Literatura académica sobre el tema "Cancers du sein triple négatifs"
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Artículos de revistas sobre el tema "Cancers du sein triple négatifs"
de Nonneville, A. y A. Gonçalves. "Cancers du sein triple-négatifs : données actuelles et perspectives d’avenir". Oncologie 21, n.º 1-4 (enero de 2019): 33–39. http://dx.doi.org/10.3166/onco-2019-0039.
Texto completoGonçalves, Anthony. "Chimiothérapie néo-adjuvante des cancers du sein HER2-positifs et triple-négatifs". Bulletin du Cancer 103, n.º 6 (junio de 2016): S76—S89. http://dx.doi.org/10.1016/s0007-4551(16)30149-7.
Texto completoBeguinot, Marie, Marie Eve Fondrevelle, Laetitia Paradisi-Prieur y Camille Archinard. "Cancers du sein triples négatifs, l’innovation thérapeutique enfin accessible". Sages-Femmes 21, n.º 2 (marzo de 2022): 41–43. http://dx.doi.org/10.1016/j.sagf.2022.01.008.
Texto completoBoisserie-Lacroix, M., G. Mac Grogan, M. Debled, S. Ferron, M. Asad-Syed, V. Brouste, S. Mathoulin-Pelissier y G. Hurtevent-Labrot. "Aspects radiologiques des cancers du sein triple négatifs : à propos de 73 cas". Journal de Radiologie Diagnostique et Interventionnelle 93, n.º 3 (marzo de 2012): 196–203. http://dx.doi.org/10.1016/j.jradio.2011.12.006.
Texto completoWeymuller, V., A. Caille, C. Diguisto, M. Chas, M. L. Jourdan, F. Arbion, G. Body y L. Ouldamer. "Influence des facteurs hormonaux sur le pronostic des cancers du sein triple négatifs". Gynécologie Obstétrique Fertilité & Sénologie 47, n.º 5 (mayo de 2019): 471–77. http://dx.doi.org/10.1016/j.gofs.2019.03.006.
Texto completoGonçalves, Anthony. "Chimiothérapie néo-adjuvante des cancers du sein triple-négatifs : une place pour le platine ?" Bulletin du Cancer 101, n.º 12 (diciembre de 2014): 1063. http://dx.doi.org/10.1684/bdc.2014.2051.
Texto completoHumbert, O., J. M. Riedinger, C. Charon-Barra, A. Berriolo-Riedinger, I. Desmoulins, I. Cochet, E. Depardon, P. Fumoleau y F. Brunotte. "Identification de biomarqueurs prédictifs de la réponse des cancers du sein triple-négatifs : intérêt de la TEP/TDM au 18FDG". Médecine Nucléaire 39, n.º 3 (mayo de 2015): 215–16. http://dx.doi.org/10.1016/j.mednuc.2015.03.032.
Texto completoGueye, M., S. M. K. Gueye, M. Mbaye, F. Niasse Dia, M. E. Faye Diémé, M. M. Niang, A. A. Diouf y J. C. Moreau. "Aspects cliniques et pronostiques des cancers du sein triple négatifs à l’unité de sénologie du CHU Le-Dantec de Dakar". Journal Africain du Cancer / African Journal of Cancer 5, n.º 1 (19 de enero de 2013): 42–47. http://dx.doi.org/10.1007/s12558-013-0252-2.
Texto completoTréchot, I., A. Cayre, F. Kwiatowski, M. M. Dauplat, C. Abrial, F. Mishellany, G. Fouilhoux, M. A. Mouret-Reynier, J. M. Nabholtz y F. Penault-Llorca. "Sub-localisation cellulaire de la P-cadhérine dans les cancers du sein triple négatifs : un marqueur de la transition épithélio-mésenchymateuse ?" Annales de Pathologie 32, n.º 5 (noviembre de 2012): S131. http://dx.doi.org/10.1016/j.annpat.2012.09.163.
