Academic literature on the topic 'Résistance aux thérapies'
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Journal articles on the topic "Résistance aux thérapies":
Massard, V., A. Harlé, L. Uwer, and J. L. Merlin. "Mutations du gène ESR1 : du fondamental à la clinique." Oncologie 21, no. 1-4 (January 2019): 29–32. http://dx.doi.org/10.3166/onco-2019-0027.
ROMÉO, É., O. GISSEROT, J. P. DE JAURÉGUIBERRY, and J. S. BLADÉ. "Principes de traitement des tumeurs métastatiques." Médecine et Armées Vol. 39 No. 1, Volume 39, Numéro 1 (February 1, 2011): 25–32. http://dx.doi.org/10.17184/eac.6429.
Boileau, M., N. Germain, S. Magne, L. Mortier, and P. Marchetti. "Implication des cellules de la lignée adipocytaire dans la résistance aux thérapies ciblées dans le mélanome métastatique." Annales de Dermatologie et de Vénéréologie 147, no. 11 (November 2020): A17. http://dx.doi.org/10.1016/j.annder.2020.08.020.
Hamann, Pierre, Michael Cerezo, Vagner Stephan, and Caroline Robert. "Rôle du complexe d’initiation de la traduction eIF4F dans la résistance aux thérapies ciblant des points de contrôle immunitaire." Annales de Dermatologie et de Vénéréologie - FMC 1, no. 8 (December 2021): A121. http://dx.doi.org/10.1016/j.fander.2021.09.547.
Leonardi, Lucas, Sophie Sibéril, Marco Alifano, Isabelle Cremer, and Pierre-Emmanuel Joubert. "L’autophagie modulée par les virus." médecine/sciences 38, no. 2 (February 2022): 159–67. http://dx.doi.org/10.1051/medsci/2022010.
Gazzeri, Sylvie. "L’EGFR nucléaire : un nouveau mode de signalisation dans les cancers." Biologie Aujourd'hui 212, no. 1-2 (2018): 27–33. http://dx.doi.org/10.1051/jbio/2018016.
Hochmann, Jacques. "Brêves réflexions sur les résistances aux thérapies corporelles." Adolescence 81, no. 3 (2012): 577. http://dx.doi.org/10.3917/ado.081.0577.
Zaccagnino, Maria, Martina Cussino, Chiara Callerame, Cristina Civilotti, and Isabel Fernandez. "Anorexie mentale et EMDR : un cas clinique." Journal of EMDR Practice and Research 12, no. 4 (November 2018): E64—E76. http://dx.doi.org/10.1891/1933-3196.12.4.e64.
Capovilla, Mathieu. "Effets secondaires carcinogènes et résistances aux thérapies ciblées anti-BRAF." Annales de Pathologie 33, no. 6 (December 2013): 375–85. http://dx.doi.org/10.1016/j.annpat.2013.09.003.
Schmitt, L., S. Prebois, and A. Yrondi. "Quelle stratégie psychothérapeutique pour les déprimés résistants aux antidépresseurs ?" European Psychiatry 30, S2 (November 2015): S22. http://dx.doi.org/10.1016/j.eurpsy.2015.09.070.
Dissertations / Theses on the topic "Résistance aux thérapies":
Geneste, Aline. "Tissu adipeux et résistance tumorale aux thérapies ciblées." Thesis, Lyon, 2018. http://www.theses.fr/2018LYSE1115/document.
Targeted therapies as tyrosine kinase inhibitors permitted an improvement of breast cancer therapies by targeting HER2. However, resistance has been observed in obèse patients for lapatinib treatment.We reproduced the effect of resistance of breast cancer cells to laaptinib in presence of adipose tissue as observed for other therapies. Tumor cells overexpressing HER2 was partly resistant to lapatinib but also for other tyrosine kinase inhibitors when in contact with adipocyte-conditioned medium. By impnating human adipose tissue nad human tumors in mice, we were able to study rhe resistance of breast tumor cells in vivo.In order to elucidate the mechanism of such resistance, we exposed the adipocytes to several metabolism modulators. The lapatinib-induced cell cytotoxicity was lower for the tumor cells exposed to the conditioned medium from adipocytes earlier exposed to alpha blockers than to the conditioned medium from adipocytes alone. In the same manner, the toxicity was lower for the agonists of alpha-adrenergic receptors , for beta-blockers and for the lipolysis inhibitors. At the opposite, the cytotoxicity was enhanced for tumor cells in contact with the conditioned medium of adipocytes exposed to the agonists of beta adrenergic receptors.At the tumor cell level, the laaptinib-induced cell cycle arrest was reduced for the tumor cells exposed to the conditioned medium regarding the G0/G1 phase. That was verified by the study of the expression of genes involved in the cell cycle progression
Lhuissier, Eva. "Chondrosarcome : mécanismes de résistance aux traitements conventionnels et thérapies innovantes." Thesis, Normandie, 2017. http://www.theses.fr/2017NORMC407/document.
