Thèses sur le sujet « Response to therapies »
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Massó, Vallés Daniel. « Inhibiting Myc and the Myc dependent inflammatory response as cancer therapies ». Doctoral thesis, Universitat Autònoma de Barcelona, 2017. http://hdl.handle.net/10803/458137.
Texte intégralThe work of this thesis was carried out in the Mouse Models of Cancer Therapies Laboratory led by Dr. Laura Soucek in the Preclinical Research Program of the Vall d’Hebron Institute of Oncology (VHIO), and comprises two differentiated parts centered on two oncogenic functions of Myc. In the first project we validated the pharmacological inhibition of mast cells as a therapeutic strategy against pancreatic ductal adenocarcinoma (PDAC). To do so, we made use of the Bruton’s tyrosine kinase (BTK) inhibitor ibrutinib in mouse models of PDAC, the most common and aggressive pancreatic tumor. Treatment with ibrutinib inhibited mast cell degranulation, reduced cell proliferation and leukocytic infiltration in the tumor stroma and dramatically reduced collagen deposition. In fibrotic mouse models of PDAC, both genetically-engineered and patient-derived, ibrutinib extended survival and synergized with chemotherapy, demonstrating the clinical applicability of this drug against pancreatic cancer. This project has led to the publication of a research paper and an editorial (Masso-Valles et al. 2015; Masso-Valles et al. 2016), as well as contributing to the initiation of clinical trials combining ibrutinib with chemotherapy in patients with metastatic PDAC (phase 1/2: NCT02562898 and phase 2/3: NCT02436668). The second project is focused on the relationship between Myc and metastasis. We studied de potential of Omomyc, a Myc dominant negative mutant that had shown extraordinary efficacy against primary tumors in multiple mouse models, against metastatic breast cancer. We demonstrated that Myc inhibition by Omomyc is a safe and effective therapy against breast cancer by impairing cell proliferation, angiogenesis, migration and invasion in vitro, dramatically reducing primary tumor and metastatic growth in immunocompromised mice, even eradicating established metastases, and preventing primary tumor and metastatic formation almost completely in immunocompetent mice. Thus, we have demonstrated for the first time the applicability of Omomyc against metastasis, challenging the pre-established notion that Myc inhibition could potentiate, rather than inhibit, invasion. Finally, we have validated TMTP1-Omomyc as the first direct-deliverable Omomyc-based drug for the treatment of metastatic triple negative breast cancer, providing a new therapeutic opportunity for patients suffering from this dreadful and incurable disease.
FATIMA, RIZWAN NARJIS. « Targeting the integrated stress response (ISR) as a therapeutic option for chronic lymphocytic leukemia ». Thesis, The University of Sydney, 2021. https://hdl.handle.net/2123/25009.
Texte intégralNji, Akindeh Mbuh. « Modeling response and delayance to parasite clearance time to artemisinin combination therapies(ACT) ». Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-168213.
Texte intégralRandall, Adrian Joseph. « A systems approach to uncovering the adaptive response of cancer to targeted therapies ». Thesis, Massachusetts Institute of Technology, 2012. http://hdl.handle.net/1721.1/72967.
Texte intégralCataloged from PDF version of thesis.
Includes bibliographical references (p. 47-53).
Tyrosine kinase inhibitors have significant promise in the fight to develop agents that can target cancer in a tumor-specific manner. A number of drugs have been and are currently in development to inhibit specific kinases that can mediate uncontrolled proliferation; however, an unfortunate eventuality for most patients receiving these treatments is the development of resistance that renders these drugs almost completely ineffective. While a number of mechanisms can evolve within a tumor to mitigate effects of kinase inhibitors, we sought to uncover what changes are occurring in the tyrosine phosphorylation network at both short timescales (minutes to 72 hours) and long timescales (120 hours+) that can be playing a role in helping a tumor become resistant to driver-kinase inhibition. It is our hypothesis that specific feedback networks are able to detect and overcome driver kinase inhibition through activation of potential other pathways, which can go on to mediate a longer term resistance phenotype. In order to probe dynamics in the tyrosine phosphorylation network, we employed mass spectrometry to analyze peptides derived from six non-small cell lung cancer cell lines that we classify as either EGFR+ or EML4-ALK+. From both mass spectrometry data and growth assays, we identified an unintuitive boost in signaling and growth in response to low inhibitor concentrations, suggestive of a cellular mechanism that is adaptive to driver kinase inhibition. Studies of EML4-ALK driven H3122 cells showed that this short-term response is not the same as the known long-term resistance mechanism to ALK inhibition, leading support to the notion that the short-term "adaptive response" may be a novel type of mechanism to aid tumor adaptation to targeted therapies. In an effort to better probe signaling events occurring downstream of the phosphotyrosine network, a new pull down technique for mass spectrometry using 14-3-3 protein against phosphoserine and phosphothreonine peptides is described. The results of these studies open up many potential avenues for further exploration into the immediate and long-term signaling response of cancer to targeted therapies.
by Adrian Joseph Randall.
