Relevant bibliographies by topics / Chemotherapy role

Academic literature on the topic 'Chemotherapy role'

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Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Chemotherapy role"

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(R.T), Dr C. S. K. Prakash, M. D. "Nasopharyngeal Carcinoma- Role of External Beam Radiotherapy (EBRT) and Chemotherapy Vs EBRT, Chemotherapy and Intraluminal Brachytherapy." Journal of Medical Science And clinical Research 04, no. 10 (October 27, 2016): 13348–61. http://dx.doi.org/10.18535/jmscr/v4i10.92.

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Nithish, Dr C., Dr G. Ajith Kumar, and Dr P. Sravani. "Fishing Clues for the Efficacy of Chemotherapy: Role of Fasting." International Journal of Trend in Scientific Research and Development Volume-3, Issue-4 (June 30, 2019): 109–11. http://dx.doi.org/10.31142/ijtsrd23581.

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Crump, Laura. "Chemotherapy treatment — the nurse's role." Veterinary Nursing Journal 27, no. 5 (May 2012): 183–85. http://dx.doi.org/10.1111/j.2045-0648.2012.00175.x.

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Hansen, H. H. "739 The role of chemotherapy." European Journal of Cancer Supplements 1, no. 5 (September 2003): S222—S223. http://dx.doi.org/10.1016/s1359-6349(03)90767-1.

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Lind, Julena, and Nancy Jo Bush. "Nursing's role in chemotherapy administration." Seminars in Oncology Nursing 3, no. 2 (May 1987): 83–86. http://dx.doi.org/10.1016/0749-2081(87)90027-1.

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Ishikawa, Kazuhiro, Mikiyo Maeda, Yumiko Goto, Amar Gajjar, and Toshitaka Nabeshima. "Role of Pharmacists in Innovative Chemotherapy :." Iryo Yakugaku (Japanese Journal of Pharmaceutical Health Care and Sciences) 33, no. 12 (2007): 987–97. http://dx.doi.org/10.5649/jjphcs.33.987.

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Aragon-Ching, JeannyB, Rita Nader, and Joelle El Amm. "Role of chemotherapy in prostate cancer." Asian Journal of Andrology 20, no. 3 (2018): 221. http://dx.doi.org/10.4103/aja.aja_40_17.

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Paiar, Fabiola, Vanessa Di Cataldo, Giacomo Zei, Eleonora Monteleone Pasquetti, Sara Cecchini, Icro Meattini, Monica Mangoni, et al. "Role of chemotherapy in nasopharyngeal carcinoma." Oncology Reviews 6, no. 1 (June 12, 2012): 1. http://dx.doi.org/10.4081/oncol.2012.e1.

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Nasopharyngeal carcinoma (NPC) is a unique malignant head and neck cancer with clinical, demographic, and geographic features distinct from other head and neck epithelial malignancies. Non-keratinizing, poorly differentiated, and undifferentiated WHO types 2 and 3 is the most common subtypes of NPC. NPC is also characterized by its relatively high sensitivity to radiation, so that in the last decades radiotherapy (RT) has been the cornerstone of treatment. However, in the majority of cases NPC is discovered at locally advanced stage. The results are disappointing when RT alone is offered. The 5-year survival rates have been reported to be about 34-52%. The poor prognosis for advanced NPC led to increasing interests in exploring the use of chemotherapy (CT). NPC has been considered to be not only radiosensitive but also chemo-sensitive and has shown high response rate to various chemotherapeutic agents. Certainly, the treatment strategies for NPC will continue to change and evolve as a better understanding is gained of the molecular and immune mechanisms that drive this disease. We reviewed the current literature focusing on the role of CT and new-targeted agents.
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Housley, Stephen Nick, Paul Nardelli, Allison B. Wang, Ann Marie Flores, Eric J. Perreault, and Tim Cope. "Cancer's role in chemotherapy-induced neuropathy." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e24064-e24064. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e24064.