Chondrosarcomas are bone malignant tumors, considered as radio- and chemo-resistant, due to their hypoxic environment. In this context, this study aimed to better understand the role of hypoxia in the resistance of these tumors to chemotherapy (cisplatin) and radiotherapy (X-rays) and to identify new therapeutic strategies to re-sensitize chondrosarcomas by epigenetic targeting of H3K27 methylation. First, we showed that, contrary to what is commonly accepted, hypoxia has differential effect on cisplatin or X-ray sensitivity in chondrosarcomas, while it increases cisplatin resistance and X-ray sensitivity only in one cell line. Secondly, 3-deazaneplanocin A (DZNep) induces apoptosis in these tumors by a mechanism independent of H3K27 methylation and its methylase EZH2 and seems to act through the Rhoβ / EGFR pathway. However, it causes side effects on male fertility. In addition, its association with cisplatin potentiates its toxic effects on chondrosarcomas. The GSK-J4, on the other hand, decreases cell growth and its association with cisplatin increases this effect.This study highlights that chondrosarcomas use different cellular regulation mechanisms, showing the importance of conducting studies on several cell lines in order to better predict the response to treatments. In addition, these studies demonstrate the anti-tumoral properties of DZNep and GSK-J4 in the treatment of these tumors
Kammerer-Jacquet, Solène-Florence. "Carcinome à cellules claires du rein : phénotype métastatique et résistance aux thérapies ciblées." Thesis, Rennes 1, 2016. http://www.theses.fr/2016REN1B038.
Clear cell renal cell carcinoma (ccRCC) is the most common kidney cancer. It is characterized by frequent inactivation of the tumor suppressor gene VHL found in 70% of tumors leading to the transcription of HIF transcription factor target genes such as VEGF. This is an aggressive tumor with 50% of metastatic patients. Sunitinib, an inhibitor of receptor tyrosine kinase antiangiogenic, is currently the most used in 1st line despite 30% of patients who progress quickly. The advent of a new anti-angiogenic targeting MET (cabozantinib) and immunomodulators (anti-PD-1 antibody, nivolumab) makes crucial discovery of predictors of response to treatment. In the first part, we studied a retrospective study of 98 consecutive ccRCC. We assessed complete VHL status and correlated it with the expression of PD-L1. Moreover, while the prognosis is different between ccRCC synchronous metastatic and metachronous, their phenotype have never been compared. In this purpose, we performed an analysis of the main pathological prognostic factors, immunohistochemical markers (CAIX, VEGF, PAR3, PD-1 and PD-L1) and molecular (VHL status: deletion, mutation and promoter methylation) correlated with specific survival. We demonstrated that non-inactivated VHL tumors (niVHL) were associated with the presence of synchronous metastases, sarcomatoid component, a dense lymphocytic infiltrate, an overexpression of VEGF, an expression of PD-L1 and a poor prognosis. We also compared the phenotypes of metachronous and synchronous metastatic ccRCC. The first ones were associated with sarcomatoid component, cytoplasmic expression of PAR-3 overexpression VEGFA and niVHL status and a poor prognosis even from the diagnosis of metastases. In the second part, we studied a retrospective study of 90 consecutive metastatic ccRCC treated with first line sunitinib to identify predictors of response or resistance. We used the same techniques as above plus the MET status (mutation in Next-Generation sequencing and expression by IHC). Patients were classified as primary-refractory, intermediate and long-term responders depending on the duration of their response as assessed by radiological criteria (RECIST). We also characterized the genetic profile of 73 ccRCC of this series by CGH array for which we had frozen tumor. Primary refractory patients often had poor prognosis (Heng criteria), liver metastases, infiltration of the hilar fat. Cytogenetically, their tumors had many more genetic alterations, both gains as losses. These recurrent alterations were gains of 5p, 7p, 8q22.1-qter and loss of 6q21-q25.3 region. The multivariate Cox model highlighted four independent factors: the score of Heng, liver metastases, infiltration of the hilar fat and gain of 8q which integrated into a prognostic nomogram had a c-index of 0.74 for survival progression-free survival and 0.77 for overall survival. In conclusion, our study identified a subtype of ccRCC with a poor prognosis with niVHL status that should be explored at the genomic level. Furthermore, we showed a phenotype difference between ccRCC synchronous and metachronous metastatic patients whereas their care is currently the same. Finally we have identified a prognostic nomogram in metastatic ccRCC treated with sunitinib in the first line. This nomogram if confirmed by a larger prospective study could have a significant clinical impact in the selection of patients most likely to benefit from anti-angiogenic therapy
Delmas, Audrey. "Rôle de la petite GTPase RhoB dans la résistance des mélanomes aux thérapies ciblées." Toulouse 3, 2013. http://thesesups.ups-tlse.fr/2465/.
