Literatura académica sobre el tema "Microenvironnement tumoralal"
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Artículos de revistas sobre el tema "Microenvironnement tumoralal"
Le Guellec, Sophie, Raphaëlle Duprez-Paumier y Magali Lacroix-Triki. "Microenvironnement tumoral". médecine/sciences 30, n.º 4 (abril de 2014): 372–77. http://dx.doi.org/10.1051/medsci/20143004009.
Texto completoBruchard, Mélanie y François Ghiringhelli. "Microenvironnement tumoral". médecine/sciences 30, n.º 4 (abril de 2014): 429–35. http://dx.doi.org/10.1051/medsci/20143004018.
Texto completoParisel, Eléonore, Laura Prudhomme y Jonathan Pol. "L’immunocytokine FAP-IL2v: Un co-traitement efficace pour pallier la résistance au trastuzumab du cancer du sein HER2+". médecine/sciences 40, n.º 6-7 (junio de 2024): 569–72. http://dx.doi.org/10.1051/medsci/2024072.
Texto completoFinak, Greg, Julie Laferrièe, Michael Hallett y Morag Park. "Le microenvironnement tumoral". médecine/sciences 25, n.º 5 (mayo de 2009): 439–41. http://dx.doi.org/10.1051/medsci/2009255439.
Texto completoFridman, Wolf H. y Catherine Sautès-Fridman. "Le microenvironnement tumoral". médecine/sciences 30, n.º 4 (abril de 2014): 359–65. http://dx.doi.org/10.1051/medsci/20143004007.
Texto completoTartour, Eric. "Vaccins anti-cancer : quel avenir dans les stratégies d’immunothérapie anti-cancéreuse ?" Biologie Aujourd'hui 212, n.º 3-4 (2018): 69–76. http://dx.doi.org/10.1051/jbio/2019002.
Texto completoKaplon, Hélène y Marie-Caroline Dieu-Nosjean. "Quel avenir pour les lymphocytes B infiltrant les tumeurs solides". médecine/sciences 34, n.º 1 (enero de 2018): 72–78. http://dx.doi.org/10.1051/medsci/20183401016.
Texto completoCoënon, Loïs, Arthur Battistoni, Agathe Poupée-Beaugé, Stéphanie Germon y Isabelle Dimier-Poisson. "Micro-organismes anti-cancéreux et armement". médecine/sciences 37, n.º 1 (enero de 2021): 47–52. http://dx.doi.org/10.1051/medsci/2020259.
Texto completoBorriello, Lucia y Yves A. DeClerck. "Le microenvironnement tumoral et la résistance thérapeutique". médecine/sciences 30, n.º 4 (abril de 2014): 445–51. http://dx.doi.org/10.1051/medsci/20143004021.
Texto completoLebecque, S., S. Goddard, J. J. Pin, J. Y. Blay y I. Treilleux. "Les cellules dendritiques dans le microenvironnement tumoral". Annales de Pathologie 24 (noviembre de 2004): 36–37. http://dx.doi.org/10.1016/s0242-6498(04)94036-9.
Texto completoTesis sobre el tema "Microenvironnement tumoralal"
Pavy, Allan. "Mécanismes cellulaires adaptatifs du microenvironnement tumoral exposé au plasma froid - Application au traitement du cholangiocarcinome". Electronic Thesis or Diss., Sorbonne université, 2024. http://www.theses.fr/2024SORUS267.
