Relevant bibliographies by topics / Resistance to therapies

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Resistance to therapies'

Author: Grafiati
Published: 16 November 2024

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Journal articles on the topic "Resistance to therapies"

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Gupta, P. D. "Reducing drug resistance should be the aim of therapies." Clinical Research and Clinical Trials 3, no. 4 (April 30, 2021): 01–05. http://dx.doi.org/10.31579/2693-4779/028.

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Over the period, due to evolutionary constrains, gene mutations, changes in micro- and mega- environment gave a tool to bacteria to adopt for survival in the hostile environment. When they are exposed with broad spectrum antibiotics, they have adopted to live and become resistant to antibiotics. In this review many preventive and curative strategies has been described to avoid antibiotics. These lines of treatments would not give chances to microbes to become drug resistant. “Prevention is better than cure” adopting this strategy we have described immunochemicals and many herbal medicines which will prevent infections. Also given importance to maintain proper balance of microbiota in the gut by replacement of the lost (may be due to many reasons) species which are considered necessary for maintaining a balance in bacterial population.
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Bartolotti, Marco, Enrico Franceschi, Rosalba Poggi, Alicia Tosoni, Monica Di Battista, and Alba A. Brandes. "Resistance to antiangiogenic therapies." Future Oncology 10, no. 8 (June 2014): 1417–25. http://dx.doi.org/10.2217/fon.14.57.

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Prasad, Rajendra, Atanu Banerjee, and Abdul Haseeb Shah. "Resistance to antifungal therapies." Essays in Biochemistry 61, no. 1 (February 28, 2017): 157–66. http://dx.doi.org/10.1042/ebc20160067.

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The evolution of antifungal resistance among fungal pathogens has rendered the limited arsenal of antifungal drugs futile. Considering the recent rise in the number of nosocomial fungal infections in immunocompromised patients, the emerging clinical multidrug resistance (MDR) has become a matter of grave concern for medical professionals. Despite advances in therapeutic interventions, it has not yet been possible to devise convincing strategies to combat antifungal resistance. Comprehensive understanding of the molecular mechanisms of antifungal resistance is essential for identification of novel targets that do not promote or delay emergence of drug resistance. The present study discusses features and limitations of the currently available antifungals, mechanisms of antifungal resistance and highlights the emerging therapeutic strategies that could be deployed to combat MDR.
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Tejpar, Sabine, Hans Prenen, and Massimiliano Mazzone. "Overcoming Resistance to Antiangiogenic Therapies." Oncologist 17, no. 8 (July 6, 2012): 1039–50. http://dx.doi.org/10.1634/theoncologist.2012-0068.

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Sledge, George W. "Resistance to Anti-HER2 Therapies." Breast 20 (October 2011): S16. http://dx.doi.org/10.1016/j.breast.2011.08.014.

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Lawrence Drew, W. "Cytomegalovirus resistance to antiviral therapies." American Journal of Health-System Pharmacy 53, suppl_2 (April 1, 1996): S17—S23. http://dx.doi.org/10.1093/ajhp/53.8_suppl_2.s17.

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Thangavadivel, Shanmugapriya, and Jennifer A. Woyach. "Genomics of Resistance to Targeted Therapies." Hematology/Oncology Clinics of North America 35, no. 4 (August 2021): 715–24. http://dx.doi.org/10.1016/j.hoc.2021.03.004.

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Guièze, Romain. "Mechanisms of resistance to targeted therapies." Hématologie 26, S3 (September 2020): 20–26. http://dx.doi.org/10.1684/hma.2020.1564.

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Fong, Chun Yew, Omer Gilan, Enid Lam, Alan Rubin, Jessica Morison, George Giotopoulos, Kym Stanley, et al. "Modelling Resistance to Emerging Epigenetic Therapies." Blood 124, no. 21 (December 6, 2014): 3546. http://dx.doi.org/10.1182/blood.v124.21.3546.3546.

