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Artykuły w czasopismach na temat "Agressivité tumorale"
Sangol Héritier, Mundeke, Musoka Kyungu Agnès, Madi Fatuma, Nyembo Luty, Kizonde Kalungwe, Yowa Muya Sandra, Kapita Izana Marie Jeanne i Chenge Borasisi. "Papilloma Inverse Nasosinusien: À Propos D’un CAS Aux Cliniques Universitaires De Lubumbashi /RDC". International Journal of Medical Science and Clinical Invention 9, nr 10 (29.10.2022): 6296–98. http://dx.doi.org/10.18535/ijmsci/v9i10.05.
Pełny tekst źródłaFalk, Alexander T., Coralie Moncharmont, Matthieu Guilbert, Jean-Baptiste Guy, Gersende Alphonse, Jane-Chloé Trone, Romain Rivoirard i in. "La radiothérapie induit-elle une agressivité accrue des cellules tumorales du glioblastome?" Bulletin du Cancer 101, nr 9 (wrzesień 2014): 876–80. http://dx.doi.org/10.1684/bdc.2014.1946.
Pełny tekst źródłaRozprawy doktorskie na temat "Agressivité tumorale"
Lesluyes, Tom. "Remodelage génomique des sarcomes pléomorphes : caractérisation transcriptomique et agressivité tumorale". Thesis, Bordeaux, 2019. http://www.theses.fr/2019BORD0074.
Pełny tekst źródłaPleomorphic sarcomas are rare mesenchymal tumors characterized by many chromosomal rearrangements. Their oncogenic process is still poorly understood, no recurrent and specific genetic alteration able to drive the tumor initiation has been identified yet. The work I did during my thesis had the objective to better understand the biology of these tumors, focusing on transcriptomic consequences of their genomic remodeling.We characterized fusion transcripts in these tumors by high-throughput sequencing (RNA-seq). This led us to identify the expression of several chimeric transcripts involving TRIO (5.1% of cases). Moreover, this analysis and the identification of expressed variants allowed us to identify frequent mutations of tumor suppressor genes such as ATRX (16% of cases) and more generally members of the SWI/SNF complex (47% of cases). Alterations of this major complex of chromatin remodeling are associated with higher genetic instability and more aggressive phenotype.In pleomorphic sarcomas, genetic instability is linked to tumor progression through the expression of a prognostic transcriptomic signature. This signature, termed CINSARC, is involved in mitosis control and chromosome segregation pathways. We wanted to determine the origin of such expression by integrating genomics and epigenetics, transcriptional and post-transcriptional regulation mechanisms. Though these mechanisms do not seem to directly regulate CINSARC expression, important changes have been highlighted. From a clinical standpoint, we demonstrated that the signature expression is a global prognostic factor of tumor aggressiveness in numerous cancer types. In addition, CINSARC is a better prognostic marker than the FNCLCC grading system, the current international standard to evaluate the metastatic risk in soft tissue sarcomas. We consequently developed a method allowing a daily clinical application of the CINSARC signature to improve the therapeutic management of these tumors
Martins, Isabelle. "Agressivité du mélamone : marqueurs pronostiques et concept de la cellule souche cancéreuse". Paris 7, 2008. http://www.theses.fr/2008PA077221.
Pełny tekst źródłaMelanoma is the most lethal of skin cancers. The main objective of this study consisted in a better definition of criteria leading to the aggressiveness of melanoma. Most melanoma express abnormally the molecules of the MHC II (major histocompatibility complex of class II). This expression has been associated with a poor survival prognosis for the patients. As the mhc ii molecules display tumor antigens at the cell-surface of melanoma, one hypothesis was that MHC II expression results from signaling cascades involved in tumor progression. We provide the first evidence that the chemical and genetic inhibition of the mapk signaling pathways significantly reduces the expression of the MHC II molecules in melanoma cell lines. In addition we show that the abnormal expression of MHC II coïncides with the activation of the nf-kb pathway and of target genes. Taken as a whole these data can explain the association between expression of MHC II molecules and a poor prognosis as it correlates with signaling cascades leading to cell proliferation and resistance against apoptosis and the expression of proteins defining aggressive stages of the tumor. Secôndly, we have studied a melanoma cell line possessing certain properties of "cancer stem cells" (expression of neural stem cell markers, growth as spheroids in a medium optimized for neural stem cells). Our data evidence numerous modulations of gene expression in spheroids versus adherent cells. In addition spheroids display differential properties in their tumorigenicity during xeno-transplantation experiments indicating that, depending on their microenvironment, melanoma can have different potential of aggressiveness
Lauriol, Jessica. "Agressivité du mélanome liée à l'expression du complexe majeur d'histocompatibilité de classe II et à la plasticité cellulaire induite par le microenvironnement". Paris 7, 2010. http://www.theses.fr/2010PA077033.