Melanoma treatment recently met a breakthrough with the approval of Vemurafenib, a BRAFV600E inhibitor. However, its efficiency is limited as patients rapidly develop resistances still misunderstood. This project reveals an original pathway involved in resistance to Vemurafenib and also to MEK inhibitors, another new therapeutic class approved in melanoma. In response to Ras/Raf/MEK/ERK pathway inhibition by B-Raf or MEK inhibitors, c-Jun is overexpressed and activated leading to RhoB overexpression by an iCCAAT box-dependent transcriptional activation. Induced RhoB favors cell survival in response to these inhibitors in an AKT-dependent manner. Inhibition of the c-Jun/RhoB/AKT pathway with siRNA or AKT inhibitors potently increases B-Raf and MEK inhibitors efficiency through apoptosis triggering. In conclusion, we identified for the first time the involvement of the c-Jun/RhoB/AKT pathway in Vemurafenib resistance and demonstrated the synergism of the Vemuranib/AKT inhibitor association. In fact, we demonstrated, at molecular level, the relevance of current clinical evaluation of B-Raf/MEK and AKT inhibitors association
Hatat, Anne-Sophie. "Epissage Alternatif d'ATG16L1b : un rôle dans l'échappement des tumeurs pulmonaires aux thérapies anti-EGFR." Thesis, Université Grenoble Alpes (ComUE), 2018. http://www.theses.fr/2018GREAV027/document.
Identifying what is a driver oncogene and developping small molecules that are able to targetits activity led to drastic changes in NSCLC treatments. EGFR is a transmembrane receptorwith Tyrosine Kinase (TK) activity allowing signal transmission from the environment towardsthe inner of the cell by signaling pathways activation. Among those signaling pathways arefound survival and proliferation pathways. Activating mutations make EGFR a driver onco-gene, which was the first protein to be identified as such. Hence numerous chemical compoundtargeting mutated EGFR (EGFR-TKI, gefitinib) have been developped. Their use in clinicsrepresent a huge improvement for patients care. However resistance mechanisms ultimatelyoccur. Transcriptomic analyses of acquired resistant models to EGFR-TKI have shown thattheir RNA transcripts expression is abnormal. Moreover results from the team have demons-trated that SR proteins (splicing factor) expression is deregulated in NSCLC. Based on thoseresults we hypothesized that SRSF2 mediated alternative splicing of mRNA could be involvedin resistance mechanims acquired by lung carcinoma in response to EGFR-TKIThe lab developped resistant clones by chronic exposure to gefitinib of EGFR mutated lungadenocarcinoma cellular models.We first observed the accumulation of the expression of SRSF2 protein in resistant clonescompared to the sensitive cell line. Secondly, sensitivity to gefitinib induced apoptosis of twoclones was resored when neutralising SRSF2. A RNA-seq analysis led us to identify Atg16L1 aspotentially being involved in the SRSF2-mediated sensitization to gefitinib-induced apoptosis.SRSF2 neutralisation modulates Atg16L1 splicing in response to gefitinib. Neutralisation ofExon 8 containing transcripts of Atg16L1 sensitizes resistant clones to gefitinib induced apop-tosis. This alternative splicing switch modulates autophagic activity of the cells in reponseto gefitinib. We have shown that exon8 containing transcripts favor autophagy inhibition inreponse to gefitinib. This work emphasize the role of Atg16L1 alternative splicing switch ofexon8 in autophagy inhibition and its correlation with a resistant phenotype in response toEGFR-TKI. SRSF2 may participate in the modulation of this alternative splicing switch inreponse to gefitinib
Guérard, Marie. "Signalisation nucléaire de l'IGF-1R et résistance aux thérapies anti-EGFR dans les cancers du poumon." Thesis, Université Grenoble Alpes (ComUE), 2016. http://www.theses.fr/2016GREAV085/document.
