Academic literature on the topic 'Tumeurs – Métabolisme'
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Journal articles on the topic "Tumeurs – Métabolisme"
Larsen, Christian-Jacques. "P53 « s'acoquine » avec le métabolisme énergétique des tumeurs." Bulletin du Cancer 97, no. 10 (October 2010): 1125–27. http://dx.doi.org/10.1684/bdc.2010.1192.
Full textLacroix, Matthieu, Laetitia Karine Linares, and Laurent Le Cam. "Rôle du suppresseur de tumeurs p53 dans le contrôle du métabolisme." médecine/sciences 29, no. 12 (December 2013): 1125–30. http://dx.doi.org/10.1051/medsci/20132912016.
Full textDubé, Nicole, and Linda Youde. "Étude de la distribution spatiale des principales causes de mortalité dans la ville de Québec (1976-1978)." Cahiers de géographie du Québec 25, no. 66 (April 12, 2005): 413–31. http://dx.doi.org/10.7202/021531ar.
Full textCordier-Bussat, Martine, Chantal Thibert, Pierre Sujobert, Laurent Genestier, Éric Fontaine, and Marc Billaud. "Même l’effet Warburg est oxydable." médecine/sciences 34, no. 8-9 (August 2018): 701–8. http://dx.doi.org/10.1051/medsci/20183408017.
Full textMalthièry, Y., and F. Savagner. "Métabolisme énergétique de la cellule cancéreuse : exemple des tumeurs endocrines riches en mitochondries." Annales d'Endocrinologie 67, no. 3 (June 2006): 205–13. http://dx.doi.org/10.1016/s0003-4266(06)72588-4.
Full textCorporeau, Charlotte, Arnaud Huvet, Vianney Pichereau, Lizenn Delisle, Claudie Quéré, Christine Dubreuil, Sébastien Artigaud, Catherine Brenner, Monique Meyenberg Cunha-De Padua, and Nathalie Mazure. "Crassostrea gigas, une huître au service de la recherche sur le cancer." médecine/sciences 35, no. 5 (May 2019): 463–66. http://dx.doi.org/10.1051/medsci/2019079.
Full textGuillaum, Benedicte, Benjamin Lemasson, Emmanuel Barbier, Alexandre Krainik, and Sylvie Grand. "Évaluation de l’oxygénation tissulaire et du métabolisme de l’oxygène de tumeurs cérébrales en imagerie par résonance magnétique." Journal of Neuroradiology 44, no. 2 (March 2017): 76–77. http://dx.doi.org/10.1016/j.neurad.2017.01.008.
Full textDeshayes, E., N. Flori, P. Senesse, M. C. Eberle, S. Guillemard, P. O. Kotzki, J. Fraisse, et al. "Absence d’impact de la nutrition artificielle sur le métabolisme glucidique des tumeurs de l’œsophage et des voies aérodigestives supérieures." Nutrition Clinique et Métabolisme 32, no. 4 (November 2018): 289. http://dx.doi.org/10.1016/j.nupar.2018.09.122.
Full textNicolas, G. "Radiothérapie métabolique des tumeurs neuroendocrines." Annales d'Endocrinologie 77, no. 4 (September 2016): 243. http://dx.doi.org/10.1016/j.ando.2016.07.027.
Full textPreti, Beatrice, Jasna Deluce, and Siddhartha Srivastava. "Type B Lactic Acidosis in a Solid-Tumour Malignancy Without Liver Metastases." Canadian Journal of General Internal Medicine 16, no. 2 (June 21, 2021): 38–42. http://dx.doi.org/10.22374/cjgim.v16i2.427.
Full textDissertations / Theses on the topic "Tumeurs – Métabolisme"
Lonjon, Michel. "Exploration du métabolisme tumoral cérébral par microdialyse : étude expérimentale et clinique." Nice, 2001. http://www.theses.fr/2001NICE5688.
Full textLussey, Charlotte. "Apport de l'imagerie multimodale à l'étude de l'angiogenèse et du métabolisme des tumeurs liées aux mutations SDHB." Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCB151/document.
