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Artykuły w czasopismach na temat "Cancer – Environnement"
Bonnaud, F., B. Melloni, A. Vergnenègre, A. Zigani i T. Daix. "Cancer bronchique et environnement intérieur". Revue des Maladies Respiratoires 24, nr 2 (luty 2007): 248–51. http://dx.doi.org/10.1016/s0761-8425(07)91052-9.
Pełny tekst źródłaLy, A. "Cancer et environnement en Afrique". Oncologie 9, nr 5 (maj 2007): 370–79. http://dx.doi.org/10.1007/s10269-007-0636-y.
Pełny tekst źródłaLecerf, Jean-Michel, Fabrice Nesslany i Stéphanie Ranque-Garnier. "Nutrition, activité physique, environnement et cancer". Pratiques en nutrition 11, nr 42 (kwiecień 2015): 29–32. http://dx.doi.org/10.1016/j.pranut.2015.03.006.
Pełny tekst źródłaRuffié, P., i J. Margery. "Cancer et environnement: le cas de l’amiante". Oncologie 9, nr 5 (maj 2007): 335–39. http://dx.doi.org/10.1007/s10269-007-0641-1.
Pełny tekst źródłaEspina, C., K. Straif, S. Friis, M. Kogevinas, R. Saracci, H. Vainio i J. Schüz. "Quatrième Code européen contre le cancer : environnement, profession et cancer". Psycho-Oncologie 10, nr 3 (wrzesień 2016): 150–64. http://dx.doi.org/10.1007/s11839-016-0579-x.
Pełny tekst źródłaSasco, A. J. "Cancer, environnement et populations à l’heure de la mondialisation". Oncologie 9, nr 5 (maj 2007): 380–91. http://dx.doi.org/10.1007/s10269-007-0693-2.
Pełny tekst źródłaBacqué, M. F., i J. Carretier. "Cancer et environnement. L’humanité face à ses choix politiques". Psycho-Oncologie 10, nr 3 (wrzesień 2016): 147–49. http://dx.doi.org/10.1007/s11839-016-0590-2.
Pełny tekst źródłaSaib, M. S., A. Cicollella, J. Caudeville i O. Ganry. "Analyse spatio-temporelle du lien environnement-cancer en Picardie (projet CIRCE)". Revue d'Épidémiologie et de Santé Publique 62 (luty 2014): S60. http://dx.doi.org/10.1016/j.respe.2013.12.078.
Pełny tekst źródłaLe Moal, J., D. Daniel Eilstein, K. Straif i M. Ledrans. "W - 1 Cancer et environnement : les tumeurs cérébrales prioritaires pour la surveillance". Revue Neurologique 163, nr 4 (kwiecień 2007): 201. http://dx.doi.org/10.1016/s0035-3787(07)90889-9.
Pełny tekst źródłaCarretier, Julien. "L’Unité « Cancer et Environnement » Pôle des Sciences Cliniques, Centre Léon Bérard, Lyon". Oncomagazine 4, nr 4 (listopad 2010): 6. http://dx.doi.org/10.1007/s11944-010-0050-y.
Pełny tekst źródłaRozprawy doktorskie na temat "Cancer – Environnement"
Dekky, Bassil. "Micro-environnement et cancer : rôle des adamalysines dans la progression tumorale". Thesis, Rennes 1, 2018. http://www.theses.fr/2018REN1B046.
Pełny tekst źródłaTumor microenvironment plays a major role in tumor growth, invasion and resistance to treatments. Understanding the mechanisms that regulate communication between tumor cells and their microenvironment is essential to develop effective therapies. In this context, Adamalysin extracellular proteases play major role in tumor progression, by modulating the extracellular matrix (ECM) remodeling and the bioavailability of cell communication mediators such as cytokines, chemokines and growth factors. My work revealed a new interaction between ADAM12, a mesenchymal marker induced during the epithelial-mesenchymal transition (EMT) dependent on TGF-β and ZO-1, a scaffolding protein expressed in tight junctions of epithelial cells. Both proteins are redistributed in invadopodia-like structures to promote ECM degradation. In a second study, we carried out an in silico screening that allowed us to identify a cluster of Adamalysin genes co-expressed in patients with hepatocellular carcinoma. Among these Adamalysins we have studied the protein ADAMTS12 in more details, and shown that this protein plays a key role in the development of liver fibrosis involving an acute or chronic inflammatory response
Guillet, Pierre. "Infections nosocomiales et cancer : rôle des facteurs environnementaux". Aix-Marseille 2, 1992. http://www.theses.fr/1992AIX20655.
