Literatura académica sobre el tema "Cellules souches mammaires"
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Artículos de revistas sobre el tema "Cellules souches mammaires"
Gagniac, L., S. Cagnet, M. Adlanmerini, F. Boudou, A. Weyl, I. Raymond-Letron, J. F. Arnal, C. Brisken y F. Lenfant. "Le récepteur des estrogènes ERα membranaire module les propriétés des cellules souches mammaires". Annales d'Endocrinologie 77, n.º 4 (septiembre de 2016): 259–60. http://dx.doi.org/10.1016/j.ando.2016.07.073.
Texto completoLotz, JP, F. Pene, C. Bouleuc, T. André, C. Gisselbrecht, H. Bonnak, Z. Merad et al. "Intensification thérapeutique et autotransplantation de cellules-souches hématopoïétiques dans le traitement des tumeurs solides de l'adulte : principes, réalisation et application au traitement des tumeurs germinales, trophoblastiques, mammaires, ovariennes et bronchiques à petites cellules. Première partie". La Revue de Médecine Interne 16, n.º 1 (enero de 1995): 43–54. http://dx.doi.org/10.1016/0248-8663(96)80663-1.
Texto completoLotz, JP, F. Pene, C. Bouleuc, T. André, C. Gisselbrecht, H. Bonnak, Z. Merad et al. "Intensification thérapeutique et autotransplantation de cellules-souches hématopoïétiques dans le traitement des tumeurs solides de l'adulte. Principes, réalisation et application au traitement des tumeurs germinales, trophoblastiques, mammaires, ovariennes et bronchiques à petites cellules. 2e partie". La Revue de Médecine Interne 16, n.º 2 (febrero de 1995): 150–62. http://dx.doi.org/10.1016/0248-8663(96)80682-5.
Texto completoBoudin, Laurys, Christian Chabannon, Patrick Sfumato, Renaud Sabatier, François Bertucci, Carole Tarpin, Magali Provansal et al. "Expérience de l’institut Paoli-Calmettes concernant la chimiothérapie à haute dose et autogreffe de cellules souches hématopoïétiques pour la prise en charge des cancers mammaires : impact du statut Her2 et BRCA1/2". Bulletin du Cancer 104, n.º 4 (abril de 2017): 332–43. http://dx.doi.org/10.1016/j.bulcan.2016.12.007.
Texto completoDeugnier, Marie-Ange, Valérie Petit, Ilaria Taddéi-De La Hosseraye, Marisa Faraldo y Marina A. Glukhova. "Vers la caractérisation des cellules souches de la glande mammaire murine adulte". médecine/sciences 23, n.º 12 (diciembre de 2007): 1125–32. http://dx.doi.org/10.1051/medsci/200723121125.
Texto completoAsselin-Labat, Marie-Liesse. "Cellules souches et progéniteurs dans la glande mammaire : rôle critique du facteur de transcription Gata-3". médecine/sciences 23, n.º 12 (diciembre de 2007): 1077–80. http://dx.doi.org/10.1051/medsci/200723121077.
Texto completoTesis sobre el tema "Cellules souches mammaires"
GRAVIS, GWENAELLE. "Chimiotherapie a haute dose avec reinjection de cellules souches hematopoietiques dans les adenocarcinomes mammaires". Aix-Marseille 2, 1994. http://www.theses.fr/1994AIX20855.
Texto completoEl, Helou Rita. "Rôle des programmes épigénétiques dans la régulation de l'identité des cellules souches cancéreuses mammaires". Thesis, Aix-Marseille, 2015. http://www.theses.fr/2015AIXM5019.
Texto completoTumor heterogeneity observed in breast cancer is the main cause of clinical failures despite a significant therapeutic arsenal. This heterogeneity is explained by the presence of a minority population of cells, the cancer stem cells (CSC). CSC are resistant to conventional therapies causing relapse and metastasis. Deciphering programs regulating the cardinal properties of these cells, self-renewal and differentiation, is a crucial step for the development of new therapies. The identity of CSC is regulated by epigenetic mechanisms. The work of this thesis focused on the study of two epigenetic mechanisms: DNA methylation and microRNAs. We first identified a signature of 68 regions hypomethylated in CSC. This signature showed an enrichment of the TGF-ß pathway and had a prognostic impact on patient survival. We then were interested in the regulation of CSC by miRNAs. We identified miR-600, a bimodal microRNAs, regulating the self-renewal-differentiation balance. MiR-600 regulates Wnt pathway via SCD1. The identification of the miR-600/SCD1/Wnt axis opens a new therapeutic perspective to target CSCs. Our work deciphered epigenetic programs, regulating breast CSC-fate and open new perspective to improve breast cancer care
Azzoni, Violette. "Cellules souches cancéreuses et résistance thérapeutique du cancer du sein : ciblage des cellules souches cancéreuses mammaires par l'inhibition de la réponse au stress réplicatif". Thesis, Aix-Marseille, 2018. http://www.theses.fr/2018AIXM0740.