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Abstract The BET inhibitors are first-in-class, epigenetic targeted therapies that deliver a new therapeutic paradigm by directly targeting protein-protein interactions at chromatin. Early clinical trials have shown significant promise, especially in AML, suggesting that these compounds are likely to form an important component of future anti-cancer regimens. Therapeutic resistance is an inevitable consequence of most cancer therapies, therefore the evaluation of resistance mechanisms is of utmost importance in order to optimize the clinical utility of this novel class of drugs. Using primary murine stem and progenitor cells immortalized with MLL-AF9, we have developed a novel approach to generate over 20 clones stably resistant to the prototypical BET inhibitor, IBET. Resistance has been established at >IC90 of the parental cell line. In parallel, we have maintained matched vehicle treated clones in addition to the parental cell line. Resistant clones maintain their clonogenic capacity in IBET and are also impervious to IBET induced cell-cycle arrest and apoptosis. Resistance to IBET confers cross-resistance to other chemically distinct BET inhibitors such as JQ1 and also resistance to genetic knockdown of BET proteins. Moreover, resistance is stably maintained across subsequent cell generations in the absence of ongoing selective pressure. Resistance is not mediated through increased drug efflux or metabolism but is demonstrated to emerge from the leukemia stem cell (LSC) compartment. Resistant clones display an immature phenotype (c-kithi/Gr1-/CD11b-) and functionally, exhibit increased clonogenic capacity in vitro and markedly shorter disease latency following primary syngeneic transplantation (Figure A, B and C). Importantly, resistant clones maintain their resistance to IBET therapy in vivo. We will present data gleaned from exome capture sequencing, ChIP-seq and RNA-seq, to demonstrate the underlying molecular mechanisms of resistance to epigenetic therapies, including genetic changes, molecular events at chromatin and the upregulation of compensatory pathways that will inform future combination therapies to obviate and/or overcome BET inhibitor resistance. In summary, we have utilized a primary murine model of MLL leukemia to derive over 20 individual clones that are resistant to BET inhibition. Our data is consistent with resistance emerging from the LSC population. This data will allow us to develop rational drug combinations to overcome resistance and enhance the therapeutic efficacy of emerging epigenetic therapies. Furthermore, our data provides novel insights into the biology of AML and provides an unprecedented opportunity to study leukemia stem cells and develop therapeutic strategies to eradicate them. Figure 1 Figure 1. Disclosures Lugo: GlaxoSmithKline: Employment. Jeffrey:GlaxoSmithKline: Employment. Gregory:GlaxoSmithKline: Employment. Prinjha:GlaxoSmithKline: Employment.
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Smith, Sinéad M., Colm O’Morain, and Deirdre McNamara. "Helicobacter pylori resistance to current therapies." Current Opinion in Gastroenterology 35, no. 1 (January 2019): 6–13. http://dx.doi.org/10.1097/mog.0000000000000497.

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Dissertations / Theses on the topic "Resistance to therapies"

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Hewlett, Mark. "The evolution of resistance to multidrug antibiotic therapies." Thesis, University of Exeter, 2015. http://hdl.handle.net/10871/21596.

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The purpose of this thesis is to explore the interaction between antibiotics at sub-lethal doses, and E.coli. Initially we focussed on pairwise antibiotic interaction, and the potential to exploit these interactions to minimise antibiotic resistance. In testing the hypothesis that antagonism will slow adaptation by reducing selection for resistance we determined that there are conditions in which this fails to be the case. We furthermore caution against treating drug interactions as anything other than a dynamic property of the bacteria-drug interaction, by showing that the relationship between two drugs may be both synergistic and antagonistic depending on a variety of factors. Whilst exploring the adaptive response to drug combinations we discovered a highly unusual effect of Doxycycline to act as a growth stimulant to E.coli AG100. Chapter 3 and 4 are devoted to determining the nature and mechanism of this stimulation, and analysing any potential genomic changes using whole genome re-sequencing. Having shown that dose response is not always a monotone function of increasing drug dose, in chapter 5 we also look at the dose response in a diffusive context, using a custom built imaging system to show the common non-monotonicity of disk diffusion type assays, that manifest themselves as bullseye patterns of growth. We use a mathematical model to explore the ecological and adaptive reasons for such patterns. Finally in chapter 6 we look at the coevolutionary history of phage and E.coli REL606 strains, by determining trade-offs caused by lambda phage and the sole carbon source maltotriose both utilising the same porin (lamB) for cell entry.
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Guix, Arnau Marta 1974. "Mechanisms of acquired resistance to anti-EGFR therapies in squamous cell carcinoma." Doctoral thesis, Universitat Pompeu Fabra, 2017. http://hdl.handle.net/10803/565440.

