_15.
Der volle Inhalt der QuelleHazebroucq, V. „Le cancer du sein en France: Problèmes médicaux légaux et responsabilités“. In Cancer du sein, 203–15. Paris: Springer Paris, 2012. http://dx.doi.org/10.1007/978-2-8178-0245-9_16.
Der volle Inhalt der QuelleKonferenzberichte zum Thema "Cancer du sein – Étiologie"
Fongaufier, C., S. Zahouily, CI Gros, S. Guihard, F. Hubelé, P. Barthélémy und F. Bornert. „Métastases mandibulaires du cancer du sein, aspects diagnostiques et thérapeutiques : réflexion autour de 3 cas“. In 65ème Congrès de la SFCO. Les Ulis, France: EDP Sciences, 2017. http://dx.doi.org/10.1051/sfco/20176502024.
Der volle Inhalt der QuelleRichard, Amélie, Karen Reilly und Sophie Jacquin-Courtois. „Que révèlent les disfluences sur le manque du mot rapporté par les patientes ayant un cancer du sein“. In XXXIVe Journées d'Études sur la Parole -- JEP 2022. ISCA: ISCA, 2022. http://dx.doi.org/10.21437/jep.2022-38.
Der volle Inhalt der QuelleBerichte der Organisationen zum Thema "Cancer du sein – Étiologie"
Corkum, Eleanor, Tiffanie Perrault und Erin C. Strumpf. Améliorer les parcours de diagnostic du cancer du sein au Québec. CIRANO, Oktober 2023. http://dx.doi.org/10.54932/tlak9928.
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