Inhaltsverzeichnis
Auswahl der wissenschaftlichen Literatur zum Thema „Inhibiteurs de la poly (ADP-ribose) polymérase“
Geben Sie eine Quelle nach APA, MLA, Chicago, Harvard und anderen Zitierweisen an
Machen Sie sich mit den Listen der aktuellen Artikel, Bücher, Dissertationen, Berichten und anderer wissenschaftlichen Quellen zum Thema "Inhibiteurs de la poly (ADP-ribose) polymérase" bekannt.
Neben jedem Werk im Literaturverzeichnis ist die Option "Zur Bibliographie hinzufügen" verfügbar. Nutzen Sie sie, wird Ihre bibliographische Angabe des gewählten Werkes nach der nötigen Zitierweise (APA, MLA, Harvard, Chicago, Vancouver usw.) automatisch gestaltet.
Sie können auch den vollen Text der wissenschaftlichen Publikation im PDF-Format herunterladen und eine Online-Annotation der Arbeit lesen, wenn die relevanten Parameter in den Metadaten verfügbar sind.
Zeitschriftenartikel zum Thema "Inhibiteurs de la poly (ADP-ribose) polymérase"
Buxeraud, Jacques, und Sébastien Faure. „Le talazoparib (Talzenna®), un inhibiteur de poly(ADP-ribose) polymérase“. Actualités Pharmaceutiques 61, Nr. 614 (März 2022): 11–12. http://dx.doi.org/10.1016/j.actpha.2021.12.040.
Der volle Inhalt der QuelleBagot, Jean-Lionel, und Jean-Philippe Wagner. „Prévention et traitement des effets secondaires des inhibiteurs de la poly-ADP-ribose-polymérase-1 (iPARP) dans les cancers du sein et de l’ovaire“. La Revue d'Homéopathie 12, Nr. 3 (September 2021): 144–50. http://dx.doi.org/10.1016/j.revhom.2021.06.002.
Der volle Inhalt der QuelleWaissi, W., A. Nicol, M. Rousseau, G. Noël und H. Burckel. „Étude de la radiosensibilisation in vitro et in vivo par la gemcitabine et un inhibiteur de la poly(ADP-ribose) polymérase après irradiation par photons et protons, dans les cancers du pancréas“. Cancer/Radiothérapie 23, Nr. 6-7 (Oktober 2019): 796. http://dx.doi.org/10.1016/j.canrad.2019.07.021.
Der volle Inhalt der QuellePozo, FJO, G. de la Rubia Sanchez, Ménissier-de Murcia J und G. de Murcia. „La poly(ADP-ribose) polymérase : un facteur de survie.“ médecine/sciences 14, Nr. 11 (1998): 1196. http://dx.doi.org/10.4267/10608/937.
Der volle Inhalt der QuelleBoulu, Roger G., Christian Mesenge, Christiane Charriaut-Marlangue, Catherine Verrecchia und Michel Plotkine. „Mort neuronale : rôle potentiel d’une enzyme nucléaire, la poly(ADP-ribose) polymérase“. Bulletin de l'Académie Nationale de Médecine 185, Nr. 3 (März 2001): 555–65. http://dx.doi.org/10.1016/s0001-4079(19)34539-x.
Der volle Inhalt der QuelleRuf, A., J. Ménissier-de Murcia, GE Schulz und G. de Murcia. „Poly (ADP-ribose) polymérase : la structure cristallographique va permettre de développer de nouveaux médicaments antitumoraux.“ médecine/sciences 12, Nr. 11 (1996): 1269. http://dx.doi.org/10.4267/10608/664.
Der volle Inhalt der QuelleVambergue, Anne. „Stress oxydatif et activation de la poly-(ADP-ribose) polymérase: grossesse normale et diabète gestationnel“. Diabetologia Notes de lecture 1, Nr. 3-4 (17.11.2009): 33–34. http://dx.doi.org/10.1007/s13116-009-0017-3.
Der volle Inhalt der QuelleGonçalves, Anthony. „Inhibiteurs de la poly(ADP-ribose) polymerase et cancer du sein : bilan et perspectives“. Bulletin du Cancer 99, Nr. 4 (April 2012): 441–51. http://dx.doi.org/10.1684/bdc.2012.1553.
Der volle Inhalt der QuelleSchreiber, Valérie, Giuditta Illuzzi, Eléa Héberlé und Françoise Dantzer. „De la découverte du poly(ADP-ribose) aux inhibiteurs PARP en thérapie du cancer“. Bulletin du Cancer 102, Nr. 10 (Oktober 2015): 863–73. http://dx.doi.org/10.1016/j.bulcan.2015.07.012.