S.M.
Breen, Michael Scott. « TISSUE RESPONSE TO INTERVENTIONAL MRI-GUIDED THERMAL ABLATION THERAPY ». Case Western Reserve University School of Graduate Studies / OhioLINK, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=case1080938405.
Texte intégralReddy, Papari Prashanth. « Non-motor symptoms in advanced Parkinson's : the natural history and response to advanced therapies ». Thesis, King's College London (University of London), 2015. http://kclpure.kcl.ac.uk/portal/en/theses/nonmotor-symptoms-in-advanced-parkinsons(b82ce682-b4f0-424d-9c7e-9f293b11bc18).html.
Texte intégralFenton, Audrey C. « The role of oncogenic kras as a determinant of response to EGER?HER2 targeted therapies ». Thesis, Queen's University Belfast, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.534743.
Texte intégralCramer, Megan L. « Novel signaling pathways in skeletal muscle : Modifiers of disease and the immune response to therapies ». The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1531790292235549.
Texte intégralMcNally, Jonathan P. « The rational targeting of the DNA damage response pathway for the selective elimination of encephalitogenic T cells ». University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1428652709.
Texte intégralBeshir, Kahlid Bushra. « Genetic polymorphisms in 'Plasmodium falciparum' associated with reduced response to artemisinin combination therapies in Western Kenya ». Thesis, London School of Hygiene and Tropical Medicine (University of London), 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558359.
Texte intégralTousignant, Kaylyn Davis. « Investigation of metabolic rewiring in prostate cancer cells during the adaptive response to androgen-targeted therapies ». Thesis, Queensland University of Technology, 2020. https://eprints.qut.edu.au/180822/1/Kaylyn_Tousignant_Thesis.pdf.
Texte intégralSavic, Sinisa. « The role of dysregulated unfolded protein response and resistance to apoptosis in the pathogenesis of rheumatoid arthritis and non- response to anti-TNF therapies ». Thesis, University of Leeds, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.534440.
Texte intégralHu, Qiuhua. « Investigating prostate tumour vasculature and oxygenation status in response to androgen-targeted therapies using photoacoustic-ultrasound imaging ». Thesis, Queensland University of Technology, 2022. https://eprints.qut.edu.au/228679/8/Qiuhua_Hu_Thesis.pdf.
Texte intégralNji, Akindeh Mbuh [Verfasser], et Ulrich [Akademischer Betreuer] Mansmann. « Modeling response and delayance to parasite clearance time to artemisinin combination therapies (ACT) / Akindeh Mbuh Nji. Betreuer : Ulrich Mansmann ». München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2013. http://d-nb.info/1049393309/34.
Texte intégralHecker, Michael [Verfasser], Reinhard [Akademischer Betreuer] Guthke, Raimund W. [Akademischer Betreuer] Kinne et Ronald [Akademischer Betreuer] Westra. « Integrative Modeling of Transcriptional Regulation in Response to Autoimmune Desease Therapies / Michael Hecker. Gutachter : Reinhard Guthke ; Raimund W. Kinne ; Ronald Westra ». Jena : Thüringer Universitäts- und Landesbibliothek Jena, 2011. http://d-nb.info/1016367775/34.
Texte intégralGiovanni, Nuciforo Paolo. « Quantitative analysis of HER family proteins using mass spectrometry as a predictive tool of response to anti-HER therapies in breast cancer ». Doctoral thesis, Universitat Autònoma de Barcelona, 2016. http://hdl.handle.net/10803/395203.