Texto completoBreast tumors are known to present a major intratumoral heterogeneity that contributes to therapy failure and disease progression. The origin of this cellular heterogeneity is mainly explained by a hierarchical organization of tumor tissues where several subpopulations of self-renewing breast cancer stem cells (bCSCs) sustain the long-term oligoclonal maintenance of the neoplasm. bCSCs drive tumor growth, resist to conventional therapies and initiate metastasis development. Thus, developing bCSC-targeting therapies is becoming a major challenge requiring the understanding of the unique molecular circuitry of bCSC as compared to non-bCSC. To better understand the biology of these cells, we isolated bCSCs from different patient–derived xenografts (PDXs), derived fom breast tumors, and established their gene expression profiles. We identified a bCSC core transcriptional program that may be implicated in the reduction of the replicative stress in CSC: overexpression of genes implicated in dNTP metabolism and homologous recombination (HR). Our results show that HR plays a major role in SR regulation of bCSC and that bCSC are more resistant to RS than non-bCSC, We realized a preclinical assay in PDX and showed that HR inhibition prevent bCSC expansion Cisplatin-induced, suggesting a sensitization of the bCSC to the chemotherapy. Our results identify replication stress as the Achilles’ heel of bCSC and highlights HR as potential targets for anti-bCSC therapy
Cascales, Élodie. "L'enzyme CD10 : un acteur clé dans l'identification et la régulation des cellules souches mammaires humaines". Phd thesis, Université Claude Bernard - Lyon I, 2010. http://tel.archives-ouvertes.fr/tel-00703178.
Texto completoCascales, Élodie. "L’enzyme CD10 : un acteur clé dans l’identification et la régulation des cellules souches mammaires humaines". Thesis, Lyon 1, 2010. http://www.theses.fr/2010LYO10313/document.
Texto completoIn breast, the existence of cancer stem cells has been demonstrated and that explain a number of observations as tumour heterogeneity. Other studies have demonstrated the resistance of radio and chemotherapy by different innate or acquired stem cell specific mechanisms that could explain relapse few years after the traitment. For all these reasons, that is very important to understand these mechanisms and to know physiological actors both implicated in the regulation of normal or cancer stem cells. CD10 is a zinc-dependant metallo-endopeptidase that inactivates a number of signalling peptides that could be implicated in mammary growth and differentiation. We have showed that CD10+ cell sorted population is enriched in Stem Cells/Early Common Progenitors/MyoEPithelial cells. We demonstrate that the protease activity of CD10 and the adhesion function of beta1-integrin are required to prevent differentiation of mammary stem cells/early progenitors. Taken together, our data suggest that integrin-mediated contact with the basement membrane and cleavage of signalling factors by CD10 are key elements in the microenvironment that maintains the progenitor and stem cell pools in the mammary gland. Adipose tissue is also a major component of the mammary microenvironment implicated in its homeostasis by the secretion of soluble factors. Our results suggested that the adipose tissue could be considered as a potential source of stem cells that differentiated into the luminal epithelial lineage involved in some breast cancers
Salvador, Marion. "Régulation épigénétique des cellules souches cancéreuses mammaires : un nouveau rôle pour l'ARN non-codant Xist". Thesis, Aix-Marseille, 2014. http://www.theses.fr/2014AIXM5078.
Texto completoThese last decades have allowed deciphering the biology of breast cancer and improving the therapeutic management. However, recurrence and metastatic progression of the disease are still not curable. The concept of cancer stem cells (CSC) could provide an explanation for these failures. CSC would resist conventional therapies (chemotherapy, radiotherapy) and would be responsible for both relapse and progression of cancer. The elimination of CSC seems to be an essential prerequisite for the treatment of patients. The identity and fate of stem cells are tightly regulated by epigenetic mechanisms. The work of this thesis investigated the consequences of deregulation of two epigenetic players: HDAC enzymes and long non-coding RNA Xist. We have shown that epigenetic modulation via HDAC inhibitor (HDACi) eliminates the CSC by inducing their differentiation. We present a new therapeutic strategy for breast cancer: differentiation therapy. We determined Xist as the predictive biomarker of response to HDACi. Xist is a key partner of cell plasticity, the work of this thesis therefore interested in the consequences of Xist deregulation in tumor initiation. We observed that Xist inhibition promotes division of normal breast stem cells. We propose a new model of tumor initiation: epigenetic deregulation is an early change without consequence on tissue homeostasis but could be the first step of the cancerous transformation
Konge, Julie. "Le TGF-β1 module la transition épithéliale-mésenchymateuse et le pool de cellules souches cancéreuses dans les cellules tumorales mammaires humaines : impact sur la radiosensibilité". Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS044.