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Targeted therapies against the Epidermal Growth Factor Receptor (EGFR) are useful to treat many human cancers such as non-small cell lung cancer, colorectal cancer and head and neck cancer. However, the efficacy of such treatments is always compromised by resistance. This doctoral thesis has focused in the mechanisms of acquired resistance to targeted therapies against the EGFR (such as the small tyrosine kinase inhibitors gefitinib and erlotinib, or the monoclonal antibody cetuximab) in squamous cell carcinomas. In the first part of the thesis, preclinical studies with cellular and xenograft models were developed to elucidate the molecular mechanisms of resistance; the second part of the thesis was performed in tumor samples from patients with advanced squamous cell carcinomas of the head and neck. The main finding from the preclinical analysis was that the activation of the insulin-like growth factor receptor 1 system, mainly through downregulation of insulin-like growth factor binding proteins, is responsible for the acquired resistance to anti-EGFR therapies. However, these results could not be validated in a small sample set of advanced head and neck cancer patients.
Els tractaments dirigits contra el receptor del factor de creixement epidèrmic (EGFR) són útils en diversos càncers en l’home, com el càncer de pulmó de cèl·lula no petita, el càncer colorrectal o els tumors de cap i coll. Però l’eficàcia d’aquests tractaments sempre està limitada per l’aparició de resistències. Aquesta tesi doctoral s’ha centrat en investigar els mecanismes de resistència adquirida a tractaments dirigits contra l’EGFR (com els inhibidors tirosina quinasa gefitinib i erlotinib o l’anticòs monoclonal cetuximab) en carcinomes escamosos. En la primera part de la tesi s’han desenvolupat estudis preclínics amb models cel·lulars i xenoinjerts per desxifrar els mecanismes moleculars de resistència; la segona part de la tesi ha inclòs estudis en mostres de carcinomes escatosos de cap i coll de pacients amb tumors avançats. La troballa principal dels estudis preclínics ha estat que l’activació del sistema del receptor del factor de creixement semblant a la insulina, principalment a través de la disminució dels nivells de les proteïnes d’unió als factors de creixement semblants a la insulina, és la responsable de l’aparició de resistència adquirida als tractaments anti-EGFR. Posteriorment, però, aquests resultats no han estat validats en una petita cohort de pacients amb tumors avançats de cap i coll.
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McGivern, Niamh. "Activation of MAPK signalling results in resistance to therapies for ovarian cancer." Thesis, Queen's University Belfast, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.695671.

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Ovarian cancer is the fifth most common cancer affecting women in the UK, and is the most lethal of all gynaecological cancers. Treatment primarily consists of debulking surgery followed by a platinum and taxane based chemotherapy, and despite initial high levels of response, the majority of women will relapse with platinum resistant disease, resulting in a poor prognosis. Few targeted therapies have entered the clinic for the treatment of ovarian cancer, however there is strong preclinical data to suggest there is a therapeutic window to target SRC tyrosine kinase in this disease. The SAPPROC trial was a phase 11 trial investigating the addition of the SRC inhibitor saracatinib (AZD0530) to weekly paclitaxel in platinum resistant ovarian cancer, however, this study showed no benefit to survival from this combination. The work presented in this thesis has investigated potential mechanisms of resistance to SRC inhibitors in ovarian cancer, and by using two complementary screening approaches, highlighted a role for activated MEK signalling in driving this resistance. Further work demonstrated that a SRC and MEK are parallel pathways, and inhibition of one leads to activation of the other. This has important therapeutic implications, and a combination of SRC and MEK inhibitors was shown to synergistically inhibit the growth of ovarian cancer cells, and so this combination may be logical in the clinic. Importantly, the SAPPROC trial was performed in platinum resistant ovarian cancer patients, and it has previously been reported that platinum resistant cells exhibit activated MAPK signalling. A novel platinum resistant ovarian cancer cell line was generated in vitro, and demonstrated activated MAPK, as well as resistance to SRC inhibition. This suggests that SAPPROC may have failed to show any benefit of SRC inhibition in platinum resistant patients has their tumours already exhibit activated MEK, and therefore did not respond to SRC inhibition. This highlights the need to further understand mechanisms of drug resistance, the the importance of this in the design of clinical trials.
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Sun, Xiaowen. "An integrin-based mechanism for sensitizing melanomas to therapies." Diss., University of Iowa, 2015. https://ir.uiowa.edu/etd/6506.

