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Статті в журналах з теми "Réponse aux thérapies"
D, Y. M. "Prédire la réponse aux thérapies ciblées en oncologie pulmonaire." Option/Bio 24, no. 490-491 (May 2013): 5. http://dx.doi.org/10.1016/s0992-5945(13)71260-1.
Повний текст джерелаGoy, Erwan, and Corinne Abbadie. "Sénescence et cancer." médecine/sciences 34, no. 3 (March 2018): 223–30. http://dx.doi.org/10.1051/medsci/20183403010.
Повний текст джерелаJean-Lionel, Bagot. "L’homéopathie, une réponse intéressante aux effets secondaires des thérapies ciblées." La Revue d'Homéopathie 8, no. 3 (September 2017): 130–36. http://dx.doi.org/10.1016/j.revhom.2017.07.020.
Повний текст джерелаLecomte, Conrad, and Tania Lecomte. "Au-delà et en deçà des techniques cognitives béhaviorales dans le traitement des troubles graves : les facteurs communs." Dossier : Schizophrénie, délires et thérapie cognitive 24, no. 1 (October 19, 2006): 19–38. http://dx.doi.org/10.7202/031583ar.
Повний текст джерелаVétizou, Marie, Romain Daillère, and Laurence Zitvogel. "Rôle du microbiote intestinal dans la réponse aux thérapies anti-tumorales." Biologie Aujourd'hui 211, no. 1 (2017): 51–67. http://dx.doi.org/10.1051/jbio/2017009.
Повний текст джерелаEhmke, Ivan, Marie-Françoise Charpin, Florent Girin, Laurent Hersent, Isabelle Odin, and Magali Briane. "Soutien des équipes de santé mentale aux équipes MCO : une expérience de la crise Covid." SHS Web of Conferences 133 (2022): 02002. http://dx.doi.org/10.1051/shsconf/202213302002.
Повний текст джерелаAubertin, Kelly, Max Piffoux, Anna Sebbagh, Jeanne Gauthier, Amanda K. A. Silva, and Florence Gazeau. "Applications thérapeutiques des vésicules extracellulaires." médecine/sciences 37, no. 12 (December 2021): 1146–57. http://dx.doi.org/10.1051/medsci/2021207.
Повний текст джерелаSaillant, Francine, Nicole Rousseau, and Danièle Desjardins. "Thérapies douces et quête des sens." II. Autres corps, autres sens, no. 24 (November 10, 2015): 63–72. http://dx.doi.org/10.7202/1033938ar.
Повний текст джерелаOrain-Pelissolo, S. "Les autres indications des thérapies de pleine conscience en psychopathologie." European Psychiatry 29, S3 (November 2014): 661. http://dx.doi.org/10.1016/j.eurpsy.2014.09.045.
Повний текст джерелаCortot, A. B. "Évaluation de la réponse à la chimiothérapie, aux thérapies ciblées et à l'immunothérapie." Revue des Maladies Respiratoires Actualités 7, no. 4 (November 2015): 455–61. http://dx.doi.org/10.1016/s1877-1203(16)30029-5.
Повний текст джерелаДисертації з теми "Réponse aux thérapies"
Girard, Nicolas. "Réponse des chondrosarcomes aux traitements conventionnels et recherche de thérapies innovantes." Caen, 2015. http://www.theses.fr/2015CAEN2070.