Texto completoKouassy, KY, O. Kimso, K. Traore, BA Oddo, A. Edoukou, DR Niang, KA Gaetan, SI Mounkeila, M. Toure y I. Adoubi. "C103: Intérêt du Paclitaxel – Bévacizumab dans le cancer du sein triple négatif métastatique à Abidjan". African Journal of Oncology 2, n.º 1 Supplement (1 de marzo de 2022): S43. http://dx.doi.org/10.54266/ajo.2.1s.c103.jsle2071.
Texto completoTesis sobre el tema "Cancers du sein triple négatifs"
Bonsang-Kitzis, Hélène. "Caractérisation moléculaire et immunité des cancers du sein triple-négatifs". Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS162.
Texto completoTriple negative breast cancer (TNBC) is the most heterogeneous and pejorative subtype of breast cancer. The cornerstone of the treatment of such tumors is based on systemic chemotherapy, more and more frequently administered before surgery, since no targeted therapy has been validated to date. Obtaining a pathological complete response (PCR) is a major favorable prognostic marker as well as an in vivo test of anti-tumor drug susceptibility. The objective of our thesis work was therefore to provide elements of understanding of this heterogeneity through the clinical, biological and molecular dissection of these tumors.We analyzed gene expression profiles of TNBCs and identified 6 distinct molecular subtypes with different biologies and prognoses. This classification used an original methodology based on both classical bioinformatic tools and biological networks. The enrichment of immunity genes from the stromal compartment of the tumor represents a major determinant of the prognosis of these tumors: a strong expression of the immunity genes is associated with a significantly more favorable prognosis.Our main contribution is based on a better understanding of immunity and tumor infiltrated lymphocytes (TILS) of these TNBCs. It is probably the most immunogenic subgroup of breast cancers with the highest TILs levels pre-NAC with HER2-positive tumors. TILS levels are also highly correlated with genes of our immune prognosis module. The predictive and prognostic value of stromal TILS is different according to the molecular subtype of breast cancer, suggesting a completely different immunity of these tumors. The rate of TILS also varies differentially within each subgroup under the influence of the NAC, indicating a complex interaction between TILS and treatments. We show that the kinetics of TILS levels with NAC is a relevant indicator of response to NAC with a response that is all the more important that a decrease in the TILS rate will be important. The most immunogenic tumors with an important immune activity are therefore the most favorable triple-negative tumors. One of the challenges of the coming years will therefore be to identify, as soon as possible, the least immunogenic TNBC that can best benefit from immunotherapies alone or in combination with chemotherapeutic treatment in order to activate or restore early a deficient immunity.Under the same denomination of TILS there are probably different phenotypic populations of lymphocytes. Indeed, after CNA, their prognostic value is opposite between the TNBC and the HER2-positive tumors: high levels of TILS are associated with an unfavorable prognosis in HER2-positive tumors whereas they have a tendency to be associated with a better prognosis for TNBC tumors. The interactions are complex between cytotoxic agents and the tumor and / or its microenvironment. The analysis of the breast or axillary lymph node residual disease represents an underutilized material that could lead to a better understanding of the mechanisms of sensitivity or resistance to treatment.Beyond the key role immunity for these tumors, our work identifies some TNBCs for which the hormonal environment, through the body mass index or the menopausal status, could play a role. Thus, the exploration of the metabolome, immune features in overweight / obese patients or the analysis of the androgen-receptor pathway (and its connections with the estrogen and progesterone-receptor pathways) of the TNBC must also be explored. This opens up possible treatment perspectives for some patients
Ashraf, Yahya. "Immunociblage de la cathepsine D dans le microenvironnement des cancers du sein triple-négatifs". Thesis, Montpellier, 2015. http://www.theses.fr/2015MONTT020.
