Littérature scientifique sur le sujet « Prostate – Cancer – Génétique »
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Articles de revues sur le sujet "Prostate – Cancer – Génétique"
Manus, Jean-Marie. « PCA3, marqueur génétique du cancer de prostate ». Revue Francophone des Laboratoires 2009, no 409 (février 2009) : 12. http://dx.doi.org/10.1016/s1773-035x(09)70178-9.
Texte intégralValéri, Antoine. « Étude génétique, épidémiologique et clinique du cancer de la prostate familial ». Bulletin de l'Académie Nationale de Médecine 186, no 4 (avril 2002) : 779–91. http://dx.doi.org/10.1016/s0001-4079(19)34297-9.
Texte intégralCussenot, Olivier, et Géraldine Cancel-Tassin. « Le point sur la prédisposition génétique pour le cancer de la prostate ». Bulletin du Cancer 102, no 1 (janvier 2015) : 53–56. http://dx.doi.org/10.1016/j.bulcan.2014.12.007.
Texte intégralJalloh, M., M. Ndoye, TA Diallo, J. Mouanza, A. Diallo, MM Mbodji, I. Labou, L. Niang et S. Gueye. « C109 : Coût annuel de la prise en charge du cancer de la prostate de 105 patients hospitalisés à l’Hôpital Général Idrissa Pouye en 2018 ». African Journal of Oncology 2, no 1 Supplement (1 mars 2022) : S45—S46. http://dx.doi.org/10.54266/ajo.2.1s.c109.opfy7382.
Texte intégralSeddik, S., L. Brureau, R. Eyraud, P. Blanchet, M. Luc et M. Romana. « Facteurs de susceptibilité génétique de récidive du cancer de la prostate : étude des variants du gène DARC ». Progrès en Urologie 28, no 13 (novembre 2018) : 611–12. http://dx.doi.org/10.1016/j.purol.2018.07.008.
Texte intégralLabrie, F., A. Belanger, A. Dupont, G. Pelletier, V. Luuthe, J. Simard, L. Cusan, C. Labrie, Y. Lachance et R. Poulin. « Synthèse périphérique des androgènes chez l'homme. Génétique moléculaire du système et sa prise en compte dans le traitement du cancer de la prostate. » médecine/sciences 6, no 3 (1990) : 261. http://dx.doi.org/10.4267/10608/4127.
Texte intégralDiallo, I., ID Diamé, C. Diouf, ST Faye, A. Thiam, A. Yaya, O. Sow, B. Fall et L. Niang. « C64 : Les cancers urogénitaux en région périphérique du Sénégal : A propos de 156 cas ». African Journal of Oncology 2, no 1 Supplement (1 mars 2022) : S28. http://dx.doi.org/10.54266/ajo.2.1s.c64.lned9685.
Texte intégralNau, Jean-Yves. « Prostate : nouvelles données génétiques sur le cancer ». Revue Médicale Suisse 4, no 145 (2008) : 489. http://dx.doi.org/10.53738/revmed.2008.4.145.0489.
Texte intégralCussenot, Olivier, et Géraldine Cancel-Tassin. « Facteurs de risque génétiques pour le cancer de la prostate ». médecine/sciences 20, no 5 (mai 2004) : 562–68. http://dx.doi.org/10.1051/medsci/2004205562.
Texte intégral« Cancer héréditaire de la prostate : une première mutation génétique identifiée ». Revue Francophone des Laboratoires 2012, no 445 (septembre 2012) : 32. http://dx.doi.org/10.1016/s1773-035x(12)71666-0.
Texte intégralThèses sur le sujet "Prostate – Cancer – Génétique"
Valeri, Antoine. « Etude génétique, épidémiologique et clinique du cancer de la prostate familial ». Paris 5, 2000. http://www.theses.fr/2000PA05CD07.
Texte intégralCornu, Jean-Nicolas. « Facteurs de risques génétiques associés à la patho-biologie du vieillissement prostatique ». Phd thesis, Université Pierre et Marie Curie - Paris VI, 2014. http://tel.archives-ouvertes.fr/tel-01037914.
Texte intégralMiet, Sophie. « Analyse d'échantillons multiples de carcinomes prostatiques : identification d'altérations génétiques précoces ». Lyon 1, 1999. http://www.theses.fr/1999LYO1T130.