Повний текст джерелаChondrosarcomas (CHS) are malignant bone mesenchymal tumors and known to be radio- and chemo-resistant. In this context, the aim of this study was to determine their sensitivity to conventional treatments (X-ray and cisplatin), to better characterize their resistance mechanisms and to identify new therapeutics targets (epigenetic therapy targeting the methyltransferase EZH2 and hadrontherapy by carbon ions). First, we showed that CHS had different sensitivities to X-rays and cisplatin. Moreover, X-rays induced apoptosis or senescence of sensitive cells whereas cisplatin induced only apoptosis. Resistance mechanisms are different and are strongly linked to CHS type. Furthermore, we showed for the first time that CHS were more sensitive in vitro to carbon ions than X-rays. Second, we investigated the efficiency of epigenetic therapy using an EZH2 inhibitor. We showed that the inhibitor reduces chondrosarcomas growth, both in vitro and in vivo. However, its molecular mechanisms remains unclear even if it is independent of EZH2. This work highlights the heterogeneity and the variety of chondrosarcomas responses to conventional treatments. Therefore, it is of importance to use chondrosarcomas with different grades and origins. Moreover, we confirm the interest of the hadrontherapy by carbon ions to treat CHS
Perkins, Géraldine. "Marqueurs moléculaires prédictifs de réponse aux thérapies ciblées dans les cancers digestifs." Phd thesis, Université René Descartes - Paris V, 2012. http://tel.archives-ouvertes.fr/tel-00829655.
Повний текст джерелаHarlé, Alexandre. "Marqueurs de réponse aux thérapies ciblées et personnalisation thérapeutique dans les cancers colorectaux métastatiques." Thesis, Université de Lorraine, 2014. http://www.theses.fr/2014LORR0267/document.
Повний текст джерелаColorectal cancer is the third most common cancer worldwide with more than one million patients diagnosed each year, among 50% will develop metastatic disease. Recent efforts to improve the treatment of metastatic colorectal cancer (mCRC) has led to the development of monoclonal antibodies such as cetuximab and panitumumab, that inhibit the activation of the Epidermal Growth Factor Receptor (EGFR) and its downstream pathways (namely RAS/RAF/MAPK and PI3K/AKT/mTOR) that promote cell growth, proliferation, inhibition of apoptosis, invasion and metastasis. However, from studies including “RAS wild-type” i.e. KRAS and NRAS wild-type tumors, the response rates to cetuximab or panitumumab therapy ranged from only 40 to 60% which results in a large fraction of patients without any known causes for treatment failure. The presence of alterations in other genes such as PIK3CA or BRAF in the EGFR-dependent signaling pathways is responsible for some of the non-responding cases. Moreover, overexpression or alterations of proteins such as PTEN, PI3K, AKT, involved in the RAS/RAF/MAPK or PI3K/AKT/mTOR signaling pathways can have a significant impact on cell proliferation or apoptosis. Absence or overexpression of proteins under their active phosphorylated forms may be of interest to predict response to anti-EGFR in RAS wild-type patients. In this work, we first developed assays to assess RAS and PIK3CA mutations in formalin fixed paraffin embedded colorectal tumors, then we validated these assays according to ISO 15189 and we finally studied expression of downstream signalling phosphoproteins and KRAS, NRAS, BRAF and PIK3CA status in 100 frozen samples of patients with mCRC and treated with anti-EGFR. Among the 100 tumor samples, 60 were RAS wild-type. Among the RAS wild-type patients, 45.0% achieved a complete or partial response, and 55.0% had a stable disease or progression (p<0.001) when treated with anti-EGFR. Patients with a RAS mutation had significant lower progression-free survival (PFS) (HR=3.04[1.91; 4.83];p<0.001) and overall survival (OS) (HR=2.49[1.56; 3.97];p<0.001). PFS and OS were significantly higher in RAS wild-type patients. Expression of pAKT, pERK1/2 and pMEK1 was significantly lower in RAS wild-type patients than in RAS mutated patients (p=0.0246; p=0.004; p=0.0110 respectively) and no significant difference was observed between RAS wild-type and RAS mutated tumors in the expression of pEGFR, pGSK3, pIGFR, pP70S6K and pP90SRK. In RAS wild-type patients, response rate was significantly higher for tumors that overexpressed pEGFR and pAKT above the calculated threshold (p=0.0258 and p=0.0277 respectively). No significant relation was found between response rate and the level of expression of the other phosphoproteins. Our study shows that combining the analysis of the expression of EGFR downstream signalling phosphoproteins, RAS, BRAF or PIK3CA status could be of interest to predict the response to anti-EGFR therapies in patients with mCRC
Abou, faycal Chérine. "Le sVEGFR1 : quel rôle dans la réponse aux thérapies antiangiogéniques dans les carcinomes pulmonaires squameux ?" Thesis, Université Grenoble Alpes (ComUE), 2016. http://www.theses.fr/2016GREAV022/document.