Texte intégralIntroduction: Dysregulated expression and activity of HER family members is frequent in breast cancer (BC). Up to 25% of BC overexpress HER2. High levels of this oncogene, almost invariably as a consequence of genomic amplification, drives aggressive disease and is an important therapeutic target. Monoclonal antibodies and small molecules kinase inhibitors are the main strategies to target HER2 in BC. Although trastuzumab treatment is associated with considerable benefits in terms survival outcomes, a significant number of patients with HER2-positive BC do not benefit from it or become resistant. Other HER2-targeted drugs (eg, lapatinib, pertuzumab, and T-DM1) have been approved for the treatment of HER2-positive metastatic BC after progression on trastuzumab. These new HER2-targeted drugs are now being tested in the adjuvant setting, alone or in dual antibody regimens without concomitant or sequential chemotherapy. Identifying which patients with BC are most likely to benefit from one or another form of anti-HER targeted therapy is crucial. Current standard methods for the determination of HER2 status (IHC and FISH) are semiquantitative, suffers from reproducibility issues, and do not predict response to trastuzumab. In the present study we sought to investigate if quantitative analysis of HER2 by mass spectrometry (MS) may improve current prediction of response or resistance to HER-targeting drugs. Methods: Using selected reaction monitoring MS, we quantified HER2 protein levels in formalin-fixed, paraffin-embedded tissue samples that had been classified as negative (HER2 0, 1+), equivocal (2+) or positive (3+) by immunohistochemistry (IHC). Receiver operating characteristic (ROC) curves were constructed by computing the sensitivity and specificity of increasing quantities of HER2 (by MS) in predicting HER2 positivity (by combined IHC/ISH) and of survival benefit after anti- HER2 therapy. Survival was modeled using the Kaplan-Meier curves and the p-value obtained by the log-rank test. Multivariate survival analysis was performed using the Cox proportional hazards model adjusted for hormone receptor status, tumor stage, lymph node status and HER2 SRM levels. Results were considered significant when p-values (p) were less than 0.05. Results: Absolute HER2 amol/μg levels were significantly correlated with both HER2 IHC and amplification status by ISH (p<.0001). Within IHC-positive (3+), a wide dynamic range of HER2 protein expression (from 163.7 to 17,446.7 amol/μg) was present. A HER2 threshold of 740 amol/μg showed an agreement rate of 94% with IHC and ISH standard HER2 testing (p<0.0001). Discordant cases (MS-negative/ISH-positive) showed a characteristic amplification pattern known as double minutes (DM). Patients showing HER2 levels by MS above the threshold of 2200 amol/mg (super-expressors) had a significant longer disease-free survival (DFS) and overall survival (OS) in an adjuvant setting and longer OS in a metastatic setting. Neither HER2/CEP17 ratio nor HER2 GCN was predictive of longer DFS or OS in the adjuvant setting. Conclusion: Accurate HER2 protein quantification can be achieved using MS and can be conducted in FFPE clinical tissue samples from BC patients. Quantitative HER2 measurement by MS correlates with protein expression by IHC but provides a wider dynamic range, thus highlighting the limited resolution of diagnostic IHC. Not all ISH-positive tumors show high HER2 protein expression despite being IHC 3+. Tumors amplified in DM show significantly lower HER2 protein levels compared to those with HSR pattern. MS is superior to IHC and ISH in predicting outcome after treatment with anti-HER2 therapy. Patients whose tumors express HER2 protein level >2200 amol/mg benefit more from anti-HER2 therapy than patients with lower HER2 expression levels.
Ma, Yuting. « The crosstalk between dying tumor cells and immune effectors within tumor microenvironment elicited by anti-cancer therapies dictates the therapeutic outcome ». Phd thesis, Université Paris Sud - Paris XI, 2011. http://tel.archives-ouvertes.fr/tel-00636891.
Texte intégralRudalska, Ramona [Verfasser], et Christiane [Akademischer Betreuer] Ritter. « Multiplex in vitro and in vivo RNAi screening to identify treatment response modifiers of targeted therapies in HCC / Ramona Rudalska ; Betreuer : Christiane Ritter ». Braunschweig : Technische Universität Braunschweig, 2014. http://d-nb.info/1175820806/34.
Texte intégralBates, Victoria. « The role of hypoxia-regulated glucose transporters and glucose metabolism in the response to hypoxia-linked therapies and as an indicator of prognosis in solid tumours ». Thesis, Liverpool John Moores University, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.531361.
Texte intégralYuting, Ma. « The crosstalk between dying tumor cells and immune effectors within tumor microenvironment elicited by anti-cancer therapies dictates the therapeutic outcome ». Thesis, Paris 11, 2011. http://www.theses.fr/2011PA11T033/document.