Texto completoCholangiocarcinoma (CCA) is a cancer with a poor prognosis and limited therapeutic options. Surgical resection is the only curative option available, but it is applicable to only a small number of patients and offers relatively low survival rates (5-year survival of 30%) due to the typically late diagnosis of this cancer. Palliative therapies, based on chemotherapy and immunotherapy, are generally ineffective, mainly because of the desmoplastic nature of CCA, which limits the entry of drugs into the tumor site. With an increasing incidence and accounting for 2% of global cancer mortality, it is crucial to develop new therapies, including local treatments targeting tumor cells and their microenvironment, for the treatment of this cancer. It is in this context that enthusiasm for the use of cold atmospheric plasma (CAP) in the treatment of CCA has emerged. Considered the fourth state of matter and generated by the partial ionization of a gas at low temperature, CAP has demonstrated promising antitumor effects in various preclinical cancer models over the past fifteen years. It is indeed capable of producing reactive oxygen and nitrogen species (RONS). A close collaboration between the Saint-Antoine Research Center (CRSA) and the Plasma Physics Laboratory (LPP) has highlighted significant antitumor effects in an immunodeficient murine model of CCA, as well as significant remodeling of the tumor stroma, a crucial element in tumor progression. Since then, a CAP device adapted for insertion into a duodenoscope has been developed, with the aim of enabling in situ treatment of CCA tumors via endoscopy in the future. The objective of this thesis was to explore the antitumor effects of this new plasma source on in vitro and in vivo models of CCA, distinguishing the direct effects of plasma on tumor cells from indirect effects on tumorigenesis, mediated by phenotypic modifications of stromal cells, including cancer-associated fibroblasts (CAFs) and tumor endothelial cells (TECs). After demonstrating the technical feasibility and biological applicability of this endoscopic source, it was observed that the oxidative stress induced by CAP altered the activation state and migratory phenotype of CAFs, while affecting the viability and angiogenic profile of TECs. The use of three-dimensional spheroid models also revealed immunogenic signatures triggered by cold plasma treatment. Indeed, it was proven in vivo, through prophylactic vaccination, that CAP could induce immunogenic cell death (ICD) of tumor cells, promoting the recruitment of immune cells to the tumor site. Preliminary results also showed that direct treatment of subcutaneous tumors slowed tumor growth while allowing the recruitment of antitumor immune cells. Finally, after elucidating the mechanisms of ICD in vitro, a new therapeutic approach combining CAP and vaccinations was proposed, demonstrating an antitumor effect accompanied by increased infiltration of immune cells. To make the use of CAP clinically accessible, tests on porcine models were conducted to verify the thermal and electrical safety of this endoscopic source, both for the patient and the clinician. Thus, CAP opens up promising new perspectives for the locoregional treatment of CCA, by modulating the immunogenicity of tumors and impacting their desmoplastic stroma
Leca, Julie. "Impact du dialogue entre microenvironnement intra-tumoral et cellules tumorales dans l'adénocarcinome pancréatique". Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM4003.
Texto completoPancreatic adenocarcinoma (PDA) is particularly resistant to current therapies. A concept suggests that its cellular composition participates in this process, limiting drugs access and affecting tumor cells behavior. Indeed, non-tumor cells, mainly mesenchymal (including Cancer Associated Fibroblasts, CAFs) and immune cells display over 70% of the tumor mass and form the intra-tumoral microenvironment or stroma. The impact of stroma in PDA development and progression is at the center of many clinical investigations. Firstly, we studied a neurogenic factor, Slit2, implicated in axon guidance pathway and secreted by CAFs. Slit2 increases Schawnn cells migration and morphologic changes of neural cells. Indeed, nerve size and density are increased in a tumor compared to a healthy pancreas, that is called, neural remodeling. Secondly, we worked on a multi-proteic complex (ANXA6/LRP1/TSP1), associated to vesicular trafficking, only expressed in stromal compartment, and mainly in CAFs. This complex is present in extracellular vesicles and confers proliferative and pro-migratory capacities to tumor cells. Data obtained during my thesis constitute an important rationale to target the crosstalk between tumor and stromal compartment, in order to sensitize tumor cells to chemotherapy and improve patient survival
Le, Nail Louis-Romée. "Caractérisation de cellules dérivées d'ostéosarcomes humains". Thesis, Nantes, 2017. http://www.theses.fr/2017NANT1032/document.