Pełny tekst źródłaBONNIER, PASCAL. "Aspects epidemiologiques et pronostiques recents des cancers du sein. La tumeur et son environnement". Aix-Marseille 2, 1997. http://www.theses.fr/1997AIX20667.
Pełny tekst źródłaEmeville, Elise. "Polluants Organochlorés et Risque de Survenue du Cancer de la Prostate. Interactions Gène-Environnement". Thesis, Rennes 1, 2014. http://www.theses.fr/2014REN1B016/document.
Pełny tekst źródłaProstate cancer (PCa) is the most frequent type of cancer in Western countries. Advanced age, ethno-geographic origin and the presence of a family history of CaP are the main clearly established risk factors. The effects of exposure to synthetic chemicals with hormonal properties, also called endocrine disruptors (EDCs), on PCa are also are suspected. The main objective of this thesis is to evaluate the relationships between plasma concentration of persistent organochlorine pollutants with hormonal properties, such as DDE (the main metabolite of DDT) and PCBs as well polymorphisms of selected genes involved in xenobiotic (GSTM1, GSTT1) and estrogens (CYP17, CYP19, CYP1B1, COMT, UGT1A1) metabolism, and the occurrence of PCa or its recurrence after treatment with radical prostatectomy. This project is based on data obtained from the population-based case-control study (KARUPROSTATE) in Guadeloupe and from cases treated by radical prostatectomy
Dumond, Aurore. "Les Neuropilines, des cibles pertinentes dans le traitement du cancer du rein à cellules claires". Electronic Thesis or Diss., Université Côte d'Azur, 2020. http://www.theses.fr/2020COAZ6033.
Pełny tekst źródłaClear cell Renal Cell Carcinoma (ccRCC) represent 80% of kidney cancers. Around 80% of ccRCC present an inactivation of the von Hippel-Lindau gene (VHL) gene, leading to the stabilization the Hypoxia Inducible Factors 1 and 2 alpha (HIF-1 and 2α) and to the overexpression of their targeted genes such as the « Vascular Endothelial Growth Factor (VEGF) », the principal angiogenic factor. Thus, ccRCC are one of the most vascularized cancers and represent a paradigm for anti-angiogenic treatments (AAT). Currently,15 different AAT have obtained FDA and EMA approval. They are divided in three different families:- antibodies targeting VEGF- tyrosine-kinase inhibitors (TKi) that target receptors involved in neo-angiogenesis such as the current reference therapy, sunitinib- decoy receptors that trap VEGFA and PlGF such as aflibercept.Overexpression of VEGF (involved in angiogenesis) and of the other member of the VEGF family, VEGFC (involved in lymphangiogenesis) is also a key phenomenon of immune tolerance. Therefore, immune-checkpoint inhibitors (anti PD-1, anti PD-L1 and anti CTLA-4) also obtained an approval for the treatment of ccRCC.However, relapse on TKi are frequently observed after a few months and immune-checkpoint inhibitors present a long-lasting effect only in 20% of patients. Hence, ccRCC is still an uncurable disease and new therapeutic strategies targeting concomitantly angiogenesis/lymphangiogenesis and immune tolerance are urgently needed. Neuropilins (NRP1 and NRP2) are co-receptors of VEGF and VEGFC and are expressed on vascular and lymphatic endothelial cells, on tumor cells and on immune cells. Hence, they may represent ideal targets to inhibit the drivers of ccRCC aggressiveness.My thesis describes the relevance of targeting the NRP1 and NRP2 signaling pathways in ccRCC by a genetic (invalidation of the two genes by CRISPR/Cas9) and by a pharmacological approach (development of a NRPs inhibitor). The preclinical results generated represent an essential first step for the initiation of early phase clinical trials for patients with treatment failure
Legendre, Claire. "Adaptation cellulaire et moléculaire des cellules d'hépatome humain HepaRG à un environnement hypoxique". Rennes 1, 2009. http://www.theses.fr/2009REN1S055.
Pełny tekst źródłaReduced oxygen level, or hypoxia, is frequently encountered in solid tumours and contributes to drug resistance. Hypoxia is also associated with invasive phenotype and correlated to poor prognosis and mortality. The role of hypoxia in hepatocellular carcinoma biology is not fully understood. Therefore, there is a need for developing in vitro models mimicking hypoxic conditions find within solid tumours using hepatic tumour cells. Highly differentiated human hepatoma HepaRG cells respond to hypoxia by a switch from aerobic to anaerobic glycolysis. Moreover, we showed that hypoxia also repressed drug-metabolizing enzymes expression. These repressions could therefore strongly compromise chemotherapy effectiveness on tumour cells within hypoxic environment. Furthermore, HepaRG cells cultured under hypoxic versus normoxic conditions might represent a new strategy to test different types of therapeutic molecules in order to predict their effectiveness
Clement-Colmou, Karen. "Impact du fractionnement de la radiothérapie sur le microenvironnement vasculaire tumoral". Thesis, Nantes, 2018. http://www.theses.fr/2018NANT1029/document.