Texte intégralJagla, Monika. « Etude de l'impact de mutations du domaine de liaison à l'ADN sur les fonctions du récepteur des androgènes dans le cancer de la prostate ». Strasbourg 1, 2007. https://publication-theses.unistra.fr/public/theses_doctorat/2007/JAGLA_Monika_2007.pdf.
Texte intégralBantsimba, Malanda Gladys. « Facteurs de susceptibilité génétique associés à la progression des cancers de la prostate ». Paris 6, 2009. http://www.theses.fr/2009PA066128.
Texte intégralSiebert, Christelle. « Détection et fonction des récepteurs des androgènes tronqués dans le cancer de la prostate ». Strasbourg, 2010. https://publication-theses.unistra.fr/restreint/theses_doctorat/2010/SIEBERT_Christelle_2010_ED414.pdf.
Texte intégralIn 2010, the number of new cases of prostate cancers (PCa) is estimated at 71 600. With 10 000 deaths per year, PCa is in France the second cause of male mortality due to cancer. The dependence of cancerous cells towards androgens is taken into account in hormonal therapies against PCa. However, physiopathology of escape from hormonal therapies may involve several types of mechanisms. One is the emergence of mutations in the androgen receptor (AR) gene to promote proliferation and survival of cancer cells in the absence of androgens. Thereby, expression of genes involved in signaling pathways of growths factors or cytokines (CXCR4, CXCL12, EGFR, HER2, HER3, ET-A, VEGFR and Wnt11) was analyzed by RT-QPCR from samples presenting truncated AR variants. This study showed significant variation in the expression of EGFR, HER2, HER3 and Wnt11. A functional test realized in yeast was developed in the laboratory to detect truncated AR variants from PCa samples, but it is long and tedious. To overcome this situation, a more suitable version for routine detection of truncated AR variants was developed. This test has also been miniaturized into a 96-well plate to facilitate its routine use and its sensitivity was increased by using 2 ADE2 and lacZ reporter systems. The first validation of the new test confirmed that the new method is faster and more sensitive than the former. The final goal is to propose this test as an innovative tool for early detection of truncated AR variants in PCa and determination of subpopulations of patients
Brureau, Laurent. « Cancer de la prostate en Guadeloupe : Facteurs de risque génétique et environnementaux de survenue et de récidive après prostatectomie radicale ». Thesis, Antilles, 2015. http://www.theses.fr/2015ANTI0018/document.
Texte intégralProstate cancer is the most common tumor pathology in West Indies. Our study aims to study risk factors of occurrence and recurrence.To carry out this study, we used the patients included in the case-control study called Karuprostate and a cohort of patients after radical prostatectomy.The main results and conclusions of my work are:a) The study of genetic factors related to the metabolism of xenobiotics and the risk of prostate cancer occurrence in Guadeloupe. The exact number (CNV) gene encoding the glutathione S transferases GSTT1 and GSTM1 were determined in 629 incident cases of prostate cancer and 622 controls. Men having 2, 3 or more copies of GSTT1 have a significantly increased risk of prostate cancer. Similarly men with 3, 4, 5 or more copies of GSTM1 and GSTT1 combined have an increased risk of disease occurrence.b) The study of genetic factors related to estrogen metabolism and the risk of prostate cancer occurrence in Guadeloupe. Five polymorphisms (SNP 3 on CYP17, CYP1B1 and COMT as well as size and UGT1A1 polymorphisms on CYP19) were studied and compared in 498 incident cases and 565 controls. Individuals with the AA genotype COMT have a significantly decreased risk of prostate cancer occurrence. No significant association was found with other studied polymorphisms. A study of 150 incident cases of prostate cancer and 150 controls from a population of Congo-Zaire was the subject of these same genotyping, with the same results.c) The influence of environmental exposure to persistent pollutants with hormonal properties of biochemical recurrence of prostate cancer after radical prostatectomy. The plasma concentrations of chlordecone, DDE (the main metabolite of DDT) and PCBs were measured in 340 subjects with prostate cancer who underwent radical prostatectomy. The exhibition (preoperative) to chlordecone was found associated with a significant increased risk of biochemical recurrence. Conversely, the increasing concentrations of DDE were found associated with a significantly decreased risk of biochemical recurrence. No association was found between exposure to PCB153 and recurrence of the disease.d) The clinical and histological risk factors of recurrence of prostate cancer were studied in 964 patients who underwent radical prostatectomy with a médian follow-up of 4.8 years. Diabetes, PSA, advanced clinical stage, high Gleason score, a high percentage of prostate biopsy, advanced pathological stage, the presence of positive margins are predictors of biochemical recurrence after radical prostatectomy.Our results show that the occurrence and recurrence of prostate cancer are Under influence of genetic and environmental factors. The specific genetic and environmental context in Guadeloupe may partly explain the high incidence of prostate cancer.In addition, further work will incorporate other genes in the future. The next ambitious project is the creation of a prospective cohort of all patients with all prostate cancer stages
Lapouge, Gaëlle. « Mécanismes d'action d'une nouvelle classe de mutations du récepteur des androgènes dans les cancers de la prostate ». Université Louis Pasteur (Strasbourg) (1971-2008), 2007. https://publication-theses.unistra.fr/public/theses_doctorat/2007/LAPOUGE_Gaelle_2007.pdf.