Texte intégralBesides exerting cytostatic or cytotoxic effects on tumor cells, some anti-cancer therapies (anthracyclines, oxaliplatin, X-Rays) could trigger an immunogenic cell death modality, releasing danger signals to alert immune system. We have shown that tumor-specific IFN- producing CD8+ T cells (Tc1) are mandatory for the success of chemotherapy to prevent tumor outgrowth. Priming of Tc1 response depends on IL-1β secretion by DC confronted with anthracycline-treated tumor cells releasing ATP. To identify the inflammatory components which link innate and cognate immune responses, we analyzed the influence of immunogenic chemotherapy on tumor microenvironment. We found an upregulated Th1- and Th17-related gene expression pattern in growth-retarded tumor after anthracycline treatment. By interfering with IFN- or IL-17A pathways, therapeutic effect of doxorubicin and oxaliplatin was abolished and dying tumor cell-based vaccine lost its efficacy to protect mice from live tumor cell rechallenge. Interestingly, we discovered that distinct subsets of T lymphocytes (V4+ and V6+) colonized tumors shortly after chemotherapy, where they proliferated and became the dominant IL-17 producers within tumor beds. In three tumor models treated with chemotherapy or radiotherapy, a strong correlation between the presence of IL-17-producing T ( T17) and IFN--producing CD8+ TIL (Tc1) was discovered. IL-17A signaling acts as upstream of IFN- since defect in IL-17RA led to complete loss of antigen specific Tc1 priming. The contribution of T17 cells (V4+ and V6+) to chemotherapy is critical as V4/6-/- mice showed reduced sensitivity to chemotherapy and vaccination. Also, tumor infiltrating T17 and Tc1 cells were reduced to basal level in this strain. IL-1β/IL-1R, but not IL-23/IL-23R, is pivotal for IL-17 production by T cells and the success of chemotherapy. Importantly, adoptive transfer of T cells could restore the efficacy of chemotherapy in IL-17A-/- mice and ameliorate the effect of chemotherapy in wild type host, provided that they retain the expression of IL-1R and IL-17A. Our research suggest a DC (IL-1β) → T cells (IL-17) → Tc1 (IFN-) immune axis triggered by chemotherapy-induced dying tumor cells, which is critical for the favorable therapeutic response. To boost the immune system, we try to combine immunogenic chemotherapy with tumor vaccine in the presence of TLR3 agonist Poly (A:U). This sequential combined therapy, which we named VCT, could significantly retard tumor growth or even completely eradicate tumor and establish long-term protection against rechallenge in highly tumorigenic models. To dissect the effect of Poly (A:U) on immune system and that on TLR3 expressing-tumor cells, we performed VCT treatment in nude mice, TRIF-/- mice and with TRIF-silencing tumors. Interestingly, our results suggested that anti-tumor effect of VCT required T cells and intact TRIF signaling pathway at the level of the host and that of tumor cells. Poly (A:U) treatment could induce high level of CCL5 and CXCL10 production from tumor cells both in vitro and in vivo, which could negatively and positively influence the therapeutic outcome. By uncoupling the effect of CCL5 from that of CXCL10, the VCT treatment can be ameliorated. Our study emphasizes that both tumor and host derived inflammatory factors participate in regulating anti-tumor response. We also highlight that therapeutic application of TLR agonists can be optimized through regulating the profile of chemokines and their downstream signaling events
Paredes, Raisa, Fritner Véliz et Aldo Lucchetti. « Comparison of the Virological Response According to the Antiretroviral Regimens in Peruvian HIV Patients Who Presented the M184V Mutation in Two National Hospitals during the Years 2008 to 2019 ». Mary Ann Liebert Inc, 2021. http://hdl.handle.net/10757/655814.
Texte intégralIntroduction: In patients with HIV in antiretroviral treatment (ART) and virological failure to the first-line regimen, establishing a therapeutic regimen after having identified the M184V mutation, which confers ART resistance, represents a dilemma. Objective: To compare the virological response of the therapeutic regimens prescribed to patients with HIV who presented the M184V mutation in two national hospitals in Lima, Peru, during the years 2008 to 2019, and to determine the risk factors associated with poor virological response. Methods: A retrospective cohort study was developed based on the information of the HIV program participants with the M184V mutation. Results: A total of 175 participants were eligible for the study. The male sex predominated (75.4%), the current median age was 41 years [interquartile range (IQR) 35.84-47.47], and the time on ART was 89 months (IQR 57.7-124.53). The median initial viral load (VL) was 4.5 log10 copies/mL (IQR 3.97-5.09) and the time between genotyping and the change of therapy was 2 months (IQR 0-3.56). The most used antiretroviral regimen was protease inhibitor plus two nucleoside reverse transcriptase inhibitors (55.4%). With the protease inhibitor plus integrase inhibitor (PI + INI) ART, 69% less risk of poor virological response was obtained [p = .019 (confidence interval 95% 0.117-0.825)]. Conclusions: In patients with HIV and the M184V mutation, the PI + INI ART has shown a greater decrease in control VL and, thus, a good virological response. The risk factors associated with a poor virological response were the delay between genotyping and change of therapy, high levels of initial VL, and poor adherence among the participants.
Revisión por pares
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.
Texte intégralBreast 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
Chhouri, Houssein. « Analysis by DNA barcoding of the heterogeneous response to anticancer drugs by different subpopulations of lung cancer cells ». Electronic Thesis or Diss., Normandie, 2022. http://www.theses.fr/2022NORMR037.
