Literatura científica selecionada sobre o tema "Génétiques des tumeurs"
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Artigos de revistas sobre o assunto "Génétiques des tumeurs"
Bourdeaut, Franck. "Prédispositions génétiques aux tumeurs osseuses". Soins Pédiatrie/Puériculture 34, n.º 270 (janeiro de 2012): 19. http://dx.doi.org/10.1016/j.spp.2012.11.002.
Texto completo da fonteRohmer, V. "Aspects génétiques des tumeurs neuroendocrines". Oncologie 15, n.º 10-11 (outubro de 2013): 515–19. http://dx.doi.org/10.1007/s10269-013-2330-6.
Texto completo da fonteRowe-Pirra, William. "Des tumeurs sans mutations génétiques". Pour la Science N° 561 – Juillet, n.º 7 (24 de junho de 2024): 13b. http://dx.doi.org/10.3917/pls.561.0013b.
Texto completo da fonteDelattre, O. "Tumeurs d’Ewing, aspects génétiques et cellulaires". Pathologie Biologie 56, n.º 5 (julho de 2008): 257–59. http://dx.doi.org/10.1016/j.patbio.2008.03.005.
Texto completo da fonteLahlou-Laforêt, K., R. Vibert, S. Richard e A. P. Gimenez-Roqueplo. "Test génétique présymptomatique chez les mineurs à risque pour la maladie de von Hippel-Lindau et surveillance des porteurs de mutation — Aspects psychologiques et éthiques". Psycho-Oncologie 15, n.º 4 (dezembro de 2021): 141–45. http://dx.doi.org/10.3166/pson-2022-0173.
Texto completo da fonteIdbaih, A., K. Hoang-Xuan, D. Psimaras, M. Sanson e J. Y. Delattre. "Aspects génétiques des tumeurs cérébrales primitives de l'adulte". EMC - Neurologie 6, n.º 2 (janeiro de 2009): 1–10. http://dx.doi.org/10.1016/s0246-0378(09)50915-3.
Texto completo da fonteThomas, G. "Dix ans de recherche sur les prédispositions génétiques au développement des tumeurs". médecine/sciences 11, n.º 3 (1995): 336. http://dx.doi.org/10.4267/10608/2213.
Texto completo da fonteCoindre, Jean-Michel, Jean-François Émile, Geneviève Monges, Dominique Ranchère-Vince e Jean-Yves Scoazec. "Tumeurs stromales gastro-intestinales : définition, caractéristiques histologiques, immunohistochimiques et génétiques, stratégie diagnostique". Annales de Pathologie 25, n.º 5 (outubro de 2005): 358–85. http://dx.doi.org/10.1016/s0242-6498(05)80145-2.
Texto completo da fonteRouprêt, M., e P. Colin. "Particularités génétiques et épidémiologiques des tumeurs urothéliales de la voie excrétrice supérieure". Oncologie 17, n.º 4 (abril de 2015): 184–90. http://dx.doi.org/10.1007/s10269-015-2506-3.
Texto completo da fonteTissier, Fréderique. "Tumeurs corticosurrénaliennes sporadiques de l’adulte : aspects génétiques et perspectives pour le pathologiste". Annales de Pathologie 28, n.º 5 (outubro de 2008): 409–16. http://dx.doi.org/10.1016/j.annpat.2008.07.005.
Texto completo da fonteTeses / dissertações sobre o assunto "Génétiques des tumeurs"
Chauveinc, Laurent. "Etudes génétiques des tumeurs radio-induites". Paris 11, 2001. http://www.theses.fr/2001PA11T040.
Texto completo da fonteRadiation induced tumors are a possible very late complications of radiotherapy. Many epidemiologist studies exists, with the evaluation of the relative risk for different tissues. But, the genetic studies are rare, and no global theory exists. With the published cases, two profiles existed, one with translocations and one with genetic material losses, evoking two different genetic evolutions. In this work, a few ways to explain the chromosomic evolution of the radiation-induced tumors were explored. In the fust part, with study of the age and the latency period of second tumor after retinoblastomas, two or more genes were modified by the irradiation. With 12 cytogenetic cases, analyzed in the laboratory, and the 25 cases of the literature, the radiation-induced tumors were characterized by genetic material losses. A anti-oncogenic evolution is probable. Only thyroid tumors did not have this evolution. The mechanism of the chromosomic material losses could be the chromosomic instability. The telomere length decreasing is a possible explanation of these phenomena. In our preliminary results, the telomere length of radiation-induced tumor did not decrease comparing to normal human cells, suggesting that telomerase activity stabilized this length
Azzouzi, Abdel-Rahmène. "Facteurs de risque génétiques des tumeurs prostatiques". Paris 11, 2003. http://www.theses.fr/2003PA11TO34.