Pełny tekst źródłaThe rising incidence of cutaneous melanoma and the low effectiveness of treatments of metastatic forms imply alternative therapies should be developed and that knowledge of its development should be improved. This thesis aims first to explain the known association between MHC class II abnormal constitutive expression by melanoma cells and unfavorable clinical outcome. This study shows that, although necessary, MAPK signalling activation is not sufficient to induce MHC class II expression and that this expression is correlated to but not regulated by NFKB activity. Moreover, MHC class II expression coincides with expression and production of chemokines associated with angiogenesis and metastasis, which provides a rationale for its association with poor prognosis. Secondly, we wondered to which extent microenvironment influences melanoma aggressiveness. In that purpose, we chose to study tumor initiating potential, invasive and differentiation abilities of melanoma cells cultured under three-dimensional condition in stem cell media. We provide evidence that this culture method increases invasive abilities of melanoma cells and directs them toward dedifferentiated phenotype marked by embryonic stem cell transcription factor expression and by an increase in differentiation potential. Finally, we put forward that the expression of embryonic stem cell transcription factors might be responsible for the observed alterations in aggressiveness properties of melanoma cells. This thesis supports actual concerns about the cancer stem cell concept and the actual hypothesis that proposes to define stem ness not as an entity but rather as a state, responding to environmental cues
Chamlali, Mohamed. "Modulation du potentiel invasif des cellules cancéreuses mammaires humaines par le canal calcique Orai3". Electronic Thesis or Diss., Amiens, 2021. http://www.theses.fr/2021AMIE0078.
Pełny tekst źródłaDuring breast cancer metastatic processes, cancer cells acquire migratory capacities through a reshaping of the cytoskeleton, but also a remodelling of the adhesive capacities highly dependent on the intracellular calcium concentration. For two decades, several studies have shown the involvement of calcium channels in the modulations of breast metastatic capacities. Recently, studies have demonstrated a role of Orai3 in several tumour processes such as resistance to chemotherapy and proliferation and apoptosis of breast cancer cells expressing oestrogen receptors. However, the role of the Orai3 calcium channel in breast tumour aggressiveness such as the metastatic process remains poorly understood.First, we characterized the entry of calcium, through the Orai3 channel, in basal-like cancer cell lines (MDA-MB-231 and MDA-MB-231 BrM2). Indeed, we have shown for the first time that the Orai3 channel is activated at the basal level, independently of the endoplasmic reticulum calcium stores, and regulates the intracellular calcium concentration. We have shown that this calcium signature regulates the cell migration of breast cancer cells. Indeed, cell migration is dependent on the entry of calcium by Orai3. Besides, we have established that this modulation of migratory capacities depends on cellular adhesive faculties. During this process, calpain (a highly calcium-dependent protease) presents a modified activity according to the expression of Orai3. During the silencing of Orai3, the activity of calpain drops, resulting in significant cell adhesiveness correlated with reduced cell migration.On the other hand, we have demonstrated an inverse correlation between the expression of Orai3 and the cell morphology of the cancer lines used. Indeed, the decrease in Orai3 expression is associated with a rounded cell morphology. Interestingly, we have discovered that this regulation of cell morphology involves a remodelling of the actin cytoskeleton in a calcium-independent manner suggesting an effect involving Orai3 as a protein (and not as a calcium channel). This result suggests the involvement of signalling proteins involved in the remodelling of the actin cytoskeleton. Indeed, the molecular inhibition of Orai3 is associated with a decrease in the expression of Focal Adhesion Kinase (FAK) without modulating its activity.In conclusion, our results reveal the pivotal role of Orai3 in the migratory processes of basal mammary cancer cells, via both calcium-dependent modulation of cell adhesion and calcium-independent actin cytoskeleton remodelling
Fabbri, Lucilla. "Rôle de la forme hypoxique VDAC1, VDAC1-∆C, dans l’expression du cil primaire et la progression tumorale". Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2019. http://www.theses.fr/2019AZUR6033.