Full textPheochromocytomas and paragangliomas (PCC/PGL) are rare neuroendocrine tumours that arise from chromaffin cells of the adrenal medulla, sympathetic and parasympathetic paraganglia respectively. Around 15% of PCC are malignant. SDHB mutations are associated with malignancy and poor prognosis. SDH deficiency leads to succinate accumulation that induces a cellular pseudohypoxic phenotype, promoting in particular VEGF and GLUT-1 expression and increasing angiogenesis and glucose metabolism. The high malignancy hazard associated with SDHB and the absence of curative treatment of metastatic forms of the disease make it essential to develop a mouse model for preclinical trials launching. The quest for a predisposed mouse model of Sdhb-deficient tumors being unsuccessful, Sdhb-/- and wild-type (WT) immortalized mouse chromaffin cells previously generated in the laboratory were propagated in the fat pad of NMRI nude mice, thereby providing the first pattern of Sdhb- deficient tumors. These mice were compared to a control group receiving non-mutated imCC (WT) and characterization was performed in vivo by multimodality imaging. Optical imaging assessing the tumor angiogenesis with Angiostamp®, an RGD fluorescent peptide, found an increased expression of integrins αvβ3 in the Sdhb-/- group 12 h after tracer injection. Dynamic contrast enhanced MRI (DCE-MRI) showed an overall tumor enhancement significantly higher in the Sdhb-/- model secondary to an increase of the tumor blood flow (F) and of the intratumoral capillary volume fraction (Vb) (compartmental analysis using PhysioD3D software). Metabolic imaging assessed by 18FDG-PET confirmed the expected high glucose consumption by Sdhb-/- tumors. Finally, magnetic resonance spectroscopy (1H-MRS) detected succinate accumulation in Sdhb-/- tumors and not in WT tumors. This result was confirmed by mass spectrometry and this innovative procedure for in vivo detection of succinate was translated into patients suffering from PCC/PGL. A succinate peak was specifically observed in SDHx-related PCC/PGL patients. In conclusion, these results show strong differences between Sdhb-/- and WT allografts and suggest that preclinical therapeutic studies could be implemented in this unique model of Sdhb-deficient tumour. Our noninvasive, highly sensitive and specific method allowing in vivo detection of succinate, the major biomarker of SDHx-mutated tumors was translated into clinical imaging
Bessière, Laurianne. "Exploration génomique et fonctionnelle des tumeurs des cellules de la granulosa ovarienne." Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCC308.
Full textFemale gametes consist of an oocyte surrounded by granulosa cells. These can form ovarial granulosa cells tumors (GCT). Two types of tumors are described: the adult form (95% of cases AGCT) or juvenile (JGCT). The AGCTs feature a FOXL2 mutation p. C134W, found in 95% o cases; no genetic marker is set for JGCTs. My PhD work was divided into two areas, according to the two types of tumors. The first was th search for a common genetic marker to JGCTs. We used a global approach to characterize th tumors and candidate genes approach, oriented towards the PI3K / AKT / mTOR pathway. W identified duplications in phase in the AKT1 protein in 60% of our samples. We they characterized the mutant proteins of AKT1: they are enriched in the membrane, under hyper phosphorylated and hyper-active form and give cells a shaggy membrane phenotype. We have also found point mutations, different from one tumor to another. The activity of these mutation remains to be characterized, as it is unclear why the found duplications are specific JGCTs. The second focus of the work was to better understand the mechanisms of action of the C134V mutation FOXL2. We have created a cell- tool containing a copy of our gene of interest unde wild or mutated form, at a specific and unchanging locus. The objective is to determine if tht mutation C134W influences the binding of the protein to DNA or affect the interaction witl partners
Bergeaud, Marie. "Etude de la nature et du rôle de l'interaction de la protéine suppresseur de tumeurs p53 avec la mitochondrie." Versailles-St Quentin en Yvelines, 2012. http://www.theses.fr/2012VERS0032.