Texto completo da fonteBarault, Ludovic. "Altérations génétiques et épigénétiques dans le cancer colique sporadique". Dijon, 2008. http://www.theses.fr/2008DIJOS025.
Texto completo da fonteCancer cells are often the result of alterations in signalling pathways implicated in cell survival or apoptosis. We successfully demonstrated in a population base of 586 colon adenocarcinomas, followed by the cancer registry of Burgundy, that activating mutation of at least one of the three genes from the MAPK signalling pathway (KRAS, BRAF, PI3KCA) was associated with a lower survival in patients bearing a tumour without microsatellite instability. In a second study, DNA Methylation, an epigenetic alteration, was evaluated in the population base (characterization of the CpG Island Methylator Phenotype). Three subgroups of methylation phenotype were identified (No-CIMP, CIMP-Low, and CIMP-High). The clinico-pathological features of cancers with MSS/No-CIMP and MSS/CIMP-Low were quite similar, but they affected survival to different degrees. The higher the level of methylation, the poorer the survival. Our work clearly showed the prognostic effect of methylation in MSS patients and the need to distinguish between the 3 groups of CIMP. These studies are all the more important since the recent use of “targeted therapies” against proteins from the signal transduction system have recently been used in cancer treatment. The identification of activating mechanisms of signalling pathways and the characterisation of epigenetic alterations involved in colon cancer are fundamental to the understanding of the molecular factors involved in colorectal cancer. Knowledge of these will have an impact on patient response and follow-up
Gad, Sophie. "Etude des prédispositions génétiques aux cancers du sein et de l'ovaire : recherche d'altérations de grande taille des gènes BRCA1 et BRCA2, recherche de facteurs génétiques modificateurs du risque de cancer de l'ovaire chez des femmes porteuses d'une mutation de BRCA1". Paris 5, 2002. http://www.theses.fr/2002PA05N028.
Texto completo da fonteGoutagny, Stéphane. "Identification des altérations génétiques impliquées dans la tumorigénèse méningée chez l'homme". Paris 7, 2010. http://www.theses.fr/2010PA077131.
Texto completo da fonteMeningiomas are the most common central nervous System tumours in the population of age 35 and older. World Health Organization defines 3 grades, predictive of the risk of recurrence. Grade 1 meningiomas account for 75-80% of cases and are slow growing benign tumours. Twenty to thirty percent are grade II, with a higher risk if recurrence. Grade III account for 2-3% of meningiomas and are associated with shorter survival. The mainstay of treatment is surgical resection, and radiotherapy in selected cases. No efficient chemotherapy is available to date. The main predisposing factor is Neurofibromatosis type 2 (NF2). About half NF2 patients harbour meningiomas, often multiple. About 2/3 of sporadic meningiomas display somatic biallelic inactivation of the NF2 tumour suppressor gene. For 1/3 of meningiomas the gene(s) involved in initiation of tumorigenesis remain unknown. The aims of this thesis were: to identify genetic events associated with meningioma malignant progression and to identify alternative pathways involved in the initiation of meningiomas tumorigenesis. We identified genetic alterations associated with histological progression of 36 paired meningioma samples in 18 patients using 500K SNP genotyping arrays and NF2 gene sequencing. Chromosome alterations acquired during progression from grade I to grade II meningioma were not recurrent. Progression to grade III was characterized by recurrent genomic alterations, the most frequent being CDKN2A/2B locus loss on 9p. Of note, the most frequent chromosome alterations observed in progressing meningioma samples are early alterations, i. E. Present both in lower and higher-grade samples of a single patient. Meningiomas displayed different patterns of genetic alterations during progression according to their NF2 status: NF2-mutated meningiomas are associated with higher chromosome instability during progression than NF2-non-mutated meningiomas, which show very few imbalanced chromosome segments. No gene or molecular pathway could be identified in initiation of meningioma tumorigenesis, but robust bioinformatic data were acquired and will be analyzed. This pattern of alterations could thus be used; as markers in clinical practice to identify tumours prone to progress among grade 1 meningiomas. Prospective validation of these prognostic criteria is a prerequisite to their clinical application
Galiana-Coudray, Corinne. "Recherche d'altérations génétiques dans les tumeurs d'oesophage : rôle éventuel des oncogènes Ras". Lyon 1, 1993. http://www.theses.fr/1993LYO1T113.