Der volle Inhalt der QuelleGirish, S., S. Desnoyers, W. Earnshaw, S. Kaufmann und GG Poirier. „La poly(ADP-ribose) polymérase (PARP): à la croisée des chemins de la réparation de l'ADN et de l'apoptose cellulaire.“ médecine/sciences 11, Nr. 10 (1995): 1487. http://dx.doi.org/10.4267/10608/2336.
Der volle Inhalt der QuelleDissertationen zum Thema "Inhibiteurs de la poly (ADP-ribose) polymérase"
Cosi, Cristina. „Rôle de la poly(ADP-ribose) polymérase dans la neurodégénérescence et de ses inhibiteurs en tant qu'agents neuroprotecteurs potentiels“. Toulouse 3, 1997. http://www.theses.fr/1997TOU30132.
Der volle Inhalt der QuelleGuillot, Clément. „Potentiel des inhibiteurs de poly(ADP-ribose) polymérases seuls ou en combinaison avec la radiothérapie comme nouvelle option thérapeutique pour le carcinome hépatocellulaire“. Thesis, Lyon 1, 2013. http://www.theses.fr/2013LYO10281.
Der volle Inhalt der QuelleHepatocellular carcinoma is the third cause of cancer related death. Due its often late diagnosis and advanced stage, a limited number of patients can benefit from curative treatments. There is thus a constant need for new treatment strategies for patients with hepatocellular carcinoma. Targeting DNA repair pathways to sensitize tumor cells to chemoor radiotherapeutic treatments is now a common strategy under investigation for cancer treatment with inhibitors of poly(ADP-ribose) polymerases (PARP) showing great potential. The aim of this work was to evaluate the potential of PARP inhibitors alone and in combination with radiation therapy as a new strategy for the treatment of hepatocellular carcinoma. We first analyzed the expression and activity of different PARP genes in a panel of liver cancer cell lines and primary human hepatocytes as well as their DNA repair capacity and assess the impact of PARP inhibitors alone and in combination with ionizing radiation in these models on cell survival. A large range in expression of PARP family members, PARP activity and sensitivity to ABT-888 in the panel of liver cells was observed as well as differential excision/synthesis repair capacity. Finally, we showed that ABT-888 sensitizes liver cancer cells to the cell killing effects of ionizing radiation. PARP inhibitors show great potential for improving radiation therapy strategies used in the management of hepatocellular carcinoma
Fernet, Marie. „Etude des mécanismes impliqués dans la réponse cellulaire précoce aux radiations ionisantes“. Paris 11, 2000. http://www.theses.fr/2000PA11T063.
Der volle Inhalt der QuelleMorice, Pierre-Marie. „Evaluation de la déficience de la recombinaison homologue et de la réponse des tumeurs ovariennes aux inhibiteurs de PARP grâce à l'utilisation de modèles de culture 3D en vue du développement d'un test prédictif Identifying eligible patients to PARP inhibitors: from NGS-based tests to promising 3D functional assays Automated scoring for assessment of RAD51-mediated homologous recombination in patient-derived tumor organoids of ovarian cancers Risk of myelodysplastic syndrome and acute myeloid leukemia related to PARP inhibitors: a combined approach using a safety meta-analysis of placebo randomized controlled trials and the World Health Organization's pharmacovigilance database The long non-coding RNA ‘UCA1’ modulates the response to chemotherapy of ovarian cancer through direct binding to miR-27a-5p and control of UBE2N levels“. Thesis, Normandie, 2020. http://www.theses.fr/2020NORMC414.
Der volle Inhalt der QuelleWorldwide each year, more than 150 000 women die from epithelial ovarian cancer largely due to emergence of resistance to chemotherapy. Approximately half of these cancers display molecular alterations that cause deficiency of DNA repair via homologous recombination (HRD), which confer sensitivity to PARP protein inhibitors (PARPi). To date, there is no test capable of fully identifying the HRD phenotype, thus limiting access to these treatments. In this context, we are developing functional assays based on the use of tumor explant slices and then, on the use of tumor organoids derived from ovarian tumors of chemotherapy-naive or previously treated patients. The culture of explants was unsuitable for this application and we then focused our work on tumor organoids. Tumor organoids were exposed to carboplatin (first-line treatment) and two PARP inhibitors (olaparib and niraparib) used for maintenance therapy. In parallel, we collected clinical data from patients (survival, platinum-free interval, RECIST, treatments) to evaluate the predictive potential of these models. The established tumor organoids responded heterogeneously to different drugs, and our results show that the organoid-based assay is capable of identifying patients highly resistant to carboplatin, suggesting that this functional assay could have a predictive value for patients treated with carboplatin. Regarding the potential of organoids in predicting PARPi response, multiple sensitivity profiles have been identified, but the correlation with clinical response has yet to be determined by studies conducted on tumor samples from patients treated with these drugs
Noel, Georges. „Effets d'un inhibiteur de la poly (ADP-ribose) polymérase 1 (PARP-1) sur la réparation des cassures double-brin de l'ADN et la létalité cellulaire radio-induite en phase S“. Paris 11, 2007. http://www.theses.fr/2007PA11T082.