Texto completoOsteosarcoma (OS) is the most frequent primitivemalignant bone tumor. We hypothesised that someMSC with cancer stem cell (CSC) characteristics maybe involved in OS development, chemotherapyresistance and metastatic progression.Adherent cells from six human OS samples wereisolated after tumor dissociation and culture. They werenamed OS derived cells (OSDC) and were compared toown patient bone marrow mesenchymal stem cells(BMMSC). We tested MSC characteristics, CSCcharacteristics, and tumor growth support capacities inan induced human OS mouse model.OSDC had the same morphologic aspect andmembrane expression profile as BMMSC. They keptdifferentiation capacities toward osteoblastic lineageand to less extend toward adipogenic and chondrogeniclineage, with variability between different OSDCpopulations. Karyotype was normal for all 6 BMMSCand for 4 OSDC. OSDC showed CSC characteristics,with sphere formations in semi solid conditions,decrease of mitochondrial metabolism in normoxiacondition. Some minimal karyotype abnormalities werefound in 2 OSDC populations. However, no tumorformation was induced in immunocompromised mice(SCID). In coinjection mouse model, 4 out of 6 OSDCincreased tumor growth compared to osteosarcomacells (MNNG-HOS) alone.OSDC that were isolated from human OS samples didnot demonstrate own tumor properties. They are highlysuspected to be part of tumor microenvironment, ratherthan the tumor origin, and to support and modulate thetumor growth. More studies are necessary to identifywhich CDOS factors influence tumor growth suggestingnew stromal targets for combined therapy
Yvonnet, Sarah. "Une approche épistémologique du microenvironnement tumoral". Thesis, Sorbonne université, 2021. http://www.theses.fr/2021SORUL163.
Texto completoCancer research has long been dominated by a genetic and molecular research approach of the disease. However, the accumulation of experimental data since 2000 also highlights the importance of another factor in carcinogenesis: the tumor microenvironment (TME). The study of the TME is accompanied by different assertions in the scientific literature: it would be an opportunity to improve therapies and enrich current knowledge or, on the contrary, it would be a new "paradigm" and would allow the development of new types of therapies.Our thesis proposes an analysis of the evolution of the field of oncology (and of the hypothesis of a potential scientific change) starting from the introduction of the study of the TME. We propose an original approach to this question by adopting two epistemological assumptions. First, we analyze both the scientific and medical communities. We study the continuum between fundamental research and clinical practice, articulating philosophy of biology and philosophy of medicine. Secondly, we conduct our philosophical analysis not only from a theoretical point of view but also as close as possible to the practices, behaviors, methods, and research organizations that participate in this scientific change. To do so, we will use methods rarely used in philosophy, such as semi-directive interviews or field observations.This approach aims to produce a philosophical analysis that contributes to both the philosophical and biomedical literature
Delorme, Solène. "Annexine A1 : dissémination et microenvironnement tumoral". Thesis, Université Clermont Auvergne (2017-2020), 2020. http://www.theses.fr/2020CLFAC042.
Texto completoAnnexine A1 (ANXA1) belongs to the annexin superfamily, which includes proteins capable of binding membrane phospholipids in a calcium dependent manner. This is a multifunctional protein initially described for its anti-inflammatory properties. ANXA1 can be nuclear, cytosolic, membrane and it can also be secreted and cleaved in surrounding environment. It presents a real interest in oncology due to its deregulation in many cancers. Depending on cancer types, ANXA1 is up- or down-regulated compared to normal tissues. It is overexpressed in triple negative breast cancer relative to other subtypes of breast tumors and in melanoma compared to melanocytes. In both pathologies, ANXA1 is associated with proliferation, migration and invasion processes, but the exact mechanism of its roles in tumors still unknown, especially those mediated by extracellular fraction. Studies carried out with Anxa1 null mice have shown the ANXA1 from stromal cells implication in tumor development and progression.The first objective of this work was to test the opportunity to block extracellular ANXA1 with a monoclonal patented antibody, VJ4B6, to decrease migration (in vitro) and dissemination (in vivo). Our results showed that VJ4B6 was unable to limit cellular migration of triple negative breast cancer (MDA-MB-231-luc) and melanoma (SK-MEL-28 and A375-MA2) cell lines presenting extracellular ANXA1. This antibody was also unable to decrease tumor development and dissemination of B16Bl6 melanoma in vivo. The second objective was to study the role of ANXA1 from tumoral and stromal cells in melanoma development and dissemination. Our results highlighted involvement of tumoral ANXA1 in proliferation of A375-MA2 and SK-MEL-28 melanoma cells in vitro. The use of Anxa1 null mice allowed to reveal that stromal ANXA1 promotes tumor development and metastases formation of murine B16Bl6 cells in vivo. Interestingly, studies of tumors showed that stromal ANXA1 absence limits both proliferation of tumor cells and angiogenesis. This could explain the decreased progression of tumors in Anxa1 null mice. Furthermore, tumors developed in these mice presented overexpression of lymphocyte markers (CD3, CD4, FoxP3, CD8a, NKp46) compared to those developed in wild-type mice. This lymphocyte influx concerned both pro- and anti-tumoral lymphocytes. Our hypothesis is that lymphocyte influx is a result of increased tumor vessels permeability in tumors from Anxa1 null mice
Castells, Magali. "Implication du microenvironnement dans la progression tumorale ovarienne". Toulouse 3, 2012. http://www.theses.fr/2012TOU30099.