Texto completo da fonteAndujar, Pascal. "Altérations génétiques des tumeurs respiratoires humaines et murines après exposition à des fibres minérales". Thesis, Paris Est, 2008. http://www.theses.fr/2008PEST0030.
Texto completo da fonteRésumé en anglais non communiqué
Bounacer, Ali. "Altérations génétiques dans les tumeurs de la thyroïde survenues à la suite d'une irradiation thérapeutique". Paris 11, 1998. http://www.theses.fr/1998PA11T044.
Texto completo da fonteCosta, Lionel. "Facteur de transcription USF1 et systèmes de réparation des dommages à l'ADN au cours de la réponse de l'hôte à l'infection par Helicobacter pylori". Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCC150/document.
Texto completo da fonteHelicobacter pylori is a gastric pathogen that infects 50% of the worlds population. H. pylori is the only bacterium known to be a class 1 carcinogenic agent, and represents the major risk factor in the development of gastric cancer. The genotoxic activity of H. pylori plays an essential role in the promotion of gastric cancer. Furthermore, H. pylori favours the proteasomal degradation of p53, a central regulator of the DNA damage response. H. pylori induces DNA hypermethylation in the promoter region of two genes encoding transcription factors, Upstream Stimulating Factors USF1 and USF2, inhibiting their expression. USF1 regulates the level of p53 and the components of the nucleotide excision DNA repair (NER) system. Moreover, in response to genotoxic stress, USF1 binds to p53 and inhibits its proteasomal degradation. My thesis project aims to elucidate the mechanisms leading to the development of gastric cancer due to H. pylori infection. This work will address the consequences of USF1 depletion during this infection, focusing on the impact on i) p53, its isoforms, and the DNA damage and repair response, and ii) the gastric carcinogenesis process. To facilitate this investigation, I have developed complementary approaches, using epithelial gastric cells for in vitro studies, and a USF1-/- mouse model for in vivo analyses. My results show a concomitant decrease in the nuclear levels of USF1 and p53, combined with a cytoplasmic delocalisation of USF1 in cells infected by H. pylori. This deregulation is accompanied by the inhibited expression of genes targeted by USF1 and p53, implicated in the DNA damage and repair response. Proximity Ligation Assay (PLA) experiments show that H. pylori alters the response of cells to genotoxic stress by inhibiting the interaction between USF1 and p53 in the nucleus following treatment with camptothecin. In parallel, H. pylori also induces the transcription of p53 isoforms. My results suggest that USF1 is a negative transcriptional regulator of the expression of these isoforms. In vivo, the absence of USF1 in USF1-/- mice exacerbates inflammation and accelerates the severity of the gastric lesions, leading to the presence of dysplasia at 9 months post-infection. These results are in agreement with the weak USF1 expression levels observed in patients with gastric cancer, which is associated with worse prognoses. In conclusion, the results obtained show the essential role played by USF1 during H. pylori infection, in the maintenance of the tumour suppressor p53 and the genetic stability of host cells. They confirm USF1 as a tumour suppressor. Finally, these findings describe not only the novel strategy by which H. pylori infection favours gastric cancerogenesis, but could also be of clinical significance, as USF1 is promising as a candidate biomarker of gastric cancer
Meunier, Katy. "Influence du statut MSI et des principales altérations génétiques des cancers coliques sur l’évolution tumorale métastatique naturelle et après chirurgie". Paris 6, 2013. http://www.theses.fr/2013PA066332.