Pełny tekst źródłaVoltage-dependent anion channel1 (VDAC1) is a porin of the mitochondrial outer membrane that plays a very important role in the regulation of cellular metabolism and apoptosis. As a consequence of hypoxia (i.e. decrease of oxygen availability), a new form of VDAC1, VDAC1-∆C, is produced from a microfusion between abnormally enlarged mitochondria and endolysosomes. Through this mechanism, the endolysosomal asparagine endopeptidase Legumain (LGMN) mediates the cleavage of VDAC1 at specific sites. Clear cell Renal Cell Carcinoma (ccRCC) is the most common form of kidney cancer characterized by loss or mutation of VHL tumor suppressor gene, occurring in both sporadic and hereditary ccRCCs. VHL inactivation is responsible for the normoxic stabilization of hypoxia-inducible transcription factors (HIFs) and thus a dysregulation of the hypoxic pathway. Moreover, ccRCC is usually characterized by loss of the primary cilium (PC) a non-motile sensory organelle of cell surface, making this cancer a model of ciliopathy. The primary cilium serves a number of key functions, among which cell signalization and cell cycle regulation are of special interest in tumorigenesis. In vitro, we demonstrated the presence of VDAC1-∆C in RCC4 cells, stabilizing both HIF1-α and HIF2-α. VDAC1-∆C was not detected in RCC4 cells re-expressing the wt pVHL (RCC4+pVHL), without HIFs stabilization. The absence of VDAC1-∆C in these cells was correlated with a low expression of LGMN and with the increase of the number of ciliated cells compared to RCC4 cell line. The silencing of VDAC1 or of LGMN in RCC4 cells abolished the presence of VDAC1-∆C and significantly increased both the number of ciliated cells and their invasive potential. In parallel, we demonstrated that a restrict group of patients, in a cohort of 19 ccRCC patients, were characterized by the absence of VDAC1-∆C, low expression of LGMN and an increase in ciliated cells.We found a gene signature based on GLI and IFT20 genes, which are markers of PC activity and formation respectively, whose overexpression (GLI1+/IFT20+) reflected the increase of PC expression. This classification, based on VDAC1, LGMN and the genes GLI1 and IFT20, was reinforced from the study of a TCGA cohort of 375 non-metastatic ccRCC. 48 patients (GLI1+/IFT20+)/375, about 12% of patients, had a poor prognosis in terms of overall survival and disease free survival. We found that an epithelial to mesenchymal transition (EMT) signature and maintenance of glycolytic metabolism were at the basis of the increase in tumor aggressiveness. Moreover, we found that patients with i) an increased expression of PC, ii) the absence of VDAC1-∆C and iii) a GLI1+/IFT20+ signature were more resistant to sunitinib, the current standard of care treatment for metastatic ccRCC, and we confirmed the same results in vitro, in ccRCC cell lines. However, since the immunophenoscore was in favor to GLI1+/IFT20+ group of patients, immunotherapy could be a particularly beneficial treatment. To understand the VDAC1-∆C -dependent restraint of PC expression, RAS-transformed mouse embryonic fibroblasts (MEF) cell lines knockout for VDAC1 (Vdac1-/-) expressing i) human VDAC1 wt (VDAC1+/+), ii) a non- cleavable form of VDAC1 (VDAC1Mut) and iii) only the truncated form of VDAC1 (VDAC1-STOP) have been engineered. We first determined that VDAC1-∆C is involved in the increase of glycolysis and respiration and that VDAC1-∆C confers the capability to metabolize more metabolites. We also demonstrated that VDAC1-∆C inhibits PC formation, thus participating to the ciliopathic phenotype of tumors. Finally, we demonstrated that the presence of VDAC1-∆C can also occur in normoxia upon silencing of the iron-sulfur biosynthetic machinery in mitochondria or with impaired iron homeostasis, attributing a new role to VDAC1 in the context of iron deprivation.Thus, my research demonstrated a new function of VDAC1 and, in particular, of VDAC1-∆C in both hypoxic and normoxic contexts
Schneider, Pascale. "Invasivité et agressivité des leucémies aigües lymphoblastiques de l'enfant : rôle de l'angiogénèse et des métalloprotéases". Rouen, 2009. http://www.theses.fr/2009ROUENR09.