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e24064 Background: For the constellation of neurological disorders known as chemotherapy-induced neuropathy, mechanistic understanding, and treatment remain deficient. This might be due to the fact that studies on the effects of chemotherapies on the nervous system have utilized experimental models that exclude cancer perhaps due to the presumption that chemotherapy alone explains the neuropathology. However, the convergence of cancer and chemotherapy on the same biological processes seems likely to yield non-linear interactions. This led us to hypothesize that clinically relevant neuropathy emerges from codependent actions of cancer and chemotherapy. Methods: We established a clinically-relevant animal model of chronic sensory neuropathy in rats with cancer (adenomatous polyposis coli in rat colon: Apc+/Pirc) and age-matched animals without cancer ( ApcWT) that were randomly assigned to receive a human-scaled course of oxaliplatin (OX) or control treatment (4 groups). We quantified behavioral deficits during precision ladder walking, a validated measure of locomotor performance. Neuronal signaling was measured during terminal in vivo experiments to examine the response of sensory neurons to physiologically-relevant stimuli. We defined statistical significance as when 95% of a highest density interval (HDI) of posterior probabilities do not overlap (hierarchical Bayesian modeling). Results: Apc+/Pirc+OX (n = 11) rats exhibited significantly higher error rate (19.2±5.6%, 95%HDI) during precision ladder walking in comparison to ApcWT+control (2.4±2.7%: n = 9) or Apc+/Pirc +control (2.5±2.9%: n = 7) and significantly exceeded the error rate observed in animals treated with OX alone (8.4±3.1%: n = 10). In contrast to the observations in all other groups, we found drastically impaired neuronal signaling in Apc+/Pirc+OX rats which manifested as significantly reduced sensitivity and attenuated static and dynamic firing patterns (95%HDI). Conclusions: We present the first evidence that chronic neuropathy cannot be explained by the effects of chemotherapy alone but instead depend on non-linear interactions between cancer and chemotherapy. This understanding is a prerequisite for developing meaningful treatment or prevention of neuropathy.
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Hussain, Syed A., Daniel H. Palmer, Andrea Stevens, David Spooner, Christopher J. Poole, and Daniel W. Rea. "Role of chemotherapy in breast cancer." Expert Review of Anticancer Therapy 5, no. 6 (December 2005): 1095–110. http://dx.doi.org/10.1586/14737140.5.6.1095.

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Dissertations / Theses on the topic "Chemotherapy role"

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Allen, W. L. "The role of Fas in response to chemotherapy." Thesis, Queen's University Belfast, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.403264.

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Tran, Cuong Duy. "Intestinal zinc and metallothionein : role in chemotherapy-induced mucositis." Title page, contents and abstract only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phc9736.pdf.

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Bowen, Joanne Marie. "Chemotherapy-induced intestinal mucositis the role of apoptosis regulators /." Click here to access, 2006. http://thesis.library.adelaide.edu.au/public/adt-SUA20060831.142913/index.html.

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Thesis (Ph.D.) -- University of Adelaide, School of Medicine, Discipline of Medicine, 2006.
Includes author's previously published papers. "March 2006" Bibliography: leaves 168-191. Also available in a print form.
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Khongkow, Pasarat. "The role of FOXM1 in breast cancer chemotherapy resistance." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/42884.

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Resistance to chemotherapeutic agents is the main obstacle to the effective breast cancer management. Therefore, it is important to elucidate the molecular mechanisms of chemoresistance and develop novel therapeutic strategies in order to overcome drug resistance. In this work, I found that FOXM1 is a critical mediator of epirubicin and paclitaxel resistance in MCF-7 breast cancer cell lines. FOXM1 expression was upregulated in both epirubicin resistant MCF-7 (MCF-7 EpiR) and paclitaxel resistant MCF-7 (MCF-7 TaxR) cells compared to sensitive MCF-7 cells. Interestingly, its depletion dramatically impaired the clonogenic survival and significantly induced cellular senescence in the resistant cells. In addition, I identified two novel downstream FOXM1 targets, NBS1 and KIF20A, involved in epirubicin and paclitaxel resistance, respectively. Firstly, I found that FOXM1 transcriptionally regulated NBS1 expression to modulate HR-mediated DSB repair and epirubicin resistance. Overexpression of FOXM1 and NBS1 lead to the enhancement of HR efficiency to eliminate epirubicin-induced DNA damage. Conversely, similar to FOXM1, depletion of NBS1 also sensitised both MCF-7 and MCF-7 EpiR cells to epirubicin by inducing cellular senescence. Secondly, I identified the mitotic kinesin KIF20A as a direct downstream target of FOXM1, participating in the mitotic spindle formation and paclitaxel resistance. Depletion of KIF20A caused mitotic spindle abnormalities, inhibition of cell growth as well as the induction of senescent cells in both MCF-7 and MCF-7 TaxR cells. Consistently, immunohistochemical analysis of breast cancer patient samples revealed that high expression levels of FOXM1, NBS1 and KIF20A are strongly correlated with poor prognosis in breast cancer, supporting a physiological role of FOXM1 and its novel targets in genotoxic drug resistance. Collectively, these findings suggests that FOXM1 and its targets, NBS1 and KIF20A, could be reliable prognostic markers for monitoring treatment efficiency as well as promising targets for therapeutic intervention to overcome epirubicin and paclitaxel resistance in breast cancer.
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Simpson, Julie Ann. "The role of population pharmacokinetic- pharmacodynamic modelling in antimalarial chemotherapy." Thesis, Open University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367218.