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Metastatic melanoma is unusually lethal with a ten year survival rate of less than 10%. Conventional DNA-damaging agents produce little improvement in patient survival. Vemurafenib (Zelboraf), a targeted therapeutic that inhibits the oncogenic BRAF demonstrates significant survival benefit. Unfortunately, it is now evident that there is both intrinsic and acquired resistance. Consequently, new strategies for sensitizing melanomas to vemurafenib are needed. Melanoma resistance to therapy is fueled in part by the integrins, the major cell surface adhesion receptors which are highly over-expressed in melanoma. Both integrin antagonists and agents that engage defective integrins increase the sensitivity of melanomas to chemotherapy. Our laboratory has identified a novel peptide, denoted vinculin activating peptide or VAP that targets integrins from within the cell and brings aberrant integrin function intact. VAP sensitizes melanoma to dacarbazine in vitro and in vivo. The effect VAP has on overcoming resistance to targeted therapies like vemurafenib, as well as the mechanism for its effects are not well understood. The goals of this project are to determine if VAP can be employed to improve sensitivity and/or overcome resistance to vemurafenib and to identify the cell surface target of VAP. Our results show that VAP not only improves melanoma sensitivity to vemurafenib but also decreases intrinsic resistance to this promising drug. In addition, we present evidence that β1 and β3 integrins are the target of VAP's effects. Since peptide-based therapies are not stable in the clinic, we explored another integrin binding partner, kindlin-2. We found that kindlin-2 is over expressed in resistant melanomas. The inhibition of kindlin-2 increases β1 integrin activation and decreases β3 integrin functions. Agents that bring aberrant β1 and β3 integrin function intact can be employed to improve sensitivity and overcome resistance to vemurafenib suggesting that combinatorial therapies that employ vemurafenib and integrin-based agents might be efficacious in combatting resistance in melanoma patients.
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Neto, João Manuel Fernandes. "Improvement of antiangiogenic therapies in colorectal cancer." Master's thesis, Universidade de Aveiro, 2015. http://hdl.handle.net/10773/15349.

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Mestrado em Biotecnologia – Biotecnologia Industrial e Ambiental
Angiogenesis is essential for tumor progression. Antiangiogenic therapies block angiogenesis and cause vessel regression, which leads to an increase of tumor hypoxia. Hypoxia is responsible for many effects in tumor biology, among which, the selection of cells that are more aggressive and more resistant to cancer therapies. In this project we aim to get some molecular insight on the mechanism(s) underlying the resistance to the combination of bevacizumab and cetuximab and to find synthetic lethal interactions with hypoxia. Our results show that: hypoxia induces resistance to EGFR inhibition in WT4 CRC cell; HIF1α is not driving the resistance phenotype; hypoxia activates RAS in WT4 CRC cells; MEK inhibitors increase the sensitivity to EGFR inhibitors in hypoxia and cytokines seem to be involved in the activation of RAS in hypoxia. We also identified four genes as potential candidates to be synthetic lethal with hypoxia. Our findings are of great clinical and biological significance and may lead to better combination therapies, improving current treatments for CRC patients and may also lead to the discovery of biomarkers of response to antiangiogenic therapies.
A angiogénese é essencial à progressão tumoral. As terapias antiangiogénicas bloqueiam a angiogénese e causam regressão dos vasos sanguíneos, o que leva a um aumento da hipóxia nos tumores. A hipóxia é responsável por diversos efeitos na biologia tumoral, entre os quais, a seleção de células cancerígenas mais agressivas e mais resistentes às terapias. Com este projeto pretendemos descobrir o mecanismo molecular envolvido na resistência à combinação de bevacizumab e cetuximab e também encontrar interações de letalidade sintética com hipóxia. Os nossos resultados mostram que: a hipóxia induz resistência à inibição de EGFR em células WT4 de cancro coloretal; o HIF1α não é responsável pelo fenótipo de resistência; a hipóxia ativa RAS em células WT4 de cancro coloretal; os inibidores de MEK aumentam a sensibilidade aos inibidores de EGFR em hipóxia e as citoquinas parecem estar envolvidas na ativação de RAS em hipóxia. Identificámos ainda quatro genes que são potenciais candidatos a terem letalidade sintética com hipóxia. Estes resultados têm uma grande importância clínica e biológica e podem conduzir a melhores terapias combinatórias, contribuindo para melhorar os atuais tratamentos de pacientes com cancro coloretal e podem ainda levar à descoberta de biomarcadores de resposta a terapias antiangiogénicas.
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Phee, Lynette. "Unorthodox antimicrobial combination therapies for the treatment of multi-drug resistant Gram-negative infections." Thesis, Queen Mary, University of London, 2018. http://qmro.qmul.ac.uk/xmlui/handle/123456789/44695.