Full textThe p53 tumor suppressor protein is found inactivated in most human cancers. Currently, there is increasing evidence for a role of p53 in metabolism regulation notably in proliferative cells exposed or not to low stress. These p53’s activities could be of major importance on p53 oncosuppressive function. We present evidence, that p53 is localized in mitochondria, in primary and tumor human and rodent cells in unstressed condition. More precisely, p53 localizes on the surface of mitochondria but also in the inter-membrane space and matrix. Furthermore this protein is mostly soluble or weakly bound to mitochondria membranes. Interestingly, we found that p53 interacts, either directly or indirectly, with a matrix protein named OSCP a subunit of F1F0-ATP synthase complex. In order to precise p53 direct role at mitochondria, we have established stably expressing cells with a matrix or inter-membrane space mitochondria-targeted p53 protein and we have investigated the effects of p53 on mitochondrial physiology. We have given rise that cells expressing matrix p53 produced less reactive oxygen species than p53 null cells. It seems that matrix localized p53 could also promote mitochondrial respiration, increase mitochondrial ATP production and favour formation of complex IV and V of OXPHOS. Conversely inter-membrane space localized p53 doesn’t seem to be implicated in these different process. Interestingly, matrix p53 interacts with OSCP, this interaction is not found when p53 localized in inter-membrane space. Taken together, our results indicate that p53 protein could have an important role in regulating mitochondrial physiology in proliferative conditions
François, Charlotte. "Rôles respectifs des oestrogènes et des gonadotropines sur la pathogenèse des tumeurs ovariennes de la granulosa et sur l'activité de l'ovaire avant la puberté." Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCC059.
Full textThe granulosa cell tumors are rare and aggressive. Recurrences may appear more than 10 years after the removal of the primary tumor, causing the death of 80% of patients. This disease is accompanied by hyperestrogenism in 70% of cases. The first part of my thesis shows that E2 limit spreading of metastases from granulosa cell tumors. Indeed, in vitro studies on cell lines-derived from a primary tumor of human granulosa (C0V434) or from metastases (KGN) highlight that E2 did not affect their proliferation, but significantly reduces the capacity of migration and invasion of KGN cells. This effect is caused by a rapid non-genomic mechanism that inhibits the activity of ERK1 / 2 via the GPER receptor (François et al. , 2015). The "mini-puberty", present in mammals after birth, is characterized by very high amounts of gonadotropins (LH and FSH) and E2. This early activation of the hypothalamic—pituitary—gonadal axis occurs at a time when the ovary contains growing follicles. The second part of my thesis shows that high levels of FSH in infantile period are essential to optimize the production of E2 by the follicles white blocking their growth and protecting them from premature maturation. Indeed, in vivo and ex vivo studies highlight that high concentrations of FSH provide significant production of E2 by increasing the expression of aromatase, but that they have no more action on the induction of the expression of cyclin D2, a key factor in the proliferation of granulosa cells (François et al. , in preparation)
Gadéa-Deschamps, Émilie. "Impact de la chimiothérapie sur le métabolisme énergétique des patientes atteintes d'un cancer du sein non métastatique : Mécanismes impliqués et conséquences métaboliques." Thesis, Clermont-Ferrand 1, 2014. http://www.theses.fr/2014CLF1MM04.
Full textToday, women face two strong epidemiological trends: a steady increase in the incidence of obesity, and an increase in the incidence of breast cancer. French women over the age of 50 face these two major public health problems, with postmenopausal obesity increasing the risk of breast cancer by 30 to 50%. Nevertheless, thanks to advances in screening and therapies, mortality is decreasing, and the number of women who have received treatment for breast cancer is increasing.Chemotherapy treatments have many side effects, including a significant change in weight during treatment (gain or loss) that seems to persist over time. Whether it is gain or loss, such weight variation has been associated with poor prognosis for these patients. Since data come mainly from American cohorts with a higher BMI than a European population, the Jean Perrin Center conducted a retrospective study to verify these results in a French population (Thivat et al., 2010). This study first confirmed that a high BMI at the time of diagnosis was associated with a poor prognosis. In addition, the weight change observed during chemotherapy treatment (gain and loss ≥5% of initial weight) was associated with a significant increase in the risk of relapse and death. Nevertheless, the causes of this weight variation and the mechanisms involved in this poor prognosis are still insufficiently understood. The objective of this work is to characterize the variation of weight in terms of body composition and to study the factors of the energy balance responsible for these variations. Biological factors associated with the change in body composition, potentially implicated in the poor prognosis, are also studied. The first chapter consists in a bibliographic review describing the pathology of breast cancer (Part I), the changes in energy metabolism following chemotherapy treatment (Part II), the role of brown adipose tissue in the regulation of energy metabolism (Part III) and finally, the impact of changes in energy metabolism on patient health (Part IV). In the second chapter the results of the studies carried out are presented. The first study, still in progress, is presented as a report, while the next two are in article form. A general discussion of all the results identifies the research perspectives to be considered in order to follow up on this work
Pham, Minh Hien. "Etudes sur le métabolisme de l'acide flavone-8-acétique (FAA), un composé à visée antivasculaire antitumorale." Paris 5, 2007. http://www.theses.fr/2007PA05P631.