Texto completoCancer is the leading cause of death in the developed world. This project focuses t on the high incidence triple-negative breast cancers (ER- and PR-negative, HER2-non amplified) who present unsatisfactory treatments. Tumor progression is known to be due to cross-talk between cancer cells and their surrounding supporting tissue, the tumor stroma. The lysosomal aspartic protease cathepsin D is over-produced and abnormally hypersecreted by epithelial breast cancer cells. This protease is an independent marker of poor prognosis in breast cancer correlated with the incidence of clinical metastasis. Cathepsin D stimulates tumor progression by both proteolytic and non-proteolytic molecular mechanisms. Our team has shown that secreted pro-cathepsin D can alter the tumor microenvironment by interacting with partners such as the LRP1 (low-density lipoprotein receptor-related protein-1) receptor, and/or by cleaving endogenous substrates like cystatin C. My pHD project aimed to target extracellular procathepsin D released in breast cancer by developing specific therapeutic antibodies to block its catalytic and binding capacities. We have isolated 50 hybridomas, that secreted IgM, a pentameric antibody format with high avidity but low affinity, and 8 anti-cath-D scFv by phage display. The anti-human cath-D scFv were selected by functional screenings for their ability to inhibit both the proteolytic activity of Cath-D and its binding to the fibroblastic LRP1 receptor. Two scFv cloned under IgG1 format (F1 and E2) inhibited wound healing, colony formation and three-dimensional outgrowth in Matrigel of MDA-MB-231 triple-negative breast cancer cells, and their tumor growth in athymic nude mice. Our findings strongly suggest that antibody-based targeting of Cath-D within the breast tumor microenvironment may have therapeutic efficacy for breast cancer treatment
Yakhni, Mohamad. "Inhibition de la synthèse des protéines, un traitement adapté aux cancers du sein triple négatifs des sous-types moléculaires autres que basal-like 1". Thesis, Université Clermont Auvergne (2017-2020), 2018. http://www.theses.fr/2018CLFAS025.
Texto completoTriple negative breast cancers (TNBC) without BRCA1/2 gene mutation or BRCAness are nowadays the breast malignancies most difficult to treat. Improvement of their treatment, for all phases of the disease, is an important unmet medical need. We analyzed the effect of homoharringtonine, a natural protein synthesis inhibitor approved for treatment of chronic myeloid leukemia, on four cell lines representing aggressive, BRCA1/2 non-mutated, TNBC genomic categories. We show that homoharringtonine inhibits in vitro growth of all cell lines for more than 80%, after 48-72h exposure to 20-100 ng/mL, the concentrations achievable in human plasma after subcutaneous drug administration. Homoharringtonine, at 100 ng/mL, strongly reduced levels of a major TNBC survival factor, anti-apoptotic protein Mcl-1, after only 2h of exposure, in all cell lines except MDA-MB-231. Other anti-apoptotic proteins, Bcl-2, survivin and XIAP, were also strongly downregulated. Moreover, in vivo growth of the least sensitive cell line to homoharringtonine in vitro, MDA-MB-231 was inhibited for 36.5% in mice, by 1 mg/kg of the drug, given subcutaneously, bi-daily, over 7 days. These results demonstrate marked antineoplastic activity of homoharringtonine in TNBC. Therefore, this drug is worth clinical evaluation in TNBC patients, as a single-agent in the metastatic or post-adjuvant maintenance setting
Hatem, Rana. "Etude des altérations moléculaires et évaluation de nouvelles thérapies ciblées dans les cancers du sein triple-négatifs". Thesis, Université Paris-Saclay (ComUE), 2015. http://www.theses.fr/2015SACLS143.
Texto completoAmong breast cancer subtypes, Triple-negative breast cancer (TNBC) has a very poor prognosis. There are currently no known targeted therapies for this subgroup of patients. In this project, we analyzed the profile of certain oncogenic alterations in the TN tumors and evaluated in vivo the therapeutic potential of targeting these alterations in TNBC.We first demonstrated that the tyrosine kinase receptor RET is overexpressed in a subset of TN and HER2+ tumors. Targeting RET by his inhibitor Vandetanib was tested in vivo in three PDX models of TNBC and one model of HER2+ BC with different expression levels of RET and EGFR. Vandetanib induced tumor regression in the three PDX models with high expression of RET or EGFR. Vandetanib effect was associated with inhibition of MAPK pathway, inhibition of angiogenesis and induction of necrosis. PI3K pathway alterations were investigated in an important number of BC PDX including TNBC PDX. PI3K pathway was shown to be activated in TNBC PDX possibly by the loss of the two pathway suppressors, PTEN and/or INPP4B. Treatment by Everolimus induced response in seven among the fifteen TNBC PDX tested. Analysis of treated tumors showed that post-treatment phosphorylation of AKT was more pronounced in responder PDX. The combination of Everolimus with chemotherapy was tested in one PDX and resulted in increased efficacy.In conclusion, in this work we showed that Vandetanib and Everolimus could be effective in treating TNBC. Further investigations are still needed to validate response related biomarkers
Mallinger, Arnaud. "Etude du mécanisme d'action d'un onco-métabolite impliqué dans la prolifération des cancers du sein triple-négatifs". Thesis, Toulouse 3, 2019. http://www.theses.fr/2019TOU30198.