Texte intégralCancer is a dynamic disease, characterized by the co-existence of multiple subpopulations of tumor cells that can evolve in response to environmental changes. This intratumor heterogeneity has dramatic consequences, not only for cancer progression and metastatic spread, but also for treatment. Specific tyrosine kinase inhibitors are effective against non-small cell lung cancers harboring activating mutations of the epidermal growth factor receptor (EGFR), but the response is not durable, and cure remains elusive because of the inevitable development of acquired resistance. During therapeutic intervention, small subpopulations of resistant or tolerant cells are selected by virtue of their higher fitness, ultimately resulting in tumor relapse.In this study, we used cellular barcoding to label several thousand populations of PC9 NSCLC cells and monitor their clonal dynamics in response to anti-cancer therapies. Our results revealed that some clones display a specific and predetermined response to treatment, indicating that cells that are primed to behave as tolerant or highly sensitive pre-exist in the original mass population. We extended these findings and showed that each type of anti-cancer drugs exerts a characteristic effect on the clonal architecture of the cell population, resulting in a specific barcode pattern that can be used as a signature to compare different compounds and investigate their mechanism of action. We have generated barcode profiles from 87 drugs targeting various pathways and used it to predict the mechanism of action of a new compound that can specifically inhibit NSCLC cell growth.In the last part of the thesis, we took advantage of CRISPR/Cas9 technology to devise Barcode-Tracker, a new strategy to identify and isolate clones of interest from a mass population based on the recognition of a specific genetic barcode. Contrary to other approaches, Barcode-Tracker doesn’t involve drug selection of the cells and it can be used to sort clones according to their intrinsic capacity to behave in a particular manner in the presence of treatment, thus mimicking the response of a therapy-naïve tumor. By providing a better understanding of how treatment can shape clonal evolution, our studies should help to improve therapeutic strategies for NSCLC patients
Hopper, Sophie. « The therapist experience of client non-response ». Thesis, University of Leeds, 2015. http://etheses.whiterose.ac.uk/10725/.
Texte intégralLandström, Birgitta, et Helene Stedmon. « Patientsuicid - : Terapeuters upplevelser och påverkan ur ett systemiskt perspektiv ». Thesis, Umeå universitet, Psykoterapi, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-118499.
Texte intégralSterner, Irit. « Client responses to therapist statements as behavioural requests ». Thesis, University of Ottawa (Canada), 1990. http://hdl.handle.net/10393/5690.
Texte intégralLaura, Bergantini. « Immune modulatory effects of novel monoclonal antibodies target therapies in severe eosinophilic asthma patients ». Doctoral thesis, Università di Siena, 2020. http://hdl.handle.net/11365/1120137.
Texte intégralCyr, Yolande. « Self-disclosure by marital therapists and consequent spouse responses ». Thesis, University of Ottawa (Canada), 1987. http://hdl.handle.net/10393/5152.
Texte intégralBancroft, Courtney. « Trainee therapist responses to the discussion of trauma in therapy ». Thesis, Pepperdine University, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=3643872.
Texte intégralResponses to disclosures/discussions of trauma can have lasting impacts on survivors who choose to share their experiences and historically have been categorized as positive, negative, and/or neutral responses with corresponding effects on the survivor. Literature recommends the use of tenets and techniques reminiscent of therapeutic common factors (e.g., listening skills, empathy, support, validation, creating a safe environment and strong therapeutic alliance) when responding to trauma. However, existing research focuses on reactions to survivors' disclosures outside of therapy and there is little research focusing on therapists' responses. Specifically, there are no studies that investigate how therapists or trainees are actually responding in psychotherapy sessions (e.g., frequency and rate of such responses).
Accordingly, the purpose of the present study was to qualitatively explore the responses of student therapists in psychotherapy sessions with trauma survivors. A sample of 5 therapist-participants from university-based community counseling centers were selected and transcribed videotaped sessions in which client- and trainee therapist-participants discussed trauma were analyzed using a qualitative and deductive content analysis. A coding system was created to categorize responses based on extant literature. Results indicated that trainee therapist-participants responded in all proposed categories (positive: validating, supportive, empathic; negative: invalidating, unsupportive, unempathetic; and neutral: clarifying questions, and reflection/summary statements). Of these, neutral responses tended to occur more frequently than positive or negative responses. Overall, positive responses followed as next most frequent and negative responses as least frequent. Other findings included that in 2 of the 5 individual sessions, negative responses were more frequent than positive responses; empathic responses were the least frequent code across all 10 coding categories; and 2 sessions had 0 recorded empathic responses. Finally, there were numerous missed opportunities for positive responding throughout the sessions.
It is hoped that this study will raise awareness around the importance of therapeutic responses to trauma survivors' discussions in psychotherapy sessions and provide insight as to how trainee therapists might apply their existing competencies to respond to clients in positive ways. Findings have implications for both future studies and clinical training practices, for example in graduate programs for trainee therapists, an area of study that is currently under-researched.
Höglund, Andreas. « Regulation of DNA damage responses by the Myc oncogene : implications for future anti-cancer therapies ». Doctoral thesis, Umeå universitet, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet), 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-44284.
Texte intégralMuller, Ilaria. « Autoimmune responses to thyroid/breast shared antigens to develop novel and specific therapies and diagnostics ». Thesis, Cardiff University, 2016. http://orca.cf.ac.uk/91002/.
Texte intégralByng-Maddick, Rachel. « Differential effects of anti-TNF therapies for inflammatory arthritides on immune responses to Mycobacterium tuberculosis ». Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10043230/.
Texte intégralQuerbach, Julia [Verfasser]. « EEG-Response-Prädiktion der medikamentösen antidepressiven Therapie mittels affektiver Stimuli bei unipolarer Major Depression / Julia Querbach ». Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2020. http://d-nb.info/1218076364/34.