Der volle Inhalt der QuelleThorel, Lucie. „Utilisatiοn de tests fοnctiοnnels pοur la prédictiοn de la répοnse des cancers οvariens à la chimiοthérapie cοnventiοnnelle et aux inhibiteurs de ΡARΡ : intérêt des οrganοides tumοraux“. Electronic Thesis or Diss., Normandie, 2024. http://www.theses.fr/2024NORMC416.
Der volle Inhalt der QuelleOvarian cancers are the second leading cause of death from gynecological cancers worldwide, primarily due to late diagnosis combined with the development of resistance to chemotherapy. Approximately half of these cancers exhibit alterations in homologous recombination (HR), making them sensitive to PARP protein inhibitors (PARPi), which are involved in DNA repair. However, identifying patients who respond to chemotherapy and selecting those eligible for PARPi remains a challenge for clinicians. In this context, the use of patient-derived tumor organoids (PDTO) for predictive functional testing represents a promising approach to guide therapeutic choices in first-line treatment and beyond. The aim of this thesis is to study the feasibility of functional tests based on PDTO to evaluate their potential applicability in precision medicine. Establishing a panel of PDTO derived from various ovarian histological subtypes has demonstrated that these models recapitulate the histological and molecular characteristics of their tumors of origin. Following direct exposure functional tests of the tumor organoids to first- and second-line treatments, we showed that these models exhibit heterogeneous responses to treatments, and particularly that PDTO identified by the predictive test as sensitive to carboplatin mainly originated from responding patients. Additionally, we investigated the results of a functional test assessing HR status, the RECAP test, and demonstrated that this test is complementary to the current method for determining HR status, which relies on NGS sequencing techniques. Although larger-scale investigations are needed to confirm the potential of tumor organoids, these results provide further support for the use of ovarian tumor organoids in the context of precision medicine
Morel, Daphné. „Identifying Synthetic Lethal and Selective Approaches to Target PBRM1-Deficiency in Clear Cell Renal Cell Carcinoma PBRM1 Deficiency in Cancer is Synthetic Lethal with DNA Repair Inhibitors Exploiting Epigenetic Vulnerabilities in Solid Tumors: Novel Therapeutic Opportunities in the Treatment of SWI/SNF-Defective Cancers Combining Epigenetic Drugs with other Therapies for Solid Tumours — Past Lessons and Future Promise Targeting Chromatin Defects in Selected Solid Tumors Based on Oncogene Addiction, Synthetic Lethality and Epigenetic Antagonism“. Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASL017.
Der volle Inhalt der QuellePolybromo-1 (PBRM1) inactivation occurs in multiple malignancies and is of particular importance in clear cell renal cell carcinomas (ccRCC), as it drives 40 to 50% of cases. Currently, no precision-medicine approach uses PBRM1 deficiency to specifically target tumour cells. To uncover novel synthetic lethal approaches to treat PBRM1-defective cancers, we performed (i) a high-throughput pharmacological screening, evaluating the sensitivity to 167 small molecules in a PBRM1-isogenic cellular model, and the (ii) systematic mapping of the whole transcriptomic and proteomic profiles associated with PBRM1 loss-of-function within this model. We further investigated the mechanism underlying this synthetic lethal relationship.We identified and validated synthetic lethal effects between PBRM1 loss and both PARP and ATR inhibition. Combinatorial use of PARP with ATR inhibitors exerted additive cytotoxic effects in PBRM1-defective tumor cells. These synthetic lethal relationships were characterized by a pre-existing replication stress in PBRM1-deficient cells associated with mitosis and DNA damage repair abnormalities, which were exacerbated upon PARP inhibition selectively in PBRM1-defective cells.These data provide the preclinical basis for evaluating PARP inhibitors as a monotherapy or in combination in patients with PBRM1-deficient ccRCC
Moreel, Xavier. „Proteomique fonctionnelle des poly(ADP-Ribose) polymerases“. Thesis, Université Laval, 2010. http://www.theses.ulaval.ca/2010/27251/27251.pdf.
Der volle Inhalt der QuelleToledano, Elie. „Régulation de la poly (ADP-Ribose) Polymérase par le phosphoadénosine phosphate“. Paris 6, 2011. http://www.theses.fr/2011PA066597.
Der volle Inhalt der QuelleIsabelle, Maxim. „Interactome des intervenants dans le métbolisme du poly(ADP-ribose)“. Doctoral thesis, Université Laval, 2012. http://hdl.handle.net/20.500.11794/24171.
Der volle Inhalt der Quelle