Texto completoOvarian cancer is rare but has a bad prognosis due to a high level of chemoresistance to the reference treatment, carboplatin. We focused on the role of the microenvironment in ovarian cancer progression. The team previously demonstrated that Hospicells are able to potentialize tumour growth and angiogenesis in vivo. My aim was to determine how Hospicells interact with tumoral cells and other microenvironment partners to promote cancer proliferation. I showed that Hospicells alone cannot induce tumoral neoangiogenesis in vitro and they promote macrophage recruitment in tumours and enhance the synthesis of several cytokines involved in angiogenesis (IL-6, IL-8 and VEGF) through macrophages. Hospicells are also involved in chemoresistance acquisition via membrane exchange and efflux pumps transfer. This original mechanism working through direct contact between cells is probably not the only one responsible for this chemoresistance. Indeed, I showed that molecules secreted by Hospicells can also induce ovarian cancer cells chemoresistance. In order to identify the mechanism through which ovarian cancer cells can become chemoresistant under microenvironment stimulation, I studied the role of Hospicells in apoptosis protection after carboplatin treatment. Hospicells conditioned medium can partially inhibit apoptosis by apoptotic signalling pathway modifications and notably a decreased activation of effector caspases (caspases 3 and 7)
Duval, Stéphanie. "Imagerie du microenvironnement matriciel tumoral : les héparanes mimétiques". Thesis, Tours, 2014. http://www.theses.fr/2014TOUR3802.
Texto completoHeparan sulfate proteoglycans (HSPG), like all proteoglycans (PG), consisting of a protein portion and a glycosaminoglycan (GAG), heparan sulphate (HS) for HSPG. They are part of the extracellular matrix (ECM). PG are able, through their GAG, to bind a number of partners such as growth factors, chemokines, cytokines or enzymes. They regulate the bioavailability of many soluble mediators and thus their biological activity. They are thus involved in the regulation of many processes such as proliferation, differentiation, tissue remodeling, angiogenesis... In addition, it was shown that the binding of proteins having a heparan binding site (HB) with HS of HSPG protect them from enzymatic degradation. However, HSPG are among the first components of the ECM to be digested by heparanase during cellular tissue damage. This digestion makes HB sites available and proteins are sensitive to proteolytic degradation. It is in order to protect the HSBP (heparan sulfate binding protein) that was developed technology heparan mimetics (HM) that will replace the degraded HS on available HB sites and protect proteins of middle injured. These HM, already used as a therapeutic agent of the ECM, are identified in this use under the symbol RGTA for regenerating agent because they increase the speed and quality of the tissue repair, potentially leading to a true tissue regeneration. During tumor development and metastasis, it has been shown that the enzymatic activity of heparanase is multiplied, leading to an increased degradation of HS. In this context, the HM will be able to fix this matrix injured hence the idea of their diagnostic use in oncology. Using labeled HM (HM*) with a radioisotope such as fluorine-18 (18F) and followed by molecular imaging PETScan (positon emission tomography with scanner associated) should allow a particularly efficient marking of the matrix surrounding metastatic and tumor cells. HM* could indeed target ECM involved, through its early degradation in the processes of tumor growth and tumor spread and become a new marker oncology in molecular imaging. To date, among the various studied cancer markers, none address the matrix compartment. The use of HM* should allow the detection of peri-tumor and find a place in the early diagnosis of cancer and the therapeutic monitoring
Papin, Antonin. "Rôle du microenvironnement tumoral dans l'expansion des lymphomes B". Thesis, Nantes, 2019. http://www.theses.fr/2019NANT1009/document.