Texto completo da fonteThe first aim was to investigate the influence of mutations characteristics of tumours displaying microsatellite instability (MSI), due to mismatch repair system (MMR) deficiency, in tumour invasion and metastatic potential. For this purpose, we set up a model of orthotopic xenograft in NOD/SCID mice using the human MSI colon cancer cell line HCT116, deficient in MLH1, a key MMR actor and its isogenic cell line obtained by transfecting a wild type MLH1 cDNA expression vector. Subcutaneous tumours were first established in mice; then, tumours were grafted onto the caecum and either left in situ to evaluate the natural evolution, or resected to assess clinical outcome after surgery. Our observations show that the expression of MLH1 improves clinical outcome of mice who underwent a curative surgical resection or when tumours were left in situ. The second objective was to compare the molecular characteristics of colon cancer with liver metastases and/or peritoneal carcinomatosis in a prospective multicentre study. Genome regions with copy number variations were identified by comparing DNA isolated from normal tissues and the different tumour sites using pan-genomic "HumanCNV370" chips. The level of genomic alterations in primary tumours is not indicative of evolution, and carcinomatosis as metastases may differ from each other and from the primary tumour. The intra-individual tumour heterogeneity has important consequences in clinics. Identifying a molecular signature in the primary tumour able to predict evolution, and defining the molecular characteristics of metastasis, should help clinicians to improve the therapeutic management of patients with colon cancer in the future
Livros sobre o assunto "Génétiques des tumeurs"
Sioud, Mouldy. RNA interference: Challenges and therapeutic opportunities. New York: Humana Press, 2015.
Encontre o texto completo da fonte1951-, Cavennee Webster, Hastie Nicholas, Stanbridge Eric J e Banbury Center, eds. Recessive oncogenes and tumor suppression. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory Press, 1989.
Encontre o texto completo da fonteP, Tonini G., Sansone Raffaele 1957-1991 e Thiele Carol J, eds. Molecular genetics of pediatric solid tumors: Basic concepts and recent advances. Chur: Harwood Academic Publishers, 1992.
Encontre o texto completo da fonteInternational, Conference on Carcinogenesis and Risk Assessment (8th 1994 Austin Tex ). Genetics and cancer susceptibility: Implications for risk assessment : proceedings of the Eighth International Conference on Carcinogenesis and Risk Assessment, held in Austin, Texas, November 30-December 3, 1994. New York: Wiley-Liss, 1996.
Encontre o texto completo da fonteSioud, Mouldy. RNA Interference: Challenges and Therapeutic Opportunities. Springer New York, 2016.
Encontre o texto completo da fonteCooper, Colin S. Translocations in Solid Tumors. Taylor & Francis Group, 2002.
Encontre o texto completo da fonteCooper, Colin S. Translocations in Solid Tumors. Taylor & Francis Group, 2002.
Encontre o texto completo da fonteCooper, Colin S. Translocations in Solid Tumors. Landes Bioscience, 2002.
Encontre o texto completo da fonteTonini, Gian. Molecular Genetics of Pediatric Solid Tumors: Basic Concepts and Recent Advances. Routledge, 1992.
Encontre o texto completo da fonteBronchud, Miguel H. Principles of Molecular Oncology. 2a ed. Humana Press, 2003.
Encontre o texto completo da fonteCapítulos de livros sobre o assunto "Génétiques des tumeurs"
Lasset, Christine, Sophie Giraud e Valérie Bonadona. "Tumeurs rares et prédisposition génétique". In Tumeurs malignes rares, 15–23. Paris: Springer Paris, 2010. http://dx.doi.org/10.1007/978-2-287-72070-3_3.
Texto completo da fonteGauthier-Villars, Marion. "Une tumeur, plusieurs prédispositions génétiques : l’exemple du médulloblastome". In Épidémiologie des cancers de l’enfant, 299–305. Paris: Springer Paris, 2009. http://dx.doi.org/10.1007/978-2-287-78337-1_37.
Texto completo da fonteRobert, J. "Génétique moléculaire des cancers : dualité hôte-tumeur". In Les biomarqueurs moléculaires en oncologie, 3–17. Paris: Springer Paris, 2014. http://dx.doi.org/10.1007/978-2-8178-0445-3_1.
Texto completo da fonte