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The rise of antimicrobial resistance (AMR) has culminated in the most pressing problem in modern medicine. The situation is most acute with regards to the management of multi- drug resistant Gram-negative infections (MDRGNB) with common infections increasingly untreatable due to rapidly dwindling therapeutic options. A solution to the problem of AMR is unlikely to be easily found, but revisiting and re-purposing existing antimicrobials is a viable approach in the medium term. This study investigated the use of unorthodox antimicrobial combination therapies for the treatment of MDRGNB, with particular focus on agents of last resort. A systematic review of clinical studies highlighted the potential for polymyxin (colistin) combination therapies (e.g. colistin-rifampicin, colistin-carbapenems), although this could not be supported in a formal meta-analysis. A systematic approach for screening MDRAB for susceptibility to novel colistin combinations using multiple methods was employed and uncovered a number that were more potent than those previously identfied. The most potent combination that was consistently identified was colistin when combined with fusidic acid, despite this drug having no useful activity against MDRGNB on its own. The combination was further evaluated in static time-kill assays against a range of Gram-negative pathogens with defined resistance mechanisms, including to polymyxins and using invertebrate (Galleria mellonella) and murine models of MDRGNB infection. Colistin and fusidic acid combination therapy was subsequently used to successfully treat a case of ventilator-associated pneumonia due to MDR A. baumannii. This work highlights how older drugs can be re-purposed to tackle the problem of AMR using a precision medicine approach. Further studies to elucidate the mechanism of action of the colistin- fusidic acid combination and a formal clinical trial are warranted to investigate the potential utility of this combination in the treatment of MDRGNB with the expressed goal of bridging the current antimicrobial development gap.
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Cerqueira, Vera. "Role of intracellular signalling pathways in conferring resistance to endocrine therapies in breast cancer." Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/4511.

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Breast cancer is the most prevalent form of cancer in women and accounts for 519,000 annual deaths (WHO Statistics). It has long been established that oestrogen (E2) stimulates tumour growth of oestrogen receptor (ER) positive breast cancer and is involved in the pathogenesis of the disease. Consequently, therapeutic approaches targeting the ER were developed. The use of endocrine therapy is an integral component in treating breast cancer however resistance to such drugs is a major limitation. Unfortunately, even initially responding tumours eventually develop resistance - acquired resistance. The aim of this study was to determine which intracellular pathways may be important in conferring acquired endocrine resistance. In order to do so, a three-stage MCF-7 cell model emulating the clinical development of acquired endocrine was used. MCF-7/LCC1 (LCC1) and MCF-7/LCC9 (LCC9) cells lines were derived from the oestrogen dependent and antioestrogen sensitive MCF-7 cell line. LCC1 cells remain responsive to endocrine therapies but their growth is not dependent on oestrogenic stimulus. LCC9 cells, on the other hand are fully resistant to endocrine therapies and completely oestrogen independent. A number of different cell membrane receptors and intracellular pathways have been implicated in endocrine resistance including HER receptor family, PI3K/Akt & MEK/ERK pathways. These pathways are of particular interest since they are able to activate ER in the absence of oestrogenic stimulus. It is likely that several pathways may be important in conferring resistance to endocrine therapies therefore the experiments in this study focussed on the transcriptional regulation of HER receptors, the activation of the Akt pathway and its implication to basic cellular processes. Following E2 treatment (48h), HER2/3/4 mRNA and protein levels were reduced in MCF- 7 and LCC1 but not in the endocrine-resistant LCC9 cell line as measured by QRT-PCR and Western blotting. The anti-estrogen fulvestrant (ICI 182,780) reversed the E2 modulation. A previous study has shown that ER and the HER2 promoter compete for limiting amounts of SRC-1 in oestrogen-responsive ZR-75-1 cells, causing HER2 repression after E2 stimulation (Newman et al.,Oncogene, 19, 490-7, 2000). ER RNAi abolished E2 repression of HER2 in MCF-7 and LCC1 cells. Furthermore, LCC9 cells have reduced SRC-1 recruitment to ER (assessed by ChIP) allowing SRC-1 to bind to the HER2 promoter. SRC-1 RNAi reduced HER2 transcription in MCF7 cells in a manner similar to E2 whilst it did not restore E2 repression in LCC9 suggesting that the latter cells have alternative mechanisms regulating HER2 transcription. RNAis against the other two p160 co-activators TIF2 and AIB1 did not restore E2 mediated HER2 repression in LCC9 cells. The importance of redundancy between p160 co-activators was also determined by performing double knockouts. SRC-1/TIF2 and TIF2/AIB1 double siRNAs had little effect on HER2 mRNA levels however SRC-1/AIB1 siRNA restored oestrogen mediated downregulation of HER2 transcription in LCC9 cells. This data indicates that SRC-1 and AIB1 co-activators play a role in the transcriptional regulation of HER receptor particularly in MCF-7 and LCC1 cells. The regulation of this transcriptional mechanism is altered in resistant LCC9 cells but, as evidenced by the double knockouts, p160 coactivators are still able to affect HER expression in these cells. This mechanism was further studied in primary breast cancer tumour material. The importance of the Akt pathway in this cell line model was also investigated as phospho-Akt levels are elevated in LCC1 and LCC9 cells. This in turn was shown to activate mTOR and ER (Ser167 residue phosphorylation) thereby contributing to increased growth and ligand independent activation of the oestrogen receptor respectively. Activation of PI3K and PTEN is unchanged in LCC1 and LCC9 cells suggesting that these proteins are not responsible for elevated Akt phosphorylation. In contrast, these cells do express higher levels of phospho-IGFR due to the high availability of receptor ligands (IGFI & IGFII). This is likely to be, at least partially, responsible for the elevated Akt activation. Moreover, the role of Akt isoforms was also determined as they are known to have different functions. The levels of Akt 2 phosphorylation are higher in endocrine resistant cell lines in comparison to parental MCF-7 cells. Interestingly, the Akt 3 phosphorylation is present in all cell lines whilst Akt 1 phosphorylation is minimal. Nevertheless, Akt RNAi studies reveal that Akt 1 and 2 siRNA dramatically reduce growth in MCF-7, LCC1 and LCC9 cells. These results suggest that Akt 2 phosphorylation may play a part in conferring endocrine resistance but the other isoforms are also important for normal cellular growth. The cell cycle profiles of LCC1 and LCC9 are very similar to MCF-7. Similarly, migration levels are unchanged in endocrine resistant cell lines. However, in the presence of antioestrogenic drugs, apoptosis in LCC1 and LCC9 cells in reduced in comparison to the parental MCF-7 cell line. Furthermore, LCC1 and LCC9 cells have higher invasion rates. The deregulation of HER receptor expression and elevated Akt activation may together confer survival advantage in LCC1 and LCC9 cells whilst also increasing their invading potential.
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Yeoman, Kathryn (Kate) Charlotte. "Working the System: Doing Postmodern Therapies in Aotearoa New Zealand." Thesis, University of Canterbury. Humanities, 2012. http://hdl.handle.net/10092/7274.