Texte intégralLeicht, Christina [Verfasser], et Arndt [Akademischer Betreuer] Hartmann. « Untersuchung molekularer Therapie-Response-Marker bei lokal fortgeschrittenen Harnblasenkarzinomen mit adjuvanter Chemotherapie / Christina Leicht. Betreuer : Arndt Hartmann ». Regensburg : Universitätsbibliothek Regensburg, 2012. http://d-nb.info/1025386175/34.
Texte intégralPachmayr, Eva Maria [Verfasser]. « Prädiktion der Therapie-Response im Patienten-abgeleiteten Maus-Xenograft-Modell bei peritoneal metastasiertem kolorektalem Karzinom / Eva Maria Pachmayr ». Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2019. http://d-nb.info/120204168X/34.
Texte intégralPachmayr, Eva [Verfasser]. « Prädiktion der Therapie-Response im Patienten-abgeleiteten Maus-Xenograft-Modell bei peritoneal metastasiertem kolorektalem Karzinom / Eva Maria Pachmayr ». Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2019. http://d-nb.info/120204168X/34.
Texte intégralKlingner, Maria Brigitte. « Untersuchung zur Vorhersagbarkeit des Therapieansprechens unter anti-TNF-Therapie bei Patienten mit Rheumatoider Arthritis ». Doctoral thesis, Universitätsbibliothek Leipzig, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-146837.
Texte intégralKluge, Regine, Lidia Chavdarova, Martha Hoffmann, Carsten Kobe, Bogdan Malkowski, Françoise Montravers, Lars Kurch et al. « Inter-reader reliability of early FDG-PET/CT response assessment using the Deauville Scale after 2 cycles of intensive chemotherapy (OEPA) in Hodgkin’s Lymphoma ». Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-204087.
Texte intégralRichard, Matthias. « Die Konzeptualisierung und Validierung von Therapie-Response und seine Bedeutung für die Behandlungsplanung in einem verlaufsorientierten Qualitätsmanagement am Beispiel von Essstörungen ». [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=961906766.
Texte intégralDüsterwald, Jan Ole [Verfasser], Achim [Gutachter] Mumme et Letterio [Gutachter] Barbera. « Überprüfung der perioperativen Response und Evaluation einer standardisierten Optimierung der antithrombozytären Therapie bei gefäßchirurgischen Patienten / Jan Ole Düsterwald ; Gutachter : Achim Mumme, Letterio Barbera ». Bochum : Ruhr-Universität Bochum, 2017. http://d-nb.info/1129452093/34.
Texte intégralHansen, Brian P. « Sudden Gains : A Pluralistic Approach to the Patient and Therapist Experience ». BYU ScholarsArchive, 2013. https://scholarsarchive.byu.edu/etd/4290.
Texte intégralRakotomalala-Andrianasolo, Andria. « Développement et caractérisation de modèles cellulaires pour l'étude du rôle de l'oncohistone H3.3 K27M dans le phénotype agressif et la réponse aux thérapies des gliomes pédiatriques diffus de la ligne médiane ». Electronic Thesis or Diss., Université de Lille (2022-....), 2024. http://www.theses.fr/2024ULILS015.
Texte intégralH3K27-altered DMG treatment is one of the most significant challenges in pediatric neuro-oncology,with no improvement in patient survival over the past 50 years. In 2012, it was shown that DMGs harbor a specific histone 3 mutation (oncohistone) called H3.3 K27M with a very high prevalence (70-80% of cases). Although theH3.3 K27M impact on the epigenetic landscape has been well described, studies are needed to understand betterits role in DMG cells’ aggressiveness and response to therapies.To study the H3.3 K27M mutation impact on DMG cell phenotypes precisely, we developed andcharacterized pediatric high-grade glioma isogenic cellular models induced and knock-out for the oncohistone.Using these models, we aimed to decipher the oncohistone impact on DMG cell biology and response to anticancertherapies, including radiation therapy, the only current standard of care for DMGs. Characterization of our H3.3 K27M-induced pediatric supratentorial glioma cell lines reveals that the oncohistone affects the response to ionizing radiations and specific targeted therapies in a cellular context-dependentway. Based on these results, we settled to characterize oncohistone biological impacts in a more relevant cellular context of DMG. In that sense, we established H3.3 K27M knock-out cellular models and characterized them regarding their parental DMG H3.3 K27M mutated cell lines. Through omic (transcriptomic and proteomic)and cell metabolism characterizations of these models, we notably showed the H3.3 K27M mutation impact on DMG cells’ lipid metabolism. In 