Повний текст джерелаVascular endothelial growth factors (VEGFs) and their receptors are regulators of physiological and pathological angiogenesis. In patients with squamous cell lung carcinoma (SCC), clinical trials evaluating anti-angiogenic therapies (AAG) have failed to identify strong benefits. Rather, these patients are at higher risk of bleeding complications when exposed to Bevacizumab (BVZ), a humanized monoclonal anti-VEGF-A antibody. The soluble VEGF receptor-1, namely sVEGFR1, is a truncated version of the cell membrane-spanning VEGFR1 that only retains the first six N-terminal Ig-like extracellular motifs of VEGFR1 owing to alternative splicing of its pre-mRNA. As a consequence, sVEGFR1 is mainly viewed as an anti-angiogenic factor that counteracts VEGF-A functions on endothelial cells. Moreover, high levels of sVEGFR1 were correlated with bad prognosis and bad response to therapies in many cancer types. Using various SCC cell lines, we showed that Bevacizumab as well as VEGFR-Tyrosine Kinase Inhibitors (Semaxanib, KI8751) increase the intra- and extra-cellular levels of sVEGFR1. We confirmed this up-regulation in NCTU-induced SCC murine tumorgrafts models treated with VEGFR-TKI (sunitinib) or anti-VEGFR2 (DC101). Of note, this effect was never observed in the lung adenocarcinoma histological sub-type (ADC), using either cell lines or a mouse model treated in the same conditions. At the molecular level, we identified the VEGF165 and SOX2 proteins as crucial upstream regulators of sVEGFR1 in response to AAG. Moreover, we unraveled an original and SOX2 proteins as crucial upstream regulators of sVEGFR1 in response to AAG. Moreover, we unraveled an original ines or a mouse model treato discriminate between AAG-sensitive or -resistant SCC cells. Finally, in a series of 77 Non Small Cell Lung Carcinoma, we provided the first description of a differential pattern of sVEGFR1 expression with 11% and 44% of SCC exhibiting no or high expression respectively, high levels of sVEGFR1 being correlated with advanced pTNM stages. As a whole, our results provide the first evidence that AAG therapies upregulate sVEGFR1 expression in SCC cells. In addition, our data highlight an unexpected pro-tumoral function of sVEGFR1 through the activation of a beta 1 integrin-dependent VEGFR autocrine loop. These results might help to understand why SCC are less responsive to anti-angiogenic drugs than ADC and to identify SCC patients eligible to these therapies
Lion, Maëva. "Biomarqueurs prédictifs de la réponse aux traitements par thérapies ciblées dans le cancer du sein." Thesis, Université de Lorraine, 2015. http://www.theses.fr/2015LORR0287.
