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Artykuły w czasopismach na temat "Cancer – Génétique"
Ferron, M., F. Praz i M. Pocard. "Génétique du cancer colorectal". Annales de Chirurgie 130, nr 10 (grudzień 2005): 602–7. http://dx.doi.org/10.1016/j.anchir.2005.02.014.
Pełny tekst źródłaJanin, N. "Prédisposition génétique au cancer". La Revue de Médecine Interne 16, nr 7 (lipiec 1995): 500–517. http://dx.doi.org/10.1016/0248-8663(96)80746-6.
Pełny tekst źródłaProbst-Hensch, Nicole M., i Alfredo Morabia. "Epidémiologie génétique et susceptibilité génétique au cancer du sein". Revue Médicale Suisse -2, nr 2378 (2002): 301–5. http://dx.doi.org/10.53738/revmed.2002.-2.2378.0301.
Pełny tekst źródłaKahn, A. "Génétique du cancer colo-rectal". médecine/sciences 10, nr 2 (1994): 228. http://dx.doi.org/10.4267/10608/2599.
Pełny tekst źródłaThomas, G., M. Muleris i RJ Salmon. "La génétique du cancer colorectal". médecine/sciences 4, nr 5 (1988): 274. http://dx.doi.org/10.4267/10608/3816.
Pełny tekst źródłaManouvrier, S., i Th Lecomte. "Endoscopie et génétique: polyposes-cancer". Acta Endoscopica 34, S2 (listopad 2004): 461–62. http://dx.doi.org/10.1007/bf03004018.
Pełny tekst źródłaViassolo, Valeria, Aurélie Ayme i Pierre O. Chappuis. "Cancer du sein : risque génétique". Imagerie de la Femme 26, nr 2 (czerwiec 2016): 95–104. http://dx.doi.org/10.1016/j.femme.2016.04.009.
Pełny tekst źródłaCanedo, P., i José Carlos Machado. "Prédisposition génétique au cancer gastrique". Acta Endoscopica 37, nr 2 (kwiecień 2007): 239–47. http://dx.doi.org/10.1007/bf02961793.
Pełny tekst źródłaCohen-Haguenauer, Odile. "Prédisposition héréditaire au cancer du sein (1)". médecine/sciences 35, nr 2 (luty 2019): 138–51. http://dx.doi.org/10.1051/medsci/2019003.
Pełny tekst źródłaGhozali, Faïza. "Cancer du poumon et prédisposition génétique". Option/Bio 19, nr 400-401 (maj 2008): 29. http://dx.doi.org/10.1016/s0992-5945(08)70151-x.
Pełny tekst źródłaRozprawy doktorskie na temat "Cancer – Génétique"
Quan, Xiao-Jiang. "Etude génétique du développement du cancer mammaire". Doctoral thesis, Universite Libre de Bruxelles, 2001. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/211526.
Pełny tekst źródłaStieber, Daniel. "Analyse génétique de la sensibilité au cancer mammaire". Doctoral thesis, Universite Libre de Bruxelles, 2005. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/211000.
Pełny tekst źródłaMaubec, Eve. "Prédisposition génétique au mélanome : de la génétique à la recherche clinique". Thesis, Paris 11, 2012. http://www.theses.fr/2012PA11T034.