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Gustafson, Heather Lynn. "Role of Manganese Superoxide Dismutase in Chemotherapy-induced Oxidative Stress." Diss., The University of Arizona, 2011. http://hdl.handle.net/10150/203510.

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Existing treatments for mantle cell lymphoma (MCL) are non-curative, demonstrating a need for a refined treatment approach. Recent clinical trials have shown promising results with the use of mammalian target of rapamycin inhibitors. I hypothesize that the anti-tumor effect of mTOR inhibitors in mantle cell lymphoma is mediated by an increase in manganese superoxide dismutase (MnSOD) protein expression and accumulation of hydrogen peroxide (H₂O₂). Findings indicate that the rapamycin-induced cytostatic effect is characterized by increased levels of MnSOD and H₂O₂, and is necessary for the full growth inhibitory effect of rapamycin. Furthermore, over-expression of MnSOD elevated the level of H₂O₂ and increased sensitivity to MnSOD. Treatment with rapamycin resulted in a loss of serine 473 phosphorylation of AKT and increased levels of MnSOD were found to be due to inhibition of the mTORC2 complex. These results are the first to suggest that long term treatment of MCL cells with rapamycin inhibits the mTORC2 complex. By understanding the key signaling molecules and affected pathways in the anti-tumor effects of mTOR inhibitors, we may be able to identify additional predictive markers to improve the therapeutic value, or study drug combinations that will enhance the effect of ROSinduced cytotoxicity. A retrospective study utilizing samples from lymphoma patients receiving standard anthracycline-based therapies, identified single nucleotide polymorphisms in oxidative stressrelated genes associated with survival. Individuals carrying minor allele SNPs in myeloperoxidase (MPO) and an aldo-keto reductase (AKR1C3) were found to be associated with shorter time to disease progression and death. This data suggest that some patients may benefit from a different therapy than the current standard of care and that regulation of the redox environment plays a role in aggressive lymphoma treatment response.
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Kwan, Stanley. "The role of ASK1 in arsenic trioxide-induced cell death." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=114442.