Повний текст джерелаBreast cancer is the most frequently diagnosed cancer in women and is a real public health problem.Advances in molecular biology have allowed the characterization of the major signaling pathways and revealed their major implication in carcinogenesis processes. Molecular targets have been identified and have enabled the development of targeted therapies, such as monoclonal antibodies, or kinase inhibitors. Despite these considerable advances that have improved the care of patients, emerging of resistance to treatments has been observed. The aim of this work was to identify new tumor biomarkers and determine their clinical significance, their theranostic interest and their impact on the response to targeted therapies. Initially, we studied the activating mutations of the PIK3CA gene. These mutations are found in 25% of breast cancers and are involved in resistance to trastuzumab, antiestrogens and mTOR inhibitors. We analyzed 149 invasive breast tumor samples for PIK3CA gene mutations by PCR-HRM (High Resolution Melting) and 118 by PCR-ARMS (Amplification Refractory Mutation System). The results achieved with the 2 techniques were consistent (k = 0.845; p <0.001) and a relationship between PIK3CA mutations and grade SBR was highlighted with a lower occurrence of mutations in SBR grade III tumors (p=0.025 in HRM and p=0.009 in ARMS). Secondly, we investigated the functional alteration of PI3K/AKT/mTOR, RAS/RAF/MAPKinases and P38MAPKinase signaling pathways. We have analyzed the expression level of phosphoproteins p-AKT, p-GSK3ß, p-S6 kinase, p-MEK1, p-ERK1 / 2, p-P90RSK, p-IGF1R and p-p38MAPK by multiplex immunoanalysis. This part includes 3 studies. The first study was a retrospective study of 45 frozen samples of invasive breast tumors in which we observed that the level of expression of P38 and p-P38 was higher in the ER + tumors. The second study was a prospective study to identify biomarkers of response to trastuzumab-everolimus association in patients with early breast cancer treated preoperatively. This study showed a statistically significant increase of the expression level of p-MEK1 (p = 0.012), p-ERK1/2 (p = 0.003) and p-p38MAPK (p<0.001) in arm treated by trastuzumab associated with everolimus. It could be explained by the repression of a negative feedback loop involving S6K, PI3K and RAS by everolimus, leading to the activation of RAS/RAF/MAPKinases signaling pathway. In the control arm investigating trastuzumab alone, no significant variations of the level of expression of phosphoproteins was demonstrated, raising the hypothesis of the implementation of a predominant immunological mechanism of action for Trastuzumab. The third study that compared effect of trastuzumab in vitro and in clinical setting confirms that trastuzumab has different modes of action when evaluated in cells and in clinical conditions. As a whole, this work showed that determining the mutation status of PIK3CA and the expression level of phosphoproteins could be useful to refine the molecular characterization of breast cancers and optimize the criteria used to personalize the prescription of targeted therapies
Gremeaux-Funck-Brentano, Elisa. "Marqueurs prédictifs de réponse aux inhibiteurs de BRAF dans le mélanome cutané métastatique." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS216/document.
Повний текст джерелаTargeted therapies have improved survival in patients with metastatic cutaneous melanoma, but some patients escape treatment. Response to treatment involves parameters dependent of the patient, the tumor biology, and the occurrence of resistance mechanisms extensively investigated. The aim of this work is to study two measurable markers in clinical practice in patient monitoring, for their predictive potential of response to BRAF inhibitors monotherapy; the first one is biological and the other one is pharmacological: mutant allele burden (MAB), defined by the ratio mutant/total, of BRAF and NRAS oncogenes, and plasma vemurafenib concentration (PVC).We report for the first time the prevalence and the mechanisms of BRAF and NRAS oncogenic allelic imbalance, defined by a high (>60%) or a low (≤30%) MAB, as opposed to a balanced “heterozygous” MAB (30 to 60%). In vitro experiments and in vivo data support the hypothesis that a BRAFV600E MAB >60% may be associated with a better response to BRAF inhibitors. NRAS MAB does not seem to be a baseline prognostic marker, but its predictive value of response to MEK inhibitors will be interesting to investigate.We demonstrated for the first time the impact of CPV assay during the monitoring of patients treated with monotherapy. A low CPV would be predictive of progression; thus, CPV appears to be an original predictive marker of response, for which the threshold value and the involved pharmacogenetic mechanisms remain to be determined
Billy, Frédérique. "Modélisation mathématique multi-échelle de l'angiogenèse tumorale : analyse de la réponse tumorale aux traitements anti-angiogéniques." Phd thesis, Université Claude Bernard - Lyon I, 2009. http://tel.archives-ouvertes.fr/tel-00631513.