Pełny tekst źródłaLes leucmies aigües lymphoblastiques reprsentent la 1ère pathologie maligne de l'enfant. Les lymphoblastes ont des caractristiques leur permettant de migrer de la MO vers le sang périphrique et les organes extra-mdullaires. Ces atteintes extra-mdullaires sont l'un des éléments qui aggravent le pronostic de la maladie. Nous anons donc étudié chez des patients des marqueurs biologiques impliqués dans les phénomènes d'invasivité cellulaire, comme le système uPA/uPAR, le CXCL-12 et son récepteur et les métalloprotéases matricielles, ainsi que leurs répercussions pronostiques. L'autre partie de notre travail a porté sur les facteurs d'angiogène impliqués dans les LAL. Après les tumeurs solides, le rôle de l'angiogenèse a été exploré également dans les hémopathies. Notre travail confirme la présence d'une angiogenèse dans les LAL. II faut définir les patients pouvant bénéficier de traitements anti-angiogéniques
Ramírez, Sevilla Cristóbal Javier. "Valor de la testosterona sérica como factor de riesgo de cáncer de próstata y de su agresividad tumoral". Doctoral thesis, Universitat Autònoma de Barcelona, 2015. http://hdl.handle.net/10803/377437.
Pełny tekst źródłaProstate cancer is the fourth most common tumour in humans and the second in male. The incidence in Spain was 21,8% in 2010. In the diagnosis of prostate cancer the patient’s medical history, digital rectal examination and serum prostate-specific antigen (PSA) detection are mandatory. The final diagnose is made by transrectal or transperineal ultrasound guided prostate biopsy. The pathology dictamen is defined with the histologic type, the Gleason grading system, number of scores, percentage of tumour, localization of the tumour and the lymphovascular and neural invasion. Testosterone is synthesized in the Leydig cells of the testis and in the adrenal gland. Functions of testosterone are the erectile function, maturation of secondary sex characteristics and testis volume differenciation. The active percentage of testosterone in serum is 1-2% and it’s called free testosterone. There are differents publications that confirm the relationship between high or low testosterone level and prostate cancer risk and its aggressiveness, but there are others that haven’t found association between testosterone and prostate cancer. The hypothesis of our study was: “There is an association between low serum testosterone level and prostate cancer detection and its aggressiveness and this relationship is best represented with free testosterone”. The objectives of the study were to analyze the results between total and free testosterone and prostate cancer detection and its aggressiveness and to compare the results between total and free testosterone. In our study 478 patients were analyzed because of a prostate-specific antigen elevation and/or abnormal digital rectal examination along 25 months. Blood samples were obtained of all patients and total testosterone level was determined by chemiluminescence immunoassay and free testosterone was determined by radioimmunoassay. The percentage of prostate cancer detection was 45,3% and it represented 216 patients. Age, digital rectal examination, total and free serum PSA, percentage of free PSA, PSA density, prostate volume, first and repeated biopsy, presence and absence of cancer in the biopsy dictamen, Gleason score 6 or less, 7 and upper than 7, total and free serum testosterone level, and low, intermediate and high risk prostate cancer aggressiveness according to the D’Amico classification were analyzed. The statistical analysis was made with non-parametric test because of the absence of normal distribution of most variables. The conclusions of this study were that neither total non free testosterone were associated with prostate cancer detection and its aggressiveness. Moreover free testosterone was not hard associated with prostate cancer diagnose. The practice of total and free serum testosterone determination cannot be recommended in patients with suspicious of prostate cancer because of an elevation of PSA and/or abnormal digital rectal examination.