Pełny tekst źródłaThis thesis had two main objectives: 1) To define groups of patients which may benefit from genetic counseling by identifying predictors of mutations of the CDKN2A gene, a major gene predisposing to cutaneous melanoma (CM) in families with only two cases. 2) Epidemiological and clinical characterization of specific entities of melanoma with the secondary objective of contributing to the identification of susceptibility genes for these entities. Coexistence of CM with renal cell carcinoma and mucosal anogenital melanomas were studied.The study populations are a collection of 293 melanoma patients that were ascertained systematically and the French collection MELARISK which is a collection including over 3000 subjects drawn from families with multiple cases of melanoma or melanoma occurring in a particular context (association with another cancer, rare locations, occurrence before the age of 20, multiple sporadic melanomas).We investigated association of three clinical features with the presence of a CDKN2A mutation in a family by extent of CM family clustering (2 versus ≥3 CM patients among first-degree relatives in a family).The study was conducted in 483 French families including 387 families with two melanoma patients, and 96 families with three or more patients with melanoma. The factors examined individually and in a joint analysis in a family were: median age at diagnosis <50 years, ≥1 patient in a family with multiple primary melanomas (MPM) or with pancreatic cancer. The frequency of CDKN2A mutations was higher in F3+ families (32%) than in F2 families (13%). While early age at melanoma diagnosis and occurrence of MPM in ≥1 patient were significantly associated with the risk of a CDKN2A mutation in F2 families, early age at melanoma diagnosis and occurrence of pancreatic cancer in a family were significantly associated with CDKN2A mutations in F3+ families. Thus this study showed that clinical features associated with CDKN2A mutations vary, in France, a country of low incidence of melanoma, according to the degree of familial clustering. Identifying predictors of CDKN2A mutations in families with two melanoma cases has helped to define subgroups of families (early age at CM diagnosis, and/or ≥1 MPM patient) in which the frequency of CDKN2A mutations is above 20% such that these subgroups of F2 families should be offered genetic testing.The analysis of two series of patients, either patients with melanoma coexisting with renal cell carcinoma or patients with anogenital mucosal melanoma identified their clinical and histological features by comparing them to a series of melanomas that were ascertained systematically. In both series, our results suggested a genetic predisposition at least partly independent of CDKN2A. The study of the c renal cell carcinoma; coexistence of CM and renal cancer in the same patient had two practical consequences for clinicians: it suggests the interest of a dermatologic screening visit in patients with renal cell carcinoma and that abdominal ultrasonography or computed tomography scanning performed at the initial workup and during the follow-up of patients with CM may be of value for the early detection of renal cancer. Regarding genetic research, this series has contributed to the identification of a germline mutation in the MITF gene that increases the risk of developing melanoma, renal cancer or both cancers and has interesting biological properties. The study of anogenital melanoma has shown that these melanomas could be associated with cutaneous melanoma in the same patient and it has also shown a high frequency of family history of melanoma associating mucosal and CM suggesting a shared genetic predisposition. Consequently dermatological screening or monitoring must include examination of both skin and mucosa in families with multiple cases of CM; and in case of a mucosal melanoma, a dermatological examination should be offered to relatives. The genetic mechanism has to be identified
Bigot, Pierre. "Approche génétique et protéomique de la carcinogénèse rénale". Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066077.
Pełny tekst źródłaKidney cancer is the 7th largest solid tumors in adults and its incidence is rising. The purpose of our research was to study renal carcinogenesis and to identify prognostic biomarkers in clear cell renal cell carcinoma.We used the isobaric tagging iTRAQ® to perform a relative quantification of kidney tumor proteins. After proteomic analysis, 928 constitutive proteins were identified and 346 had a modified expression in tumor compared with that of normal tissue. Pathway and integrated analyses indicated the presence of an up-regulation of the pentose phosphate pathway in aggressive tumors. In total, 14 proteins were excreted and could potentially become biomarkers. Among them, we confirmed that TGFBI was significantly associated with oncologic outcomes.To understand renal carcinogenesis, we investigated the 12p11.23 renal cancer susceptibility locus. The first step was to confirm this locus by an independent study. Then we performed a functional analysis of the 12p11.23 region in relation to RCC risk. Our results suggest rs7132434 is a functional SNP at 12p11.23 responsible for the GWAS RCC signal, and that this locus acts as an enhancer of SHARP1 expression by binding c-Jun. Further investigations will be necessary to understand the role of SHARP1 in renal carcinogenesis
Lefèvre, Jérémie. "Génétique du cancer colorectal : polyposes adénomateuses non liées à APC et cancers de survenue précoce". Phd thesis, Université Pierre et Marie Curie - Paris VI, 2012. http://tel.archives-ouvertes.fr/tel-00833304.
Pełny tekst źródłaShafei-Benai͏̈ssa, Effat. "La naevomatose basocellulaire : prédisposition génétique au cancer et instabilité chromosomique". Poitiers, 1997. http://www.theses.fr/1997POIT2280.
Pełny tekst źródłaValeri, Antoine. "Etude génétique, épidémiologique et clinique du cancer de la prostate familial". Paris 5, 2000. http://www.theses.fr/2000PA05CD07.
Pełny tekst źródłaNicolle, Rémy. "Regulatory networks driving bladder cancer". Thesis, Evry-Val d'Essonne, 2015. http://www.theses.fr/2015EVRY0009/document.