Responsible of 1.6 million deaths each year worldwide, lung cancer is today the leading cause of cancer mortality in the world. Non-small-cell lung cancers account for about 85% of lung cancer and have a very bad prognosis (5-year survival rate inferior to 10%). EGFR-TKI (EGFR tyrosine kinase inhibitors, gefitinib) are a real medical advance for lung cancers treatment. However, these treatments are efficient in a small subgroup of patients. So, one of the current issues is to identify primary resistance mechanisms involved in tumors.Tyrosine kinase receptors (RTK) activate intracellular signaling pathways from the plasma membrane. These last years, a nuclear translocation of the RTK was shown. Recent works suggest that RTK nuclear signaling could contribute to tumors resistance in response to anti-cancerous therapies.In our team, it was shown that activation of IGF-1R signaling is associated with lung adenocarcinoma progression and that gefitinib induces IGF-1R nuclear accumulation in a mucinous adenocarcinoma cell line. On the basis of these results, we hypothesize that nuclear IGF-1R could play a role in the resistance of mucinous lung adenocarcinoma to EGFR-TKI.Our results indicate that more than 70% lung adenocarcinoma tumors present a positive IGF-1R nuclear staining. Thanks to EGFR-TKI-resistant cell lines, we show that gefitinib induces the nuclear accumulation of IGF-1R in mucinous adenocarcinoma. This nuclear translocation involves clathrin-mediated endocytosis and a complex between IGF-1R, importin β1 and pro-amphiregulin. Amphiregulin silencing prevents IGF-1R nuclear translocation in response to gefitinib and restores gefitinib-induced apoptosis in vitro and in vivo. Our whole results identify that IGF-1R intracellular trafficking is a new component of response to EGFR-TKI and strongly suggest that a nuclear IGF-1R/amphiregulin signaling contributes to mucinous lung adenocarcinoma progression in response to EGFR-TKI
Blandin, Anne-Florence. "Rôle de l'intégrine α5β1 dans la biologie du glioblastome et dans la résistance aux thérapies anti-EGFR." Thesis, Strasbourg, 2015. http://www.theses.fr/2015STRAJ066/document.
Glioblastoma multiforme (GBM) is the most common primary brain tumor. Alteration of the EGFR pathway and high invasive potential are hallmarks of GBM. Unfortunately, trials using anti-EGFR therapies for the treatment of GBM reveal limited efficacy. We previously showed that overexpression of the fibronectin receptor, α5β1 integrin, is associated with a poor prognosis for patients and is responsible for chemoresistance to temodal. Integrins can cross-talk with growth factor receptors and amplified their oncogenic activity. Here, we sought to determine the potential role of α5 integrin in resistance to anti-EGFR therapy. Using U87 GBM cell line, we first confirmed that fibronectin-mediated integrin activation potentiated EGFR signaling. Loss of α5 integrin expression sensitized U87 cells to anti-EGFR drugs (cetuximab, gefitinib) in soft agar clonogenic assay. α5 expression can trigger resistance to both drugs on cell migration. To go further, we developed a new assay based on the quantification of cell evasion from tumor spheroids. α5 depletion increased U87 cell sensitivity to gefitinib and erlotinib, 2 EGFR-selective reversible TKI, but had not effect on lapatinib efficacy, an irreversible TKI that target EGFR, ErbB2, ErbB3 and ErbB4. Confocal microscopy revealed a strong impact of gefitinib on EGFR and integrin endocytosis. These results suggested that α5 expression may trigger resistance to TKI either by activating ErbB pathways or by controlling EGFR membrane trafficking. We also showed that to promote cell adhesion, α5 integrin stimulated fibronectin fibrillogenesis. As cells moved away from the spheroids, α5 became strictly engaged in cell-substratum adhesion sites where it recruited activated FAK. Our work highlights the pivotal role of fibronectin/α5β1 integrin in invasivity of GBM and resistance to anti-EGFR drugs
Diazzi, Serena. "Le cluster pro-fibrotique miR-143/145 favorise la plasticité phénotypique associée à la résistance des mélanomes aux thérapies ciblées." Thesis, Université Côte d'Azur, 2021. http://theses.univ-cotedazur.fr/2021COAZ6006.