Texto completoBreast cancer is the leading cause of cancer death in women. There are three subtypes of breast cancer: those that express estrogen hormone receptors (REα +), those that amplify the human epidermal growth factor receptor 2 (HER2) and those that don’t express any of these receptors, triple negative cancers (TN). For the last subtype, there is no targeted therapy. Cholesterol metabolism is deregulated in breast cancer compared to normal tissue. Indeed, in normal mammary tissues, cholesterol-5,6-epoxides (ECs) are transformed by cholesterol epoxide hydrolase (ChEH) into cholestan-triol (CT). In mammary tumor tissue, CT is converted into an onco-metabolite, 6-oxo-cholestan-3β, 5α-diol (OCDO), by the enzyme 11β-hydroxystéroïde déshydrogénase type 2 (11βHSD2). 11βHSD2 is known to regulate glucocorticoid metabolism by converting cortisol, an active glucocorticoid receptor (GR) agonist, to inactive cortisone. In addition, the OCDO stimulates the proliferation of different models of breast cancer TN by the GR. Data from the literature indicate that overexpression of GR correlates with poor progression-free survival and overall survival in patients with TN breast cancer. The purpose of my thesis was to characterize the mechanisms involved in OCDO-mediated tumor proliferation by the GR. I then showed that the AP-1 mitogenic pathway is activated by OCDO by the GR and has a major role in the tumor progression of these cell models in vitro and in vivo. Thus, targeting GR and the AP-1 pathway may represent new therapeutic strategies for TN breast cancers
Marques, Pinheiro Alice. "Implication du métabolisme de la sérotonine dans les cancers du sein triple négatifs et perspectives cliniques". Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS265.
Texto completoTriple negative breast cancer (TNBC) is the most aggressive form of breast cancers. It accounts for 15-20% of breast cancers. No progress in survival has been achieved since the advent of standard chemotherapy protocols. TNBC is an important clinical challenge. They have the worst outcome among breast cancer subgroups. Given their poor prognosis, their assumed hetetogeneity, and absence of any alternative specific targeted therapy, chemotherapy remains the only TNBC treatment. Despite an often good initial response to treatment, more than a half of patients do not achieve a pathological complete response, with a frequent and fast tumor relapse. Several therapeutic approaches have been identified preclinically, but none of these molecules have been shown to be effective on all of these patients. There is a urge for the identification of new treatments.An interesting strategy is the repurposing of medical compounds that were initially not intended for the treatment of a given disease. This strategy takes advantage of the extremely expensive initial research and development effort. This process is potentially efficient and cost-effective as previous clinical trials have been performed and pharmacokinetics/pharmacodynamics and toxicity have been already explored. In order to develop new treatment schemes we addressed the following question: Is there available drugs with strong activity in TNBC? To do so, we performed a high-throughput drug screening on 12 TNBC cell lines to reflect the dramatic heterogeneity of the disease. From this drug discovery program, several interesting compounds were identified with significant anti-tumor potential against TNBC. More particularly, psychoactive compounds regulating serotonin metabolism (ie antidepressant drugs and notably serotonin selective reuptake inhibitors-SSRIs) were found to be highly effective “hits”.My thesis work turned to the comprehension of serotonin implication in TNBC physiopathology to understand if modulating its metabolism could be of therapeutic interest for TNBC management. Different biological aspects were investigated concerning serotonin effects on TNBC cellular models (serotonin adjunction in vitro or endogenous synthesis inhibition). In addition, I established a comprehensive map of the serotonergic landscape in TNBC (biosynthetic capacity, transporters, receptors) that led to the identification of therapeutic targets that would be of interest in the treatment of cancer: HTR1D and HTR1B. Indeed, by blocking these promising targets (with chemical inhibitors or siRNA knockdown) we observed a strong reduction in cell viability in our large panel of TNBC cell lines. Remarkably, we found that their expression levels were associated to poor prognosis in breast cancer, and notably in TNBC subtype with huge dichotomy observed in the outcome, allowing future stratification of TNBC patient management and selection for further targeted therapies. These results pinpoint HTR1D and HTR1B as strong prognosis biomarkers in TNBC. Immunohistochemistry staining was also conducted to confirm the presence of these targets at the protein level in tumor samples. Moreover, I could identify a microRNA regulating one of these receptors: has-miR-599. Consistently, expression levels of this microRNA demonstrated a prognostic impact on TNBC survival. While ex vivo data of one SSRI and the dual antagonist of HTR1D/HTR1D receptors shown encouraging efficacy, their preclinical evaluation assessed in a TN PDX model could not allow to demonstrate any significant effect on tumor growth in vivo. As a matter of fact, serotonin metabolism is a complex system and TNBC heterogeneity does not permit to conclude on the therapeutic proof of concept of the serotonergic modulation in TNBC with this first attempt. A scientific manuscript of this work is being prepared for publication