3D spheroid models, this H3.3 K27M-induced lipid metabolism rewiring appeared conditioned by microenvironment factors still under investigation.On the other hand, a functional pharmacological screen identified H3.3 K27M-driven dependencies tospecific DNA repair pathways. In addition, ongoing radiobiological characterization of our models indicates anH3.3 K27M-associated radiosensitivity correlating with a decrease in DNA repair efficiency following ionizingradiations. Beyond this DNA repair impact, our pharmacological screen also revealed an H3.3 K27M-relatedsensitivity to cardiac glycoside drugs. This result makes sense with our transcriptomic data showing enrichmentin genes involved in cardiomyopathies and ion homeostasis among differentially expressed genes with theoncohistone. In this context, we began unraveling the molecular and biological processes underlying thisH3.3 K27M-driven effect.Finally, we used our isogenic cellular models to show that the H3.3 K27M oncohistone drives lipidmetabolism modifications. These metabolic changes could prime H3K27-altered DMG cells to specific regulatedcell death pathways (e.g., ferroptosis) and affect the response to certain therapies. Moreover, the H3.3 K27Mseems to drive specific sensitivities, notably to radiation therapy and cardiac glycoside drugs. Understanding the underlying molecular mechanisms governing these H3.3 K27M-associated Achille heels could highlight newinsights into the oncohistone role in DMG cells and provide rationales for developing new therapeutic strategies
Daheim, Mathias Stefan Moritz [Verfasser]. « Ausnutzung molekularer Defekte in der DNA damage response ATM-mutierter Zellen durch gezielte Therapie einer starken non-oncogene addiction von PRKDC / Mathias Stefan Moritz Daheim ». Köln : Deutsche Zentralbibliothek für Medizin, 2014. http://d-nb.info/1049199340/34.
Texte intégralMeyrath, David [Verfasser], et Knut [Akademischer Betreuer] Schnell. « Response einer Therapie mit Olanzapin bei schizophrenen Psychosen in Abhängigkeit von vorangegangenem Cannabiskonsum und dessen Impact auf das endogene Cannabinoidsystem / David Meyrath ; Betreuer : Knut Schnell ». Heidelberg : Universitätsbibliothek Heidelberg, 2019. http://d-nb.info/1177043769/34.
Texte intégralSaiger, David [Verfasser]. « Lithiumtherapie und Nierenfunktion bei Patienten mit Bipolarer Störung : Einfluss der Therapiedauer auf die glomeruläre Filtrationsrate im Kontext von somatischer Komorbidität und Therapie-Response / David Saiger ». Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2017. http://d-nb.info/1140486802/34.
Texte intégralHope, Roslyn. « Professionalism, evidence and power : key themes influencing the management of a mental health programme in the National Health Service in England ». Thesis, University of Hertfordshire, 2012. http://hdl.handle.net/2299/13903.
Texte intégralWaiczies, Sonia. « Modulation of human antigen-specific T-cell response therapeutic implications for multiple sclerosis / ». Doctoral thesis, [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=969681844.
Texte intégralHenke, Henning. « Löslicher Interleukin-2-Rezeptor-[alpha] [Interleukin-2-Rezeptor-alpha] als möglicher prognostischer Marker des virologischen Ansprechens einer Therapie mit PEG-Interferon-a-2b und Ribavirin bei Patienten mit chronischer Hepatitis C, die auf eine vorangegangene Therapie mit Interferon-alpha und Ribavirin nicht angesprochen haben (Non-Responder) ». [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=966445570.
Texte intégralMüller, Christine-Susanne. « Course of clinical response during primary systemic therapy with a dose-dense 4 cycles regime of adriamycin and docetaxel in patients with operable cancer of the breast Zeitlicher Verlauf der Klinischen Response während der Primären Systemischen Therapie des Operablen Mamma-Karzinoms mit einem Dosis Dichten Therapieregime aus 4 Zyklen Adriamycin und Docetaxel / ». [S.l. : s.n.], 2005. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB12168001.
Texte intégralSitaru, Ana Gabriela. « Modulation der T-Zell-Reaktivität durch MHC-Klasse-I Peptide und ihre Varianten Perspektiven für eine antigen-spezifische Therapie in der Transplantation = Modulation of the T cell response with MHC class I peptides and their analogues / ». Doctoral thesis, [S.l.] : [s.n.], 2003. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-4561.