Full textFlavone-8-acetic acid (FAA) was shown to be very active against solid tumours in the mouse, but was not active in man. Because metabolism could be responsible for this interspecies difference, our aim was to compare FAA metabolism in mouse and man. We showed that FAA is metabolized into 6 new metabolites using mouse microsomes. Compared with human microsomes, FAA was a better substrate for mouse microsomes and yielded more metabolites. Several cytochrome P450s and epoxide hydrolase were identified in FAA metabolism in vitro. Several metabolites were also identified in vivo in the mouse. In vitro, biological results of major FAA metabolites suggest that FAA metabolism could be involved in the marked difference in anticancer activity observed between the two species
Dayot, Stéphanie. "Rôle antitumoral de l'orexine A et des ligands biaisés dans les cancers digestifs : Impact sur le trafic intracellulaire d'OX1R." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCC301.
Full textOrexins are hypothalamic neuropeptides, which have two isoforms, A and B (OxA and OxB, respectively). They interact with two G protein-coupled receptor (GPCR) subtypes, OX1R and OX2R. Once activated, these two receptors induce the mobilization of intracellular Ca2+ via the Gq protein. In the team, where I began my PhD, it was clearly show that the orexins/OX1R system had anti-tumor properties in some cancers including colon cancer (Voisin et al., 2011). It has been showed that OxA but also OxB induce mitochondrial apoptosis via OX1R. These results mean that the orexins/OX1R system represents a potential target in the treatment of colon cancer.My first objective was to study the role of orexins and in particular OxA on pancreatic ductal adenocarcinoma (PDAC) in human. This work showed that OX1R was expressed in 96% of PDACs tested. In addition, I have shown that OX1R is expressed early in pre-cancerous lesions (PanIN). I have demonstrated that the PDAC-derived human cell line, the AsPC-1 line, expressed OX1R, and that OxA was able to induce mitochondrial apoptosis comparable to that observed in colon cancers (Voisin et al. 2011). Finally, suprisingly, my results show that almorexant, a DORA antagonist, has antitumor properties identical to OxA, the natural agonist of OX1R. The unexpected results of the almorexant with regard to its anti-tumor properties challenged me and thus determined the axis of my second objective. So I wanted to know if this effect was only related to the PDAC or if it was more widely effective in other cancers in particular colon cancer. For this, I studied the effect of almorexant in cell lines derived from human colon adenocarcinoma, lines HT-29 and LoVo. In addition, in collaboration with B. Robert's group (CRCM, INSERM U1194, Montpellier)we have developed, by a "phage display" strategy, an agonist antibody that mimicked the effects of OxA on the same cancer cells. My third objective was to study the phenomena of OX1R internalization under the action of OxA and its intracellular traffick by confocal microscopy and images analysis approaches. Indeed, so far, little or nothing is known. Several vesicle markers associated with the internalization of proteins have been used. Of course, in view of the almorexant unexpected effects, it seemed important for me to study its impact on the regulation.To conclude, the OX1 receptor is a potential target for the therapeutic treatment of human adenocarcinoma of the colon and pancreas. In addition, the demonstration that almorexant and the C2 antibody mimic the proapoptotic and antitumor effects of OxA, represents a very good alternative to the natural peptide whose disadvantages in terms of stability and administration may represent a brake in its possible therapeutic use. In addition, the membrane expression of the OX1 receptor within the cell and its fate is different depending on the ligand. These data are therefore of interest for a therapeutic point of view because the almorexant as the antibody C2 allow the OX1 receptor to stay expressed on the cell surface and thus to be available for its proapoptotic activity
Rémy, Chantal. "Intérêt de la spectroscopie RMN pour l'étude in vivo du métabolisme cérébral dans le cas de pathologies globales et localisées." Grenoble 1, 1990. http://www.theses.fr/1990GRE10110.