Tabet, Imene. "Exploration de la sensibilité au stress réplicatif dans les cancers du sein triple négatifs BRCA déficients". Electronic Thesis or Diss., Université de Montpellier (2022-....), 2023. http://www.theses.fr/2023UMONT015.
Texto completoAbout 15% of triple negative breast cancers (TNBC) are BRCA defective and show Homologous Recombination DNA repair Deficiency (HRD) and increased sensitivity to genotoxic drugs. We hypothesized that BRCA-defective TNBC are highly sensitive to replicative stress inducing drugs, which could open therapeutic perspectives. Our results show that BRCA1-deficient (BRCA1-Def) TNBC, as well as BRCA1-Def ovarian cancer cell lines showed increased sensitivity to Gemcitabine. Noticeably, Gemcitabine induced increased cell death in BRCA1-Def cells, associated with mediocre replicative stress management. Indeed, up to 80% of BRCA1-Def cells displayed persistent gH2AX staining even 48h after washing off Gemcitabine, compared with their BRCA1-WT counterpart in which staining had decreased significantly. Furthermore, Gemcitabine treated BRCA1-Def cells showed a persistent imbalance between RPA32-positive and gH2Ax-positive cells, suggesting unresolved replication stress in these cells and occurrence of replication catastrophe in a substantial fraction of the cells. Furthermore, an important fraction of gH2AX+ cells displayed pan-nuclear staining, which numbers steadily increased over time in Gemcitabine treated BRCA1-Def cells, while they decreased in the BRCA1-WT counterpart. Interestingly, nearly 90% of gH2AX pan-nuclear cells were completely negative for RPA32 and showed a strong BrdU staining in non-denaturing conditions, indicating an important accumulation of single stranded DNA specifically in these cells. Noticeably, an important number of cells with pan-nuclear gH2Ax staining were also negative for RAD51 foci, but were positive for both 53BP1 and FANCD2 foci. The opposite landscape was observed in the BRCA1-WT cells in which gH2AX pan nuclear cells were RAD51+ and 53BP1- and FANCD2-. These results indicate an acute replicative stress response in the BRCA1-Def context that induces replication forks arrest. This could lead to replication fork collapse and possibly massive DNA Double Strand Breaks (DSB). To test this hypothesis, we performed Pulse Field Gel Electrophoresis experiments that clearly showed important accumulation of DSBs in the BRCA1-Def cells 48h after Gemcitabine release. These DSBs did not result from the apoptotic cleavage of DNA as joint treatment with Gemcitabine and the apoptosis inhibitor Z-VAD FMK did not modify the DSB level, suggesting that DSBs resulted from an accumulation of unprotected ssDNA. Next we tested whether the accumulation of ssDNA resulted from over-resection caused by uncontrolled activity of the exonuclease MRE11 in BRCA-Def cell and applied a joint treatment of Gemcitabine and Mirin. As a matter of fact, inhibition of MRE11 with Mirin resulted in a specific decrease of the number of cells presenting the pan-nuclear gH2AX staining. Finally, we noted that BRCA1-Def cells were prone to mitotic slippage leading to mitotic catastrophes illustrated by an important accumulation of micronuclei in these cells. Noticeably, micro-nuclei showed double positive BrdU and pan nuclear gH2AX staining indicating that they corresponded to fragmentation of nuclei with elevated ssDNA content. We have also been able to show that the hypersensitivity of BRCA1-Def cancers to acute replication stress is reproducible in vivo in PDX models, which displayed a pan-nuclear gH2AX staining profiles, in accordance with their Gemcitabine response status. Hence, we propose that pan-nuclear gH2Ax staining could be a marker of replication catastrophe in treated tumors and could possibly be considered as a biomarker of the response to replicative stress. Hence, in a BRCA-Def context Gemcitabine treatment has combined lethal consequences, massive replicative and mitotic catastrophe
Mansouri, Hanane. "Ciblage de la protéase cathepsine D par des anticorps monoclonaux humains pour la thérapie des cancers du sein triple-négatifs". Thesis, Montpellier, 2018. http://www.theses.fr/2018MONTT069.