Texte intégralUrsache der Transplantatabstoßung ist in erster Linie die genetische Differenz im Haupthistokompatibilitätskomplex (MHC) zwischen Transplantatspender und Empfänger. Dabei stellen die aus den Fremd-MHC-Molekülen durch empfänger-eigene antigenpräsentierende Zellen prozessierten MHC-Peptide einen wichtigen Stimulus zur Aktivierung alloreaktiver T-Lymphozyten des Transplantat empfängers dar. Für die Transplantation bedeutsam ist, dass sowohl diese, als auch synthetische MHC-Peptide, wenn sie die genetische Differenz zwischen einer bestimmten Spender-Empfänger-Kombination repräsentieren, die Alloimmunantwort induzieren und damit die Abstoßung fördern. Das Ziel dieser Arbeit war, dass bereits in zahlreichen Experimentalmodellen für Autoimmunerkrankungen erfolgreiche Konzept der antigenspezifischen Immuntherapie mit Peptidvarianten oder altered peptide ligands auf die Transplantation zu übertragen. Anders als bei Autoimmunerkrankungen basiert die Alloimmunantwort aber nicht auf ein einyelnes Peptidantigen und darüber hinaus beeinflußt die jeweilige Spender-Empfänger-Kombination sehr stark dieses Peptidantigen-Repertoire. Um die Frage zu klären, welche der potentiellen MHC-Peptidantigene in der Alloimmunaktivierung dominieren, wurden Untersuchungen im Nagermodell für die allogene Spender-Empfänger-Kombination Wistar-Furth (WF, RT1u) und Lewis (LEW, RT1l) durchgeführt. Für die Transplantation wird erwartet, dass solche gezielt hergestellten Peptidvarianten sowohl die Aktivierung alloreaktiver T-Lymphozyten als auch weitere Funktionen, wie z. B. die Produktion von Cytokinen, hemmen. Dieser antigenspezifische, und wahrscheinlich auch nebenwirkungsfreie Therapieansatz könnte möglicherweise zur langfristigen Erhaltung der Transplantatfunktion führen. Durch Vergleich der Sequenzen für das MHC-Klasse-I Molekül beider Ratten-Stämme wurden für die a1 und a2 Domäne - dies ist der extrazelluläre, für die Bindung von Peptiden unterschiedlichster Herkunft verantwortliche Bereich des Moleküls - insgesamt 34 Positionen identifiziert, in denen beide Stämme unterschiedliche Aminosäuren aufweisen. Diese Differenzen werden von sieben synthetischen, mit den entsprechenden Bereichen des Spender MHC-Klasse-I Moleküls identischen MHC-Peptiden repräsentiert, welche zwischen 13 und 24 Aminosäuren lang sind. Die immunstimulierende Wirkung dieser Peptide (P1 bis P7) wurde im Proliferationsassay und im Transplantationsmodell bestimmt. Ausschließlich das Peptid mit der Bezeichnung P1 induzierte mit über 20.000 cpm die stärkste, mit einen Th1-dominierten Cytokinmuster (IL-2 und IFN-g) einhergehende T-Zellproliferation. Lewis-Empfänger, die vor der Transplantation mit diesem Peptid immunisiert wurden, stießen ihre von WF-Spendern stammenden heterotopen Herztransplantate beschleunigt ab. Von sieben potentiellen Peptidantigenen induzierte somit ausschließlich Peptid P1 eine dominante Alloimmunaktivierung und erscheint als Peptidantigen zur Herstellung von Peptidvarianten prädestiniert. P1 weicht in drei Aminosäurepositionen von der entsprechenden Sequenz der Lewis-Ratte ab. Durch sequentiellen Austausch dieser drei in der WF-Sequenz befindlichen allogenen Aminosäuren durch die entsprechenden syngenen Aminosäuren in der LEW-Sequenz führte zu sechs Peptidvarianten. Diese Empfänger-angepassten Varianten A1.1 bis A1.6 wurden anschließend auf ihre Fähigkeit untersucht, eine peptidspezifische T-Zellproliferation zu inhibieren, die möglicherweise mit einer protektiven Wirkung auf die Transplantatfunktion einhergeht. Von diesen Peptidvarianten induzierte nur Variante A1.5, sie besitzt noch eine allogene Aminosäure an Position 5, eine reduzierte T-Zellproliferation von 11.450 cpm, die mit einem Th2-dominierten Cytokinmuster (IL-4 und IL-10) korreliert. Zusätzlich hemmte A1.5 die Proliferation der P1-spezifischen T-Lymphozyten. Im Gegensatz zum Ausgangs-peptid P1 beeinflußte A1.5 nicht die Abstoßung heterotoper Herztransplantate und konnte, wurde es in Kombination mit P1 appliziert, die P1-induzierte Transplantatabstoßung verzögern. Um diese immunmodulatorische Fähigkeit der Variante A1.5 weiter zu untersuchen, wurde das Peptid in einem T-Zellrezeptor-Modulationsassay sowie in einem MHC-Kompetitionsassay getestet. Die Ergebnisse zeigten, dass A1.5 nicht die T-Zellproliferation über den T-Zellrezeptor inhibiert, sondern über die verstärkte Bindung an das MHC-Klasse-II Molekül, wodurch das Peptid P1 wahrscheinlich aus der Bindungstasche verdrängt wird. Dieses Ergebnis wurde von weiteren in vivo Daten unterstützt. Wurden beide Peptide getrennt und nicht im Gemisch appliziert, konnte A1.5 die abstoßungsinduzierende Wirkung von P1 nicht mehr kompensieren, und das Transplantat wurde zum gleichen Zeitpunkt nach Transplantation abgestoßen wie in P1-immunisierten Tieren