Because of its intrinsic plasticity and resistance to treatment, melanoma is one of the most aggressive cancers. Due to the MAPK pathway hyperactivation, targeted therapies counteracting this signaling cascade are efficient in most patients harboring BRAFV600E metastatic melanoma. However, innate and acquired resistances constitute major therapeutic challenges. Acquired resistance to MAPK-targeted therapies arises from de novo genetic lesions and non-genetic events such as transcriptional reprogramming and epigenetic changes. Upon MAPK inhibitors exposure, melanoma cells assume functionally different phenotypic states defined by master transcription factors differential activity and fixed by epigenetic events. Among them, the emergence of a poorly differentiated cell state is strongly associated with resistance acquisition and tumor recurrence. Our team has previously shown that melanoma cells switching to a dedifferentiated phenotype in response to MAPK-targeted therapies display features of cancer-associated fibroblasts (CAFs) like extracellular matrix (ECM) remodeling and markers observed in fibrotic diseases, allowing them to generate a drug tolerant microenvironment.This fibrotic state is characterized in vitro and in vivo by increased deposition and altered ECM organization associated with a mechanophenotype regulated by the mechanotransducers YAP and MRTFA. However, post-transcriptional signaling networks that underpin this mesenchymal-like phenotype are still unknown and effective therapeutic treatments to overcome MAPK-targeted therapy resistance are missing. Given the tumorigenic role of ECM in cancer progression and resistance, therapies aimed at “normalizing” the tumorigenic ECM represent promising strategies to overcome non-genetic resistance to MAPK inhibitors. Based on the role of miRNAs in post-transcriptional regulation, I focused on the characterization of a pool of miRNAs, defined as “FibromiRs,” which have been shown to participate in the onset and progression of fibrotic diseases. Their crucial role in the fibrogenic process and the possibility to therapeutically manipulate them make them promising druggable targets to prevent the onset of resistance to MAPK-targeted therapies in melanoma. Starting from a screening designed to compare the expression of “FibromiRs” in MAPK inhibitors resistant mesenchymal melanoma cells compared to therapy-naive parental cells, we have identified the profibrotic miR-143/145 cluster as overexpressed in mesenchymal resistant cells. We then explored the profibrotic function of miR-143/145 cluster in the mesenchymal-like resistant cell state and melanoma phenotypic plasticity. First, we analysed the regulation of miR-143 and miR-145 in melanoma, identifying a negative regulation of the MAPK pathway on its expression and the involvement of signaling pathways typical of the mesenchymal resistant state, such as TGFβ and PDGF signaling, in the activation of their expression. Next, we investigated the function of the cluster in the context of adaptive and acquired resistance, showing its contribution in ECM reprogramming, activation of mechanotransduction pathways, and in driving the switch from a differentiated proliferative phenotype to a dedifferentiated invasive one with decreased sensitivity to MAPK inhibition. We characterized its mechanism of action, identifying FSCN1 as a key target gene of both mature miR-143 and miR-145 in the acquisition of the mesenchymal invasive phenotype. Finally, we tested the cluster as a potential therapeutic target in vitro and in vivo through antisense oligonucleotide-mediated inhibition of its expression or pharmacological modulation combined with MAPK inhibitors administration. Overall, this work highlights the importance of a FibromiR cluster in the acquisition of a dedifferentiated phenotype resistant to MAPK-targeted therapies and proposes new therapeutic strategies based on the inhibition of FibromiRs to overcome such resistance mechanism
Ben, Jouira Rania. "Implication de la matrice extracellulaire tumorale dans la transition phénotypique et la résistance aux thérapies ciblées du mélanome." Thesis, Université Côte d'Azur (ComUE), 2017. http://www.theses.fr/2017AZUR4140.