Texto completoTriple-negative breast cancer (TNBC) accounts for 15-20% of all breast cancer cases, and chemotherapy is the only available treatment. Thus identification of new therapeutic targets is required to improve TNBC outcome. In breast cancer, the aspartic protease cathepsin D (cath-D) is a marker of poor prognosis associated with metastatic risk. This protease is overexpressed by breast cancer cells and is abnormally hypersecreted into the tumor microenvironment. Cath-D affects both cancer and stromal cells in the breast tumor microenvironment by increasing the proliferation of breast cancer cells, fibroblast invasive outgrowth, tumor growth and angiogenesis, and metastasis formation. Many studies indicated that extracellular cath-D displays oncogenic activities, suggesting it could represent a novel therapeutic target in TNBC. In order to block its oncogenic actions, the laboratory generated human IgG1 antibodies against extracellular cath-D by phage display (International patent N° PCT/EP2016/061454). The aims of my PhD project was i) to validate the potential value of cath-D as a tumor-specific extracellular target in TNBC, ii) to evaluate the therapeutic activity, and iii) to characterize the mechanisms of action of these anti-cath-D human antibodies.We showed that elevated CTSD mRNA levels correlated with shorter recurrence-free survival. Using proteomics analysis and anti-cath-D immunohistochemistry performed on Tissue Micro-Array, we observed that extracellular cath-D was detected in the tumor microenvironment of TNBC, but not in matched normal breast stroma samples. Our results thus indicate that cath-D is a tumor cell-associated extracellular biomarker and strongly suggest that it could be a good candidate for antibody-based therapy in TNBC. We found that anti-cath-D human antibodies, F1 and E2, accumulated in TNBC MDA-MB-231 tumor xenografts in athymic mice by SPECT-CT (Single Photon Emission Computed Tomography) and biodistribution analysis. F1 and E2 antibodies inhibited tumor growth of MDA-MB-231 tumor xenografts and improved mice survival without apparent toxicity. F1, the best antibody candidate, inhibited tumor growth of two TNBC patient-derived xenografts (PDX). Mechanistically, F1 treatment modulates immune tumor microenvironment in the MDA-MB-231 tumor cell xenograft model. Together, our results indicate that antibody-based targeting of cath-D may have therapeutic efficacy for TNBC treatment
Vinet, Mathilde. "Analyse de la protéine arginine méthyltransférase 5 comme cible thérapeutique dans les cancers du sein triple-négatifs". Thesis, Paris Sciences et Lettres (ComUE), 2019. https://tel.archives-ouvertes.fr/tel-02631827.