Texto completoThis works aims at characterizing radioresistant cells within human breast cancer development that is responsible for treatment failure and cancer recurrences. Although the literature is flourishing with papers tightly linking the presence of "Cancer Stem Cells" to cancer treatment resistance, the intrinsic radioresistance of those "CSC" and the mechanism involved have yet to be established.Dr. Weinberg and his team have developed an in vitro cell model that produces mammary tumor cells noted « CD24-CD44+ » after an epithelial-to-mesenchymal transition (EMT) induced by TGF-β1. This model is based on healthy human mammary cells that have been immortalized and transformed.Within this context, my Ph.D. project has focused on using this new model in order to compare the radiosensibility of two cell lines: the « CD24-CD44+ » cells and the « CD24+CD44- » one. Underlying this choice is the fact this model allows for a comparison of two cellular populations at distinct stage of the tumor’s development.This work has shed light on apoptotic and detoxification mechanism involved in the radio resistant behavior of the « CD24-CD44+ » cells. After a brief introduction of key concepts required to the understanding of this work, this manuscript will begin by presenting the characterization of the chosen model, then a study of the radiation response that enabled a first description of the « CD24-CD44+ » cell radioresistant phenotype through a mild stop at the G2/M stage of the cell cycle, the presence of polypoid cells and a high progeny generation ability after exposure to radiation.Furthermore, this works shows implications of apoptotic mechanism of « CD24-CD44+ » cells with a radioresistance phenotype. Hence, we were able to show that reduced cell death observed for the « CD24-CD44+ » cells is linked to a lower activation of apoptotic pathways.Finally, the last part will present detoxification mechanism involved in « CD24-CD44+ » radioresistance phenotype, showing an altered transcriptional signature of two detoxication genes SOD2 and HMOX1 after exposure to radiation
Bresson, Laura. "Rôle de la Podoplanine dans le développement et la tumorigenèse mammaires". Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS403/document.
Texto completoStem cells (SC) drive mammary development, giving rise postnatally to an epithelial bilayer composed of luminal and basal myoepithelial cells. The molecular identity of SCs and the factors regulating their function remain poorly defined. We identified the transmembrane protein, Podoplanin (Pdpn), as a specific marker of the basal compartment, including multipotent SCs, and found Pdpn localized at the basal-luminal interface. Embryonic deletion of Pdpn targeted to basal cells diminished basal and luminal SC activity and affected expression of several Wnt/b-catenin (Wnt/b-cat) signaling components. Moreover, Pdpn deletion attenuated mammary tumor formation in a mouse model of b-cat-induced breast cancer, limiting tumor-initiating cell expansion and promoting molecular features associated with mesenchymal-to-epithelial cell transition. In line with the loss-of-function data, we demonstrated that mechanistically, Pdpn enhanced Wnt/b-cat signaling in mammary basal cells. Overall, our study reveals a role for Pdpn in mammary development and tumorigenesis through the control of Wnt/b-cat-responsive SCs
Cagnet, Stéphanie. "Etude du rôle des intégrines liant la laminine dans le développement et la tumorigenèse mammaires". Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T079/document.
Texto completoThe improvement of breast cancer therapy requires thorough analysis of the pathways leading to tumorigenesis and clear understanding of the molecular and cellular mechanisms involved in normal mammary gland development. Mammary epithelium is surrounded by a specifically organized extracellular matrix (ECM), basement membrane, and secreted glycoproteins, laminins, are among its major constituents. Integrin-mediated interactions between mammary epithelial cells and ECM have been shown to play an essential role in the control of mammary development and tumorigenesis. However, specific roles played by distinct integrin heterodimers are yet poorly understood. My thesis project aimed to define the functions of laminin-binding integrins, i.e., heterodimers, containing 3 or 6 subunits, in normal mammary gland development, in control of mammary stem and progenitor cell functions in adult gland, and in mammary tumorigenesis. The results of my work suggest that: (i31 integrin has a unique function in the control of the myoepithelial cell contractile activity during lactation; it contributes to the activation of the FAK/Rac1/PAK1 pathway leading to MLCK inhibition required for myoepithelial cell relaxation, thereby, permitting further contractile cycles. (ii) integrin-mediated interactions of mammary basal cells with laminins are essential for the regeneration of the mammary epithelium. However, 31 and 6-contaning integrins have redundant functions in mammary stem cells.(iii) 31 integrin plays a major role in mammary tumorigenesis, it promotes survival and proliferation of tumor cells activating intracellular signaling pathways involving FAK/Rac1/PAK1, MAPK and JNK pathways. Altogether, these data provide new insights into the molecular mechanisms of mammary development, adult gland function and tumorigenesis
Dubernard, Gil. "Influence du microchimérisme fœtal sur les adénocarcinomes mammaires associés à la gestation". Paris 6, 2008. http://www.theses.fr/2008PA066300.
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