Cutaneous melanoma remains one of the most challenging and difficult cancers to treat because of its high plasticity, metastatic potential and resistance to treatment. New therapies targeting oncogenic BRAFV600E mutation have shown remarkable clinical efficacy. However, drug resistance invariably develops. Thus, the need for improving existing therapies remains critical. Recent studies have indicated that tumor resistance arises from the tumor microenvironment in which the extracellular matrix (ECM) is a determinant factor. Here, we found that BRAF inhibitor (BRAFi)-resistant melanoma cells, but not BRAFi-sensitive cells display an increased mechanosensitivity associated with a capacity to produce and remodel a 3D ECM displaying increased levels of matrix proteins such as fibronectin (FN) and collagen fibers. Interestingly, our results show that this 3D ECM is able to protect therapy-sensitive cells from the anti-proliferative effects of MAPKi. In addition, short exposures of naive melanoma cells to MAPKi augment matrix proteins production and assembly in vitro and in vivo. This 3D ECM also promotes drug tolerance within BRAFi sensitive cells. In conclusion, our results suggest that a subset of resistance to MAPK targeted therapies is associated with the production by melanoma cells of a pathological fibrotic matrisome that may affect cell behavior and therapeutic response
Combès, Eve. "Mise en évidence d’intéractions létales par criblage phénotypique dans le contexte de la résistance aux thérapies du cancer colorectal." Thesis, Montpellier, 2017. http://www.theses.fr/2017MONTT134/document.
Today, treatments for metastatic colorectal cancer have evolved through the combination of conventional chemotherapy 5-FU, oxaliplatin and / or Irinotecan and targeted therapies directed against the EGF receptor or VEGF. Despite an improved survival rate through the combination of these drugs, innate and acquired resistance to treatment is a common cause of therapeutic failure.In order to discover new therapeutic targets we carried out several phenotypic screenings using cellular resistance models acquired to chemotherapies (oxaliplatin and irinotecan) generated in the laboratory as well as the HCT116 line which exhibits an innate resistance to anti-EGFR therapies (cetuximab , panitumumab, Erlotinib). The ultimate goal of this project is to reveal genes, whose inhibition restores sensitivity to one of these treatments, thus displaying a lethal interaction with the drug.Once the kinases potentially involved in resistance to CCR therapies identified, specific inhibition by shRNA and / or a specific inhibitor was performed to confirm the potential therapeutic targets and / or biomarkers for response to treatments. The most promising target, identified as a determinant of resistance to oxaliplatin is the ATR protein (Ataxia-telangiectasia mutated and rad3 related). A protein that plays a key role in DNA repair and is activated in response to the presence of persistent single stranded DNA (ssDNA) or replicative stress, which can be generated by certain anti-cancer therapies.The inhibition of ATR via its pharmacological inhibitor VE-822 (VX-970) combined with oxaliplatin was then studied by the use of cytotoxic tests supplemented by an additivity study. Thus, we demonstrated that the inhibition of ATR combined with oxaliplatin leads to a strong synergy in the HCT116-R1 cell line in both 2D and 3D. This effect is also found in other oxaliplatin resistant clonal lines (HCT116-R2, SW48-R) as well as in the cell lines originating from them (HCT116, SW48).We have also shown that the synergistic effect of oxaliplatin and VE-822 in the HCT116-R1 line is accompanied by an increase in the presence of single-stranded DNA followed by numerous double-stranded DNA breaks, stopping proliferation and inducing apoptosis. The occurrence of this damage to DNA is also correlated with activation of the ATM pathway, p53 and inhibition of CDK2 activity. Moreover, in vitro the double treatment causes an induction of the molecular signals triggering the immunogenic cell death equivalent or superior to the treatments by oxaliplatin alone.Finally, the combination of oxaliplatin + VE-822 is also effective in vivo in immunodeficient mice xenografted with HCT116-R1 cells as well as in immunologically competent mice with a higher synergistic effect indicating that immune death (ICD ) is part of the mechanism of this combination of drugs.In conclusion, all these data confirm the interest of phenotypic screening in the discovery of new therapeutic targets by demonstrating for the first time the functional role of ATR in sensitivity to oxaliplatin
Book chapters on the topic "Résistance aux thérapies":
LEBOEUF L’ANTHOËN, Isabelle, Marie DOBIGNIES, and Pascal ANTOINE. "Compassionate Mind Training." In Le patient et son entourage, 41–52. Editions des archives contemporaines, 2023. http://dx.doi.org/10.17184/eac.7536.
Trybou, Vincent. "Chapitre 15. Conseils aux thérapeutes dans le dépistage des résistances en thérapie." In Comprendre et traiter les TOC, 215–40. Dunod, 2016. http://dx.doi.org/10.3917/dunod.trybo.2016.01.0215.