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Arsenic trioxide (ATO) is an effective treatment for acute promyelocytic leukemia (APL). While it is undergoing clinical trials for numerous malignancies including multiple myeloma, myelodysplastic syndrome, lymphoma and solid tumors, it has demonstrated only limited efficacy as a single agent. However, it may hold promise as part of a combination therapy. Thus investigation to elucidate the mechanisms of action underlying these clinical responses may lead to generation of rational combination therapies to increase its therapeutic spectrum. Previous work has described a pathway required for ATO-induced apoptosis in APL cells involving the generation of reactive oxygen species (ROS), and the subsequent induction of a specific mitogen-activated protein kinase (MAPK) cascade that includes both stress-activated protein kinase (SAPK)/ERK kinase 1 (SEK1) and c-Jun N-terminal kinases (JNK) activation. However, the link between ROS production and activation of SEK1 remains to be elucidated. Apoptosis signaling kinase 1 (ASK1) is a MAP3K upstream of SEK1 that has been implicated in the induction of stress-induced signaling.Using murine embryonic fibroblasts (MEFs) derived from ASK1-/- mice; we provide evidence that ASK1 is a strong mediator for ATO-induced apoptosis and JNK activation. In an APL cell line, we show that ATO activates ASK1 in a dose- and time-dependent manner. However, knockdown of ASK1 in APL cells enhanced susceptibility to ATO, undergoing apoptosis and growth inhibition more than their wild type counterparts. The same impact was observed in the knockdown of SEK1, a direct downstream MAP2K of ASK1, and the knockdown of ASK1 in MCF-7 cells, a human breast cancer cell line. This led us to postulate that ASK1 had a pro-apoptotic function in non-transformed fibroblasts, but was pro-survival in malignant cells. Indeed, transformation of ASK1-/- MEFs restored their sensitivity to ATO-induced apoptosis and growth inhibition. Taken together, these results suggest that ASK1 can have both pro-apoptotic and anti-apoptotic roles depending on the transformation state of the cells.One model of ASK1 regulation suggests that ASK1 is kept in an inactive form by reduced thioredoxin-1 (Trx1). During oxidative stress, Trx1 is oxidized and releases ASK1 for activation. Immunoprecipitation of ASK1 followed by immuoblotting for Trx1 in APL cells shows a strong basal association that is lost with ATO treatment. Furthermore, the activity of thioredoxin reductase 1 (TrxR1), an enzyme that converts oxidized Trx1 into reduced Trx1, is significantly decreased following ATO treatment. This suggests that ATO activates ASK1 signaling by ROS-mediated oxidation of Trx1 and by maintaining Trx1 in its oxidized state by decreasing TrxR1 activity. In addition, we show that inhibition of TrxR1 with the TrxR1 inhibitor Auranofin sensitizes APL cells to ATO-induced apoptosis. Overall, our results suggest that targeting Trx1 may enhance ATO-induced apoptosis in a novel combination therapy.
L'arsenic trioxyde (ATO) est un traitement efficace contre la leucémie promyélocitaire aïgue (APL). Alors qu'il est testé dans le cadre de plusieurs essais cliniques sur différents cancers comme le myélome multiple, le syndrome myélodysplasique, le lymphome et les tumeurs solides, il ne montre qu'une efficacité limitée en tant qu'agent unique. Quoiqu'il en soit, il pourrait être prometteur au sein d'une thérapie combinée. Ainsi, l'étude des mécanismes d'action responsables des bénéfices cliniques apportés par l'arsenic trioxide pourrait mener à la mise au point de nouvelles thérapies combinées afin d'élargir le spectre thérapeutique d'ATO. Des travaux antérieurs ont décri une voix de signalisation, requise pour l'induction de l'apoptose par l'arsenic dans des cellules d'APL, qui implique la génération d'espèces actives de l'oxygène (ROS), ainsi que l'induction subséquente d'une cascade de protéine kinases mitogène-activées (MAPK) spécifique qui inclut à la fois la protéine kinase stress-activée (SAPK)/ERK kinase 1(SEK1) ainsi que l'activation de la kinase c-jun N-terminal (JNK). Néanmoins, le lien entre la production de ROS et l'activation de SEK1 reste à être élucidé. La kinase de signalisation de l'apoptose (ASK1) est une MAP3K en amont de SEK1 qui a été impliquée dans l'induction de la signalisation induite par le stress. En utilisant des fibroblastes d'embryions de souris (MEFs) dérivées de souris ASK-/-, nous montrons qu'ASK1 est un médiateur fort de l'apoptose et de l'activation de JNK par ATO. Dans une lignée cellulaire APL, nous montrons qu'ATO active ASK1 en fonction du temps et de la dose. Par contre, une sous-régulation d'ASK1 dans des cellules APL augmente la susceptibilité envers ATO, ce qui se traduit par une diminution de la croissance et une augmentation de l'apoptose par rapport aux cellules APL sauvages. Un impact similaire est observé lors d'une sous régulation de SEK1, une MAP2K directement en aval d'ASK1, ainsi que lors d'une sous régulation d'ASK1 dans des cellules MCF-7, des cellules de cancer du sein humain. Cela nous a conduit à postuler qu'ASK1 a une fonction pro-apoptotique dans les fibroblastes non-transformés, mais anti-apoptotique dans des cellules malignes. En effet, la transformation des cellules MEFs ASK-/- a restauré leur sensibilité envers l'arrêt de la croissance et l'apoptose induits par ATO, ce qui souligne les différences entre les cellules normales et les cellules transformées. Dans l'ensemble, ces résultats suggèrent qu'ASK1 a un rôle important dans la sensibilité à l'ATO qui dépend du contexte. Un des schémas de régulation d'ASK1 suggère qu'ASK1 est séquestré sous une forme inactive par la thioredoxine-1 réduite (Trx1). Durant le stress oxydatif, Trx1 est oxydée et libère ASK1 afin qu'il puisse être activé. L'immuno-précipitation d'ASK1 suivie d'un immuno-marquage for Trx1 dans des cellules APL montre une association basale forte qui est perdue lors du traitement avec ATO. De plus, l'activité de la réductase de la thioredoxine (TrxR1), une enzyme qui convertit Trx1 oxydée en Trx1 réduite, est diminuée de façon significative après traitement avec ATO. Cela suggère qu'ATO active la signalisation d'ASK1 en oxydant Trx1, via les ROS, ainsi qu'en inhibant la réduction de Trx1 en diminuant l'activité de TrxR1. De plus, nous montrons que l'inhibiteur de TrxR1, Auranofin, sensibilise les cellules APL à l'apoptose induite par ATO. Cela suggère que la régulation d'ASK1 dépend du statut redox de Trx1. Dans l'ensemble, nos résultats suggèrent que le fait de cibler Trx1 pourrait augmenter la signalisation d'ASK1 et l'apoptose induite par ATO au sein d'une nouvelle thérapie combinée.
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Wong, Chung-lim, and 黃仲廉. "The role of GEP on chemotherapy induced alterations in hepatocellular carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/197132.