Full textBerthe, Julie. "Rôle de la protéine immuno-régulatrice PD-L1 sur le métabolisme des cellules tumorales." Thesis, Lille, 2018. http://www.theses.fr/2018LIL2S006.
Full textEvolving to a neoplastic state, normal cells acquire many characteristics; indeed, tumor cells follow abnormal metabolic pathways and exhibit the ability to avoid immune destruction, partly by exploiting immune checkpoints. Many of these are currently under clinical investigation for new cancer treatments, notably the PD-1/PD-L1 axis.Programmed Death-Ligand 1 (PD-L1) molecule belongs to the B7 immunoregulatory proteins family and was originally described as mediating tumor immuno-escape through interaction with its receptor PD-1 on T cells. Associated with poor cancer outcome, aberrant PD-L1 expression has been observed in hematologic malignancies and in multiple solid tumor types. Actually, this protein has been shown to regulate tumor cell proliferation and resistance to chemotherapy through apoptosis inhibition, without interacting with PD-1. However, cellular mechanisms modulated by PD-L1 and involved in these functions are still unclear. Abnormal metabolic pathways are known for contributing to tumor growth and therapy resistance; therefore, the objective of my PhD thesis was to investigate the impact of PD-L1 in breast cancer cell metabolic reprogramming.Using genome editing, we knocked-out the CD274 gene encoding PD-L1 in breast cancer cell line MDA-MB-231 and investigated metabolic functions after PD-L1 overexpression in the same cells. We observed that PD-L1 induces a shift from oxidative phosphorylation to glycolysis, indicating this molecule promotes the Warburg effect in these tumor cells. To validate PD-L1 metabolic reprogramming, we performed metabolomic profiling that highlighted significantly increased levels of glycolysis intermediated such as F6P, F1,6P, GAP, DHAP, PEP and pyruvate in PD-L1-expressing cells, confirming our latter results. Moreover, in agreement with an increasing mitochondrial reactive oxygen species (ROS) production, transcriptomic study suggested that PD-L1 represses NRF2-mediated oxidative stress response pathway, especially NQO2, GSTM3 and ABCC2 genes. Furthermore, in silico analysis of breast cancer patients databases highlighted a correlation between PD-L1/CD274 gene and oxidative stress gene signature (GSTM3; CYBB) or glucose transporters genes (SLC2A1; SLC2A3) expressions, supporting our results. Besides, glucose is mostly used by cancer cells to favor biosynthesis of diverse biomolecules required for cellular proliferation; the above results could explain our human breast cancer cells xenograft experiments in Nude mice demonstrating that PD-L1 increases tumoreginicity.Thus, the work presented in this thesis evidences novel PD-L1 intrinsic tumor-promoting functions, suggesting that therapeutic agents inhibiting these mechanisms would be promising for breast cancer treatment
Books on the topic "Tumeurs – Métabolisme"
Mundy, Gregory R. Calcium homeostasis: Hypercalcemia and hypocalcemia. London: Dunitz, 1989.
Find full textSies, Helmut, and Regina Brigelius-Flohe. Diversity of Selenium Functions in Health and Disease. Taylor & Francis Group, 2015.
Find full textSies, Helmut, and Regina Brigelius-Flohe. Diversity of Selenium Functions in Health and Disease. Taylor & Francis Group, 2015.
Find full textSies, Helmut, and Regina Brigelius-Flohe. Diversity of Selenium Functions in Health and Disease. Taylor & Francis Group, 2019.
Find full textDiversity of Selenium Functions in Health and Disease. Taylor & Francis Group, 2015.
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