Texto completoMantle cell lymphoma (MCL) is an aggressive non-Hodgkin lymphoma associated with poor prognosis, and despite recent improvements in the therapeutic strategies for treating MCL, its management remains challenging. While improvements in next generation sequencing technologyhave greatly increased our understanding of the intrinsic abnormalities of MCL, the role of extrinsic signaling remains largely unknown. Recent studies have highlighted the central role of the MCLmicroenvironment in tumor cell survival, drug resistance and proliferation. Characterization of the diverse MCL tumoral niches and comprehension of the crosstalk between tumor cells and surrounding cells within the MCL microenvironment are needed to increase treatment efficacy. In this work, we present a revue of MCL microenvironment and our results on the role of tumoral niches in B lymphomas. This knowledge could be rapidly translated into new therapeuticstrategies to overcome drug resistance during MCL treatment
Augustin, Jérémy. "Caractérisation du microenvironnement tumoral immunitaire des carcinomes hépatocellulaires réséqués". Electronic Thesis or Diss., Sorbonne université, 2021. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2021SORUS409.pdf.
Texto completoHepatocellular carcinoma (HCC) shows globally low response to immunotherapy and HCC immune microenvironment is not well characterized. Our objective was to connect immune, viral and morphologic aspects of HCC and understand how they intervene in sensitivity to immune checkpoint blockade. In this study, we performed a transcriptomic analysis of onco-immune genes to characterize the tumor microenvironment of 170 HCC: 23% hepatitis B (HBV), 29% hepatitis C (HCV), 16% metabolic syndrome, 17% alcohol consumption related, and 14% of undetermined etiology. We correlated gene expression profiles with clinical, morphological and viral features. We did not observe difference of immune microenvironment at a global scale, between etiologies. But within HBV group, we identified 3 Clusters. None of of these clusters expressed ϒ-interferon (compared to 25% of HCC of all etiologies combined). Cluster 1 showed an ambivalent « hot » and exhausted profile with higher expression of exhaustion markers but lower densities of T lymphocytes by immunostaining. This Cluster was associated with HBV transcription and patients from this Cluster showed higher recurrence. Cluster 2 was enriched with macrotrabecular massive subtype and was immunologically “cold” and was also associated with higher recurrence. At last, Cluster 3 was developed much more on cirrhotic liver and showed an intermediate level of immune cells infiltration, with no marker of exhaustion. It was associated with lower recurrence. In conclusion we highlight viral related specificities within HBV HCC, associated with prognostic significance
Bouakka, Ibrahim. "Ciblage thérapeutique de l’Hepatic Leukemia Factor (HLF) dans les cancers du sein triple négatifs". Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL017.
Texto completoThe intricate interplay between the immune response and tumor progression, particularly in the context of triple-negative breast cancer (TNBC), has been a focal point of oncological research over the last decade. Our preceding investigation highlighted the role of the HLF gene within a quartet gene signature, identifying its inverse association with the infiltration of immune cells within the tumor milieu. During my thesis, we investigated more precisely its implication in the immune response and TNBC tumor development. The bioinformatic analysis of clinical data from patients with TNBC demonstrated that low levels of HLF expression were associated with an overexpression of genes related to the mechanisms of attraction and activation of the immune system. The implication of neutrophils in cancer is contentious, as they can function either as active anti-tumoral partners or as pro-tumoral agents promoting immunosuppression and tumor growth. The duality of the immune system’s role in cancer, oscillating between antitumor action and support for tumor growth, reflects its great complexity within the tumor microenvironment. In this study, we employed CRISPR/Cas9 technology to inactivate the HLF gene in TNBC cell lines, enabling us to explore the repercussions on the chemokine network regulating the presence and activity of different immune populations in the tumor microenvironment. Finally, in vivo experiments conducted on immunodeficient mouse models demonstrated that reducing HLF in certain TNBC subtypes hindered tumor progression. Altogether, our results suggest that a reduction of HLF expression can lead in the early steps of tumor development to the awakening of the anti-tumoral function of the immune system to enforce the necessary immunological tone to tumor elimination. Thus, HLF emerges as a promising therapeutic target to promote the engagement and effectiveness of a competent immune response against aggressive subtypes of TNBC
Capítulos de libros sobre el tema "Microenvironnement tumoralal"
Martin, P. M. y L’H Ouafik. "Interactions entre les cellules tumorales et le microenvironnement tissulaire : « Quand le dialogue remplace le monologue »". En Cancer du sein avancé, 97–123. Paris: Springer Paris, 2007. http://dx.doi.org/10.1007/978-2-287-72615-6_11.
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