Повний текст джерелаChastel, Carine. "Développement de thérapies anti-angiogéniques combinées à l'irradiation : étude de la réponse de promoteurs aux radiations ionisantes." Université Joseph Fourier (Grenoble), 2003. http://www.theses.fr/2003GRE10071.
Повний текст джерелаFrenel, Jean-Sébastien. "Evaluation de l'ADN circulant tumoral (ADNct) comme biomarqueur de réponse aux thérapies ciblées développées en phase précoce en oncologie." Thesis, Nantes, 2018. http://www.theses.fr/2018NANT1013/document.
Повний текст джерелаCirculating cell free DNA (ccDNA) deriving from tumor can be isolated in plasma of cancer patients. This circulating tumor DNA (ctDNA) shared the same genetics and epigenetics characteristics with the tumor and represents virtually a liquid biopsy. We evaluated whether targeted next-generation sequencing (NGS) of circulating tumor DNA (ctDNA) could be used for patient selection and as a tumor clone response biomarker in 39 patients with advanced cancers participating in early-phase clinical trials of targeted drugs. Overall, 159 plasma samples were sequenced with a mean sequencing coverage achieved of 1,685X across experiments. At trial initiation (C1D1), 23 of 39 (59%) patients had at least one mutation identified in cfDNA. Out of the 44 mutations identified at C1D1, TP53, PIK3CA and KRAS were the top three mutated genes identified, with 18 (41%), nine (20%), eight (18%) different mutations, respectively. In the second part of this work, we performed sequential NGS of ctDNA for the 23 patients with cfDNA mutation identified at C1D1. The monitoring of mutation allele frequency (AF) in consecutive plasma samples during treatment with targeted drugs demonstrated potential treatment associated clonal responses. Longitudinal monitoring of cfDNA samples with multiple mutations indicated the presence of separate clones behaving discordantly. Molecular changes at cfDNA mutation level were associated with time to disease progression. Targeted NGS of ctDNA has potential clinical utility to monitor the delivery of targeted therapies and future directions are discussed
Chrétien, Anne-Sophie. "Fonctionnalité de la signalisation en aval des récepteurs HER : implication dans la réponse cellulaire et tumorale aux thérapies ciblées." Thesis, Nancy 1, 2011. http://www.theses.fr/2011NAN10050/document.
Повний текст джерелаTargeted therapies, monoclonal antibodies and tyrosine kinase inhibitors, directed against the Human Epidermal Growth Factor Receptors (HER) family, represent a major advance in oncology. Their efficacy depends on their ability to inhibit oncogenic signalling, including the RAS/RAF/MAPK and PI3K/AKT signalling pathways. Regardless of the expression of the molecular target, the efficacy of targeted therapies is independent on the genetic abnormalities of the tissue which are able to disrupt tumour cell signalling, and the research of these abnormalities is now included in the prescription criteria. The aim of this work was to evaluate the usefulness of assessing HER downstream signalling functionality using multiplex analysis of the phosphorylated forms of key intracellular kinase signalling. Proof of concept was first introduced with genetically modified cell lines models, showing the consequences of tumour genetic abnormalities on RAS/RAF/MAPK and PI3K/AKT signalling pathways and on response to cetuximab. In the second part of this work, after validation of the techniques used in clinical situation, we demonstrated the relevance of system biology approach, combining molecular biology and functional analysis with principal component analysis. Our results obtained in a retrospective clinical study in metastatic colorectal cancer, suggests that the use of data from the evaluation of HER downstream signalling pathways functionality could eventually find applications as predictive markers of clinical response to anti-HER targeted therapies
Частини книг з теми "Réponse aux thérapies"
"Les psychothérapies individuelles indiquées dans les troubles psychiques post-traumatiques de guerre." In Médecine et Armées Vol. 46 No.1, 91–96. Editions des archives contemporaines, 2018. http://dx.doi.org/10.17184/eac.7373.
Повний текст джерела