Pełny tekst źródłaThe tumour blood vessels are immature and dysfunctional, limiting the distribution and efficacy of anticancer drugs. Conventional radiotherapy (2Gy / day) improves their structure, reduces hypoxia and improves the biodistribution of concomitant treatments. However, hypofractionated radiotherapy, using higher doses per fraction, tends to replace conventional schedules. Their consequences on the tumour microenvironment are poorly understood. Our goal was to define the impact of different fractionation schedules on the tumour vascular microenvironment. A fractionation scale, ranging from 2 to 12Gy per fraction, was implemented on two cancer models (prostate and lung). Several phenotypical and functional aspects of the vasculature and anti-tumour efficacy were studied. A radiation-induced vascular maturation was observed, including an increased pericyte coverage and an improved distribution of doxorubicin. In both models, tumour control was better for hypofractionated schedules. Vascular pseudo-normalization was poorly sensitive to fractionation, but hypoxia was improved in a dose-dependent manner. The depth and duration of the improvement was greater in the slow-growing prostate cancer model: hypoxia seemed to depend as much on the kinetics of repopulation of the model as on the quality of the blood supply. Our results highlight the mutual influence of tumour and vascular responses to irradiation. They will be useful to optimize the future delivery schedule of anticancer treatments
Atieh, Youmna Marie Lyne. "Interplay between cancer cells and cancer-associated fibroblasts in tumor invasion and metastasis formation". Electronic Thesis or Diss., Paris 6, 2017. http://www.theses.fr/2017PA066140.
Pełny tekst źródłaCancer-associated fibroblasts (CAFs) are the most abundant cells of the tumor stroma. Their capacity to contract the matrix and induce invasion of cancer cells has been well-documented. However, it is not clear if CAFs remodel the matrix by other means (degradation, matrix deposition or stiffening). This project demonstrates that CAFs induce cancer cell invasion through assembly of FN into the matrix. CAFs assembled fibronectin (FN) mainly via integrin α5 but integrin αvβ3 was necessary for initial mechanosensing and fibrillar adhesion formation. In the absence of FN, contractility of the matrix by CAFs is preserved. When degradation is impaired, CAFs retain the capacity to induce invasion in a FN-dependent manner. In all cases, the levels of expression of integrin β3 and the amount of assembled FN was directly proportional to the invasion induced by fibroblast populations. Our results highlight FN assembly and integrin β3 as new hallmarks of CAFs. We also noticed that cancer cells migrate towards CAFs suggesting a possible chemotactic response. Using Dunn’s chemotaxis chamber, we found that cancer cells migrate along a gradient of CAF-conditioned media and a gradient of fibronectin. Finally, orthotopic injections of cancer cells and CAFs in the colon wall of mice revealed that CAFs stimulate metastasis of cancer cells to the liver. In conclusion, our data show that CAFs promote cancer cell invasion by depositing fibronectin that can guide cancer cells favoring metastasis formation
Tcheandjieu, Gueliatcha Catherine Ines. "Etude des facteurs de risque génétiques et des interactions gène-environnement dans les cancers différenciés de la thyroïde". Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS064.