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This thesis documents a qualitative research study of twenty postmodern therapy practitioners in Aotearoa New Zealand, focusing on their experiences in the wider field of therapy. The participants were aligned in their subscribing to postmodern critiques of therapy as a instrument of power, and in their interest in, and use of, therapy techniques and approaches that have grown out of those critiques – including narrative therapy, critical psychology, “Just Therapy”, and feminist poststructuralist therapy approaches. I argue that these practitioners represent a social movement within the field of therapy. The thesis examines the nature of the wider therapy field in Aotearoa New Zealand, analysing the perspectives of the participants. I demonstrate how this field has become increasingly dominated by the twin forces of neoliberalism and bio-science, making postmodern therapy work difficult, particularly within public sector services. In the final substantive part of the thesis, I critically examine and appraise the strategies used by participants to negotiate and resist these forces. This discussion is divided into two main chapters, dealing first with the participants who have difficulty in engaging in official politics and who consequently attempt to operate “under the radar” of management surveillance: these participants are characterised as “battlers”, “burn-outs” and “blow-outs”. Then, I turn my attention to the second group of participants – “infiltrators”, “outsiders” and “accepters” – who strategically utilise symbolic capital to pose resistance, or simply leave the public system. I also consider the professed abilities of this second group to cultivate a postmodern sensibility and to tolerate contradiction and compromise. I conclude this investigation of the possibilites for resistance to neoliberal and bio-scientific discourses by recommending greater strengthening of this local postmodern therapy movement.
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Söderhäll, Thomas. "Antibiotic combination therapies against carbapenamse producing Klebsiella pneumoniae." Thesis, Uppsala universitet, Institutionen för biologisk grundutbildning, 2021. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-452424.