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Hepatocellular carcinoma (HCC) is the fifth most common malignancy and the third leading cause of cancer related death worldwide. Chemo-therapy has been commonly used to treat unresectable HCC but with limited efficacy. Therefore, there is an urgent demand for the development of better therapeutic approaches. Granulin-epithelin precursor (GEP) is a novel growth factor with over-expression in more than 70% of HCCs and has been demonstrated as potential therapeutic target. The aims of this study are to examine the role of GEP in chemo-resistance and the therapeutic potential of GEP antibody therapy in combination with chemo-therapy in HCC. The role of GEP in HCC chemo-resistance has been examined by HCC in vitro models in the first part of the study and by in vivo human HCC xenograft models in immunocompromised mice in the second part of the study. It was shown that the chemo-therapeutic agents selected HCC cells in vitro and in vivo resulted in increased cellular expression of GEP, ABCB5, hepatic cancer stem cell (CSC) marker CD133/EpCAM positive populations and demonstrated enhanced CSCs properties including colony formation ability and chemo-resistance. Over-expression and knockdown of GEP expressions respectively demonstrated that GEP levels were important in conferring resistance to the chemo-therapeutic agents and the drug-induced apoptosis. GEP antibody therapy not only sensitized the parental HCC populations but also the chemo-resistant subpopulations to chemo-therapy induced apoptosis. Importantly, combination of GEP antibody therapy with chemo-therapy inhibited the chemo-therapy induced GEP, ABCB5 and heaptic CSCs marker over-expression through neutralization of the secretary GEP levels in the culture supernatant, and the serum GEP levels in the HCC orthotopic mice model. In human HCC xenograft models, GEP antibody treatment alone is consistently able to inhibit the tumor growth, but is unable to eliminate the established intrahepatic tumor. Cisplatin treatment, low and high dose respectively, was only able to eradicate a fraction of the intrahepatic tumor and the residual tumors grew aggressively after chemo-drug withdrawal. Combination of GEP antibody with low dose of cisplatin resulted in significant proliferation inhibition and apoptosis induction respectively. Importantly, combination of GEP antibody with high dose of cisplatin resulted in eradication of all established intrahepatic tumor. In addition, chemo-therapy induced the Akt/PKB and MEK/ERK prosurvival pathways, disturbed the balanced between the ratio of pro-apoptotic (Bax) to anti-apoptotic (Bcl-2) member through the induction of Bcl-2. Nonetheless, combination GEP antibody therapy suppressed the chemo-therapy induced phosphorylation of PDK1, Akt, MEK, ERK, and Bcl-2 levels. It was shown that Wortmannin, the PI3K/Akt inhibitor, suppressed the expression of ABCB5 and Bcl-2 induced by chemo-therapy but showed no effect on GEP expression levels. In summary, the study demonstrated the chemo-therapy treatment alone induced the expression of growth factor GEP, drug transporter ABCB5, hepatic cancer stem cell markers expressions, and the residual cancer cells showed enhanced CSCs properties. Combination treatment with GEP antibody reversed the signaling and cancer stem cell properties induced by chemo-therapy alone. Therefore, further investigations of this combination treatment approach may lead to the development of novel therapeutic approach for the clinical treatment of chemo-resistant HCC.
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McDermott, Ultan. "The role of Fas in chemotherapy-induced colorectal cancer cell death." Thesis, Queen's University Belfast, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.426703.