Pełny tekst źródłaCarcinogenesis is a consequence of the unceasing activation of cell proliferation. In normal cells, mito-genic stimuli are processed by a complex network of protein interactions and enzymatic reactions, often referred to as pathways, which can eventually trigger the activation of new genes to engage the cell into mitosis. During developmental or wound healing processes, this complex regulation of cellular phenotypes results in a tight control of the number and behavior of cells and therefore contributes to the maintenance of a functional and healthy tissue architecture. Based on genomic, transcriptomic and proteomic profiles of bladder tumors and transcriptomes of nor-mal urothelial cells at various states of proliferation and differentiation, I devised novel methodologies to characterize the pathways driving bladder cancer. I first developed a set of tools to identify and visualize sample and subtype-specific transcriptional pro-grams through the inference of a co-regulatory network and the prediction of transcription factor activity. These methods were embedded in a Bioconductor package entitled CoRegNet (bioconductor.org). The measure of transcriptional activity is based on the influence of a transcription factor on the expression of its target genes and was used to characterize the most active regulators of each bladder cancer subtypes. The integration of genomic profiles highlighted two altered transcription factors with driver roles in lumi-nal-like and basal-like bladder cancer, one of which was experimentally validated. The use of CoRegNet to model the contribution of regulatory programs of normal proliferation and diffe-rentiation in bladder cancers underlined a strong preservation of normal networks during tumorigenesis. Furthermore, a regulator of normal proliferation was found to be constitutively activated by genetic al-terations and its influence on bladder cancer cell proliferation was experimentally validated. In addition, a master regulator of urothelial differentiation was found to have a loss of activity in nearly all tumors. This was then associated to the discovery of frequent inactivating mutations and further analysis unco-vered a major role in differentiated tumors. In order to characterize signaling pathways from proteomic pull-down assays, I then designed a novel algorithm to grow a densely connected network from a set of proteins and a repository of protein interac-tions. The proposed algorithm was made available as a Cytoscape application named Pepper for Protein Complex Expansion using Protein- Protein interaction networks (apps.cytoscape.org). Finally, using both a proteomic pull-down assay of the bladder cancer oncogene FGFR3 and a transcrip-tomic profiling of its downstream regulated genes, I applied Pepper to characterize the full FGFR3 signa-ling pathway from its protein partners to the downstream transcriptional regulators. In particular, this uncovered a regulatory link between FGFR3 and the tumor suppressor TP53
Robiou, du Pont Sébastien. "Étude d'association cas-témoins pour l'identification de gènes de prédisposition au cancer colorectal sporadique". Nantes, 2009. https://archive.bu.univ-nantes.fr/pollux/show/show?id=e4d7dcbe-e008-4983-be95-e2a6b6ad6947.
Pełny tekst źródłaColorectal cancers (CRC) constitute the third most frequent cancer in France. Two distinct forms of CRC can be distinguished: the family forms (25%), due to deleterious mutations in known high-risk genes, and sporadic forms (75%), induced by the combined effect of both genetic and environmental risk factors not identified yet. In order to determine the genetic component of sporadic CRC, we conducted a case-control association study using low-penetrance genetic variants. By a “candidate gene approach”, we demonstrated the CRC-predisposing effect of 5 SNPs (Single Nucleotide Polymorphism) located genes PTGS1, IL8, MTHFR, PLA2G2A, PPARG, almost all involved in procarcinogenetic inflammatory events. By focusing on metabolic pathway,we highlighted a gene-environment interaction between cytochromes P450 SNPs and great red meat consumption. By a genome-wide association study based on DNA pools, we eventually showed, in our population, the involvement of two others SNPs located in CDH13 and UTP6, the predisposing effect of the CDH13 SNP being strengthened by a genotype-mRNA expression rate correlation. The fact that CDH13 belongs to the cadherin superfamily, whose members have a clear role in cancer, leads us to continue our investigations by analyzing the involvement of other SNPs of cadherin genes in CRC
Valent, Alexander. "Évolution génétique du neuroblastome au cours de la progression tumorale". Paris 12, 1998. http://www.theses.fr/1998PA120047.
Pełny tekst źródłaKsiążki na temat "Cancer – Génétique"
K, Cowell John, red. Molecular genetics of cancer. Oxford: Bios, 1995.