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The treatment options for multidrug resistant bacteria are dwindling and it is an important issue of research in medicine to solve. One of the more problematic bacterial species is Klebsiella pneumoniae, it can cause infections with high morbidity that are difficult to treat. Common antibiotics for treatment of these infections are carbapenems but K. pneumoniae can produce enzymes called carbapenemases that can hydrolyze carbapenems and most other beta-lactam antibiotics. In this study carbapenemase genes were introduced chromosomally to a previously susceptible K. pneumoniae strain using λ-Red recombineering. Further constructs were made with non-functional porins to examine how they affect combination treatment with carbapenems. Antibiotic combination therapy was evaluated against constructed carbapenemase- (KPC-2, NDM-1 and OXA-48) producing K. pneumoniae strains. Screening was done using time-lapse microscopy (oCelloScope), and combinations with better effect than treatment with a single antibiotic were chosen for time-kill assays. The results shows that a triple combination of colistin, meropenem and the beta-lactamase inhibitor avibactam gives an improved effect, up to twice the effect compared to monotherapy and up to 1.8 times increased effect compared to double combination. The synergistic effect was greater when adding colistin to treat the strains with non-functional porins, indicating that colistin can increase the permeability for other antibiotics into the cell. This is an interesting finding that need to be researched further.
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Salazar, Marcela d'Alincourt. "Genomic Effects of Hormonal Adjuvant Therapies that Could Support the Emergence of Drug Resistance in Breast Cancer." University of Toledo Health Science Campus / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=mco1280929084.

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Books on the topic "Resistance to therapies"

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Xavier, Ana C., and Mitchell S. Cairo, eds. Resistance to Targeted Therapies in Lymphomas. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-24424-8.

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Ling, Silvia CW, and Steven Trieu, eds. Resistance to Targeted Therapies in Multiple Myeloma. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-73440-4.

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Villanueva, Augusto, ed. Resistance to Molecular Therapies for Hepatocellular Carcinoma. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56197-4.

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Prosperi, Jenifer R., ed. Resistance to Targeted Therapies in Breast Cancer. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-70142-4.

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Tivnan, Amanda, ed. Resistance to Targeted Therapies Against Adult Brain Cancers. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-46505-0.

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Szewczuk, Myron R., Bessi Qorri, and Manpreet Sambi, eds. Current Applications for Overcoming Resistance to Targeted Therapies. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-21477-7.

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Ferreri, Andrés J. M., ed. Resistance of Targeted Therapies Excluding Antibodies for Lymphomas. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-75184-9.

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Cappuzzo, Federico. Guide to Targeted Therapies: Treatment Resistance in Lung Cancer. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-20741-4.

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Scardino, Peter T. Targeted Therapies for Castration-Resistant Prostate Cancer. Unitec House, 2 Albert Place, London N3 1QB, UK: Future Medicine Ltd, 2011. http://dx.doi.org/10.2217/9781780840109.

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Michael, Neenan, ed. Working with resistance in rational emotive behaviour therapy: A practitioner's guide. London: Routledge, 2012.

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Book chapters on the topic "Resistance to therapies"

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Weber, Georg F. "Drug Resistance." In Molecular Therapies of Cancer, 407–21. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-13278-5_16.

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McEwan, Ashley, and Silvia CW Ling. "Bone Targeted Therapies." In Resistance to Targeted Anti-Cancer Therapeutics, 105–27. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-73440-4_8.

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Pepper, John W. "Somatic Evolution of Acquired Drug Resistance in Cancer." In Targeted Therapies, 127–34. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60761-478-4_7.

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Kroll, David S. "Treatment Resistance and Advanced Therapies." In Caring for Patients with Depression in Primary Care, 61–73. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-08495-9_6.

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Qadri, Hafsa, Manzoor Ahmad Mir, and Abdul Haseeb Shah. "Antifungal Therapies and Drug Resistance." In Human Fungal Diseases, 130–45. Boca Raton: CRC Press, 2024. http://dx.doi.org/10.1201/9781032642864-10.

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Dai, Yun, and Steven Grant. "Rational Combination of Targeted Agents to Overcome Cancer Cell Resistance." In Targeted Therapies, 171–95. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60761-478-4_10.

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Lage, Hermann, and Carsten Denkert. "Resistance to Chemotherapy in Ovarian Carcinoma." In Targeted Therapies in Cancer, 51–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-46091-6_6.

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Lyons, Anna T., and Jenifer R. Prosperi. "Targeted Therapies in Breast Cancer." In Resistance to Targeted Anti-Cancer Therapeutics, 139–54. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-70142-4_6.