Texte intégralTurpin, Anthony. « Étude des gènes réprimés par le récepteur aux androgènes dans les cancers de la prostate résistants à la castration et leur évolution neuroendocrine ». Thesis, Lille, 2021. http://www.theses.fr/2021LILUS012.
Texte intégralThe presence of fusion genes, resulting from TMPRSS2:ERG chromosomalrearrangements in more than 50% of cases, leads to deregulation of the prostate cancertranscriptome. Androgen receptor (AR), a member of the nuclear receptor family, remains themajor actor in the development of prostate cancer.Our objective is to identify genes that may be involved in the evolution of prostate cancer, in relation to the TMPRSS2:ERG fusion and AR.Using a transcriptomic analysis, derived from a PC3c prostate tumour cells line model over expressing TMPRSS2:ERG fusion, we have identified two genes regulated by the fusion:Plexin A2 (PLXNA2), already described in the literature by the team (Tian et al. Oncogene.2014), and also Fascin-1 (FSCN1) coding for a protein that groups actin filaments together and isinvolved in migration and tumour invasion phenomena through invadopods formation. Wesearched for functional partners of PLXNA2, performing an in silico study with Ingenuity Pathway Analysis® software, and have identified Neuropilin-1 (NRP1) as a potentially deregulated gene by fusion. On the other hand, we have evaluated the involvement of FSCN1,associated with the evolution of several cancers but poorly known in prostate cancer.For each selected gene, we have determined, for clinical validation, their expression inhuman samples of primary prostate cancers, also by analyzing published cohort data andmonitoring their expression in vivo by immunohistochemistry in advanced cancers. We havealso studied their functional role in vitro, in hormone-independent and neuroendocrine cellmodels. Finally, we performed a bioinformatics analysis and searched in the published ChIPseq-ERG and -AR data, the existence of ERG or AR factor binding on the 2 genes NRP1 andFSCN1. Once identified, we have performed in vitro ChIP experiments using the availablecellular models and we have demonstrated the direct regulation of NRP1 and FSCN1 by AR.Together, our results highlight NRP1 and FSCN1 as genes repressed by AR, which arere-expressed in the phase of resistance to castration and are potential actors of neuroendocrinedifferentiation when the level of AR is low or inactive. Their regulation by the TMPRSS2:ERGfusion and its precise mechanisms, in relation to AR and co-factors, need to be furtherdemonstrated. However, these two genes could play a role in the mechanisms of resistance tohormone-based therapies such as androgenic deprivation or selective competitive silentantagonist of AR, and could constitute therapeutic targets in the future
Grelet, Elise. « Identification des mécanismes moléculaires et cellulaires sous jacents à la perte de Pten dans l’épithélium prostatique murin et étude du rôle de la Vitamine D dans la carcinogenèse prostatique ». Thesis, Strasbourg, 2018. http://www.theses.fr/2018STRAJ111.
Texte intégralProstate cancer is the 2nd leading cause of cancer-related deaths in males of western societies. Mutations or deletion of the PTEN locus are common in prostate cancer, and are associated with metastasis and resistance to therapeutic castration. Our results show that Pten-loss induces the proliferation of PEC leading to the formation of PIN. The hyperproliferation of PEC induces DDR followed by senescence entry of PEC. Epidemiological studies highlighted that low Vitamin D levels correlate with aggressive prostate cancer. We show that Vdr and Gemini-72, an hypocalcemic Vitamin D analog, have anti-proliferative and anti-inflammatory activities during PIN formation. Moreover, the Gemini-72 induces apoptosis in senescent cells, modulates the immune response and consequently decreases the number of High Grade PIN and reduces the stromal reaction. Thus, our study demonstrate the major role of Vitamin D signaling in prostate carcinogenesis