Znajdź pełny tekst źródłaPhilippe, Pierre. Les familles à cancer. Montréal, Qué: Presses de l'Université de Montréal, 1989.
Znajdź pełny tekst źródłaSarma, Ramaswamy H. DNA double helix & the chemistry of cancer. Schenectady, N.Y: Adenine Press, 1988.
Znajdź pełny tekst źródłaFelix, Mitelman, red. Cancer cytogenetics. Wyd. 2. New York: Wiley-Liss, 1995.
Znajdź pełny tekst źródłaFelix, Mitelman, red. Cancer cytogenetics. Wyd. 3. Hoboken, N.J: John Wiley & Sons, 2009.
Znajdź pełny tekst źródłaFelix, Mitelman, red. Cancer cytogenetics. New York: A.R. Liss, 1987.
Znajdź pełny tekst źródłaCancer: The evolutionary legacy. Oxford: Oxford University Press, 2000.
Znajdź pełny tekst źródłaT, Lynch Henry, i Kullander Stig, red. Cancer genetics in women. Boca Raton, Fla: CRC Press, 1987.
Znajdź pełny tekst źródłaJohn, Swansbury, red. Cancer cytogenetics: Methods and protocols. Totowa, N.J: Humana Press, 2003.
Znajdź pełny tekst źródłaVarmus, Harold. Genes and the biology of cancer. New York: Scientific American Library, 1993.
Znajdź pełny tekst źródłaCzęści książek na temat "Cancer – Génétique"
Gauthier-Villars, Marion. "Introduction aux prédispositions génétiques". W Épidémiologie des cancers de l’enfant, 135–38. Paris: Springer Paris, 2009. http://dx.doi.org/10.1007/978-2-287-78337-1_13.
Pełny tekst źródłaNowak, F. "Plateformes de génétique moléculaire des cancers". W Les biomarqueurs moléculaires en oncologie, 81–90. Paris: Springer Paris, 2014. http://dx.doi.org/10.1007/978-2-8178-0445-3_6.
Pełny tekst źródłaRobert, J. "Génétique moléculaire des cancers : dualité hôte-tumeur". W Les biomarqueurs moléculaires en oncologie, 3–17. Paris: Springer Paris, 2014. http://dx.doi.org/10.1007/978-2-8178-0445-3_1.
Pełny tekst źródłaGauthier-Villars, Marion. "Le rétinoblastome: Le modèle de la prédisposition génétique". W Épidémiologie des cancers de l’enfant, 139–44. Paris: Springer Paris, 2009. http://dx.doi.org/10.1007/978-2-287-78337-1_14.
Pełny tekst źródłaGauthier-Villars, Marion. "Une tumeur, plusieurs prédispositions génétiques : l’exemple du médulloblastome". W Épidémiologie des cancers de l’enfant, 299–305. Paris: Springer Paris, 2009. http://dx.doi.org/10.1007/978-2-287-78337-1_37.
Pełny tekst źródłaNoguès, C. "Prédisposition génétique au cancer du sein". W Cancer du Sein, 13–19. Elsevier, 2016. http://dx.doi.org/10.1016/b978-2-294-74449-5.00002-2.
Pełny tekst źródła"Bibliographie". W Psychanalyse et prédiction génétique du cancer, 271–75. Érès, 2017. http://dx.doi.org/10.3917/eres.vital.2017.01.0271.
Pełny tekst źródłaRousset-Jablonski, Christine. "Prédispositions génétiques aux cancers". W La Ménopause en Pratique, 263–68. Elsevier, 2019. http://dx.doi.org/10.1016/b978-2-294-74372-6.00041-2.
Pełny tekst źródłaFlahault, Cécile. "La place du psychologue dans la démarche de dépistage de prédispositions génétiques au cancer". W La pratique du psychologue et l’éthique, 97–109. Mardaga, 2009. http://dx.doi.org/10.3917/mard.bourg.2009.01.0097.
Pełny tekst źródłaRaporty organizacyjne na temat "Cancer – Génétique"
Corkum, Eleanor, Tiffanie Perrault i Erin C. Strumpf. Améliorer les parcours de diagnostic du cancer du sein au Québec. CIRANO, październik 2023. http://dx.doi.org/10.54932/tlak9928.
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