Pełny tekst źródłaContext : Differentiated thyroid cancer (DTC) incidence is characterized by considerable geographic and ethnic variations. Particularly high incidence rates were observed in Melanesian women of New Caledonia. Except for the exposure to ionizing radiation in childhood and obesity, the role of other DTC risk factors is not clearly established. Genetic factors have been suggested to play an important role in DTC risk since epidemiological studies have shown that DTC has a higher familial relative risk than any other cancers. Linkage studies in multiple-case DTC families and candidate gene studies have identified polymorphisms in several genes but very few have been replicated so far. Genome-wide association studies (GWAS) also identified several DTC susceptibility loci with the most robust associations reported on the loci 9q22 and 14q13. Only few susceptibility loci were highlighted by GWAS and the identified variants were shown to account less than 10% of the DTC familial risk, emphasizing that much remains to be discoveredObjectives: The main objective of this work was to study the role of genetic risk factors and their interaction with environmental factors in DTC risk. More specifically, we aimed to: 1) replicate the association between DTC risk and polymorphisms reported in candidate gene and GWAS studies in 2 case-control studies conducted in Metropolitan France and New Caledonia; 2) identify potential causal variants of DTC risk in GWAS loci 9q22 and 14q13 using fine-mapping approach; 3) identify new genetic risk factors for DTC in women using pathway approach by pooling data from 2 case-control studies conducted in France and USA..Materials and methods: The analysis of the candidate genes and of the GWAS loci were based on a European population of 508 cases and 621 controls from 2 case-control studies conducted in metropolitan France (CATHY study) and in New Caledonia (NC study) and, a Melanesian population of 156 cases and 114 controls from the NC study. The pathway analysis was conducted in a first step on European women from the CATHY study (365 cases/376 controls) and from the Young-Thyr study (83 cases /93 controls) both conducted in metropolitan France. In a second step, we pooled the data from CATHY/Young-Thyr study and USRT/UTMDACC study (332 cases/443 controls) conducted in the United States.Results: In Europeans and Melanesians, we found no association with polymorphisms reported previously by candidate genes studies. However, we observed that among these genes, GSTM1 and GSTT1 may modulate the associations between DTC risk and obesity or alcohol consumption. Some polymorphisms identified in GWAS studies at loci 9q22, 14q13 and 2q35 were replicated in Europeans and in Melanesians. In the GWAS loci 9q22 and 14q13, we identify new variants that can be functionally related to DTC pathogenesis in Europeans and Melanesians. We also reported interactions between some of these variants and parity or tobacco smoking. The analysis of candidate pathways in European women showed interactions between alcohol consumption or tobacco smoking and genes involved in the metabolism of these compounds and, between age at first menarche or oral contraception and genes involved in biosynthesis and metabolism of sex steroid hormones
Masson, Olivier. "Cancer du sein et micro-environnement tumoral : rôle de la protéase cathepsine D adipocytaire et de son récepteur LRP1". Thesis, Montpellier 1, 2010. http://www.theses.fr/2010MON1T027.
Pełny tekst źródłaThe aspartyl protease cathepsin D, overexpressed and hyper-secreted by epithelial breast cancer cells is a poor prognosis factor in breast cancers and stimulates cancer cell growth and metastasis formation. It also affects the tumor microenvironment, inducing the fibroblasts invasive outgrowth. Our works have shown that the LDL receptor-related protein1, LRP1, is the fibroblastic receptor for cathepsin D. LRP1 is highly expressed in adipocytes. Clinical studies indicate that obesity is a risk factor in many cancers, including breast cancer in postmenopausal women.During this thesis, we studied the role of cathepsin D and LRP1 in adipocytes, which are the prominent cell type in the tumor microenvironment of breast cancers. Our results indicate that cathepsin D and LRP1 are overexpressed in human and mouse obese adipose tissue. Furthermore, the expression of cathepsin D is increased during adipocyte differentiation. Finally, the inhibition of the cathepsin D and LRP1 expression inhibits adipogenesis indicating their key role in this process.All these results suggest that cathepsin D and its receptor LRP1 could be potential therapeutic targets in the treatment of obesity
Książki na temat "Cancer – Environnement"
Agence franc ʹaise de se curite sanitaire de l'environnement et du travail (Maisons-Alfort). Cancer et environnement. Paris: Les e d. Inserm, 2008.
Znajdź pełny tekst źródłaManzur-ul-Haque, Hashmi, i United Nations Environment Programme, red. The state of the environment. London: Butterworths, 1987.
Znajdź pełny tekst źródłaMendelsohn, Mortimer L. Mutation & The Environment Pt.d: CARCINOGENESIS (DISCONTINUED (Progress in Clinical and Biological Research)). Redaktor Mortimer Mendelsohn. John Wiley & Sons, 1990.
Znajdź pełny tekst źródłaCzęści książek na temat "Cancer – Environnement"
Praud, Delphine, Béatrice Fervers i Pauline Vidican. "Chapitre 34. Cancers". W Environnement et santé publique, 889–912. Presses de l’EHESP, 2023. http://dx.doi.org/10.3917/ehesp.goupi.2023.01.0889.
Pełny tekst źródła"CHAPITRE 1. Les cancers hormonodépendants". W Hormones, santé publique et environnement, 11–66. EDP Sciences, 2020. http://dx.doi.org/10.1051/978-2-86883-895-7-009.
Pełny tekst źródła"CHAPITRE 1. Les cancers hormonodépendants". W Hormones, santé publique et environnement, 11–66. EDP Sciences, 2020. http://dx.doi.org/10.1051/978-2-86883-895-7.c009.
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