Texto completoTriple-negative breast cancers (TNBC) are highly heterogeneous and aggressive breast cancers for which no targeted therapy yet exists. Protein arginine methyltransferase 5 (PRMT5), an enzyme which catalyzes the methylation of arginines on histone and non‐histone proteins, and its cofactor methylosome protein 50 (MEP50), have recently been attributed oncogenic functions. This thesis analyzes PRMT5/MEP50 expression and localization in a cohort of 150 breast tumors, and explores the therapeutic potential of PRMT5 targeting in TNBC, using siRNA and the specific, small-molecule inhibitor EPZ015666. We show that TNBC express similar levels of PRMT5 and MEP50 proteins compared to healthy breast tissues and to other breast cancer subtypes, but with a distinctively low nuclear component, suggesting a prognostic value of PRMT5/MEP50 localization in breast cancers. We find PRMT5 to be a relevant therapeutic target, alone or in combination, for a subset of TNBC. Finally, we identify putative novel PRMT5/MEP50 partners, whose function merit further investigation in the context of TNBC
Tolza, Claire. "Fra-1 et Fra-2 dans les cancers du sein triple négatifs : mécanismes transcriptionnels et identification de cibles thérapeutiques potentielles". Thesis, Montpellier, 2016. http://www.theses.fr/2016MONTT094/document.
Texto completoTriple negative breast cancers (TNBC) are characterized by a poor prognosis and no targeted therapy is currently available. The identification of new diagnostic and therapeutic targets is crucial for the treatment of these cancers. Fra-1 and Fra-2, two members of the AP-1 transcriptional complex, are frequently overexpressed in TNBC, where they contribute to the tumorigenic phenotype. The panel of genes under the control of Fra-1 and/or Fra-2 in TNBC, as well as the molecular mechanisms by which they control their target gene expression are mostly unknown. The aim of my thesis was to identify the panel of genes controlled by Fra-1 and/or Fra-2 in TNBC and to characterize the binding sites of Fra-1 and Fra-2 on chromatin to select direct targets for further studies, by using transcriptomic and ChIP-seq approaches combined to RNAi in the model cell line MDA-MB231. The results allowed us to select target genes for transcriptional and functional studies. The study of the transcriptional mechanisms governed by Fra-1 and/or Fra-2 was carried out on the HMGA1 gene, already known for its crucial role in the aggressiveness of epithelial tumours. The fonctional study was focused on CD68, as its expression in highly induced by Fra-1 and Fra-2. CD68 encodes a transmembrane protein which cellular fonction is still not known and its potential role in tumorigenesis has not been studied yet
Capítulos de libros sobre el tema "Cancers du sein triple négatifs"
Campone, M., E. Bourbouloux, D. Berton-Rigaud, S. Sadot, J. S. Frenel y P. Juin. "Cancers du sein triples négatifs: Une revue de la littérature". En Cancer du sein, 571–88. Paris: Springer Paris, 2012. http://dx.doi.org/10.1007/978-2-8178-0245-9_37.
Texto completoVincent-Salomon, A. "Cancers du sein triples négatifs: Jusqu’où doit-on aller dans le bilan histologique?" En Cancer du sein, 565–70. Paris: Springer Paris, 2012. http://dx.doi.org/10.1007/978-2-8178-0245-9_36.
Texto completoBachelot, T., S. I. Labidi, O. Tredan, I. Ray-Coquard y J. P. Guastalla. "Cancers du sein métastatiques « triples négatifs ». Critères cliniques et biologiques additionnels nécessaires pour prendre une décision thérapeutique. Stratégies thérapeutiques, place des anti-angiogéniques et nouvelles thérapeutiques ciblées". En Cancer du sein en situation métastatique, 233–42. Paris: Springer Paris, 2010. http://dx.doi.org/10.1007/978-2-8178-0076-9_23.
Texto completoDelozier, T. "Les cancers du sein N−, HER2 négatifs, RH+: Quelles hormonothérapies? Quand faut-il faire une chimiothérapie?" En Cancer du sein, 457–70. Paris: Springer Paris, 2012. http://dx.doi.org/10.1007/978-2-8178-0245-9_29.
Texto completoBonnefoi, H. "Nouveaux marqueurs pronostiques et prédictifs dans les cancers luminaux (HER2 négatifs) : signatures et tests multiparamétriques". En Cancer du Sein, 109–16. Elsevier, 2016. http://dx.doi.org/10.1016/b978-2-294-74449-5.00013-7.
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