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Gunther, Edward. "Interrogating Resistance to Targeted Therapy Using Genetically Engineered Mouse Models of Cancer." In Targeted Therapies, 135–53. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60761-478-4_8.

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Srivastava, Rupali, Ananya Padmakumar, Paloma Patra, Sushma V. Mudigunda, and Aravind Kumar Rengan. "Phytonanotechnologies for Addressing Antimicrobial Resistance." In Medicinal Plants and Antimicrobial Therapies, 191–225. Singapore: Springer Nature Singapore, 2024. http://dx.doi.org/10.1007/978-981-99-7261-6_9.

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Conference papers on the topic "Resistance to therapies"

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Brugge, JS, T. Muranen, J. Zoeller, D. Worster, M. Iwanicki, L. Selfors, and G. Mills. "DL1-1: Adaptive Resistance to Targeted Therapies." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-dl1-1.

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Li, Zhenghong, Carrie Qi Sun, Rebecca Arnold, John A. Petros, and Carlos S. Moreno. "Abstract 284: Combination therapies to prevent resistance to androgen deprivation therapies in prostate cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-284.

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Li, Zhenghong, Carrie Qi Sun, Rebecca Arnold, John A. Petros, and Carlos S. Moreno. "Abstract 284: Combination therapies to prevent resistance to androgen deprivation therapies in prostate cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-284.

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Zhang, Baolin, Junjie Chen, Xu Di, and Yaqin Zhang. "Abstract B246: Overcoming cancer resistance to death receptor targeted therapies." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-b246.

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Brown, Wells S., and Michael Wendt. "Abstract B49: Epithelial-mesenchymal plasticity primes inherent resistance to targeted therapies." In Abstracts: AACR Special Conference on Tumor Metastasis; November 30-December 3, 2015; Austin, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.tummet15-b49.

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Luna, Augustin, Özgün Babur, Gonghong Yan, Emek Demir, Chris Sander, and Anil Korkut. "Abstract 2838: Discovery of adaptive resistance pathways and anti-resistance combination therapies in cancer from phosphoproteomic data." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2838.

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Montero, Joan, Cecile Gstalder, Daniel J. Kim, Dorota Sadowicz, Wayne Miles, Michael Manos, Justin R. Cidado, et al. "Abstract 62: Destabilization ofNOXAmRNA as a common resistance mechanism to targeted therapies." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-62.

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Zamanian, Roham T., Mehdi Skhiri, Andrew Hsi, vinicio de Jesus Perez, and Francois Haddad. "Impact Of PAH Specific Therapies On Insulin Resistance In Pulmonary Arterial Hypertension." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5919.

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Politi, Katerina A. "Abstract IA10: Modeling sensitivity and resistance to systemic therapies in lung cancer." In Abstracts: AACR Special Conference on the Evolving Landscape of Cancer Modeling; March 2-5, 2020; San Diego, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.camodels2020-ia10.

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Luna, Augustin, Heping Wang, Ozgun Babur, Chris Sander, and Anil Korkut. "Abstract 3820: Discovery of adaptive resistance pathways and anti-resistance combination therapies from phosphoproteomic data using graphical models." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3820.

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Reports on the topic "Resistance to therapies"

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Li, wanlin, jie Yun, siying He, ziqi Zhou, and ling He. Effect of different exercise therapies on fatigue in maintenance hemodialysis patients:A Bayesian Network Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0144.

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Review question / Objective: Population: maintenance hemodialysis patients. Intervention: exercise therapy (resistance exercise； aerobic exercise； resistance combined aerobic exercise； muscle relaxation training； Baduanjin ). Comparison: simple routine nursing. Outcome: fatigue； sleep quality. Study design: randomized controlled trial. Eligibility criteria: Inclusion and exclusion criteria： RCT of study type exercise intervention in MHD patients' fatigue； Study subjects： MHD patients ≥18 years old, regardless of gender, nationality or race； The intervention measures were exercise therapy, including resistance exercise, aerobic exercise, resistance combined aerobic exercise, Baduanjin, muscle relaxation training, etc. The control group was conventional nursing measures or the comparison of the above exercise therapy； Outcome indicators： The primary outcome indicator was fatigue score, and the secondary outcome indicator was sleep quality score； Exclusion criteria： Literature using non-exercise intervention; Non-Chinese and English documents; Unable to obtain the full text or repeated publication of literature; The data cannot be extracted or the extraction is incomplete; There are serious defects in the design of the research experiment.
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