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Gomes, Ana Rita. "The role and regulation of FOXO3a in cancer and chemotherapy resistance." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/14582.

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Drug resistance is the major impediment to the success of cancer therapy. The PI3K/AKT pathway mediates a plethora of cellular functions, including cell survival, proliferation and differentiation. However, increased activation of this pathway has been correlated with drug resistance mechanisms. This pathway regulates the activity of FOXO transcription factors in a negative manner through AKT-dependent phosphorylations. The modulation of FOXO activity leads to a variety of cellular outputs, including cell cycle arrest and apoptosis that define this transcription factor as a tumour suppressor. Importantly, FOXO has also been shown to mediate the effect of many anti-cancer drugs, suggesting that it has an additional role in drug sensitivity and resistance. With this work, by studying the PI3K/AKT/FOXO axis in breast cancer, I have characterised its impact in drug sensitivity and resistance. I found that this axis is deregulated in breast cancer resistant cells. By extending my in vitro findings to clinical samples, I further elucidated the potential role of AKT and FOXO3a as indicators and predictors of treatment response in breast cancer. In addition, I have also characterised three novel downstream targets of FOXO3a - FOXP1, FOXM1 and VEGF – with important roles towards breast cancer progression and in the development of drug-resistance. By characterising these FOXO3a effectors, I unravelled a potential general mechanism by which FOXO3a represses gene target expression.
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Books on the topic "Chemotherapy role"

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Ettinger, David S. The role of chemotherapy in non-small cell lung cancer. Syracuse, NY: Bristol Laboratories Oncology Products, Bristol-Myers Oncology Division, 1986.

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International Symposium on the Expanding Role of Folates and Fluoropyrimidines in Cancer Chemotherapy (1988 Buffalo, N.Y.). The expanding role of folates and fluoropyrimidines in cancer chemotherapy. New York: Plenum Press, 1988.

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Rustum, Youcef, and John J. McGuire, eds. The Expanding Role of Folates and Fluoropyrimidines in Cancer Chemotherapy. New York, NY: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5607-3.

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A, Howell, ed. The Role of antihormones. Carnforth, Lancs, UK: Parthenon Pub. Group, 1991.

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Bunn, Paul A. VePesid (etoposide injection), its role in small cell lung cancer. Syracuse, N.Y: Bristol-Myers, Oncology Division, 1985.

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Chang, David. Targeting regional chemotherapy to hypovascular hepatic tumours: The role of degradable starch microspheres. Manchester: University of Manchester, 1993.

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E, Garfinkel Paul, and Garner David M, eds. The Role of drug treatments for eating disorders. New York: Brunner/Mazel, 1987.

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1946-, Garfinkel Paul E., and Garner David M. 1947-, eds. The Role of drug treatments for eating disorders. New York: Brunner/Mazel, 1987.

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Richard, Beasley, and Pearce Neil, eds. The Role of beta receptor agonist therapy in asthma mortality. Boca Raton: CRC Press, 1993.

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Tetrahydrobiopterin: Basic biochemistry and role in human disease. Baltimore: Johns Hopkins University Press, 1997.

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Book chapters on the topic "Chemotherapy role"

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Mann, Koren K., and Maryse Lemaire. "Role in Chemotherapy." In Arsenic, 315–45. Hoboken, NJ: John Wiley & Sons, Inc, 2015. http://dx.doi.org/10.1002/9781118876992.ch14.

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Fiorentini, Giammaria, Maurizio Cantore, Francesco Montagnani, Andrea Mambrini, Michelina D’Alessandro, and Stefano Guadagni. "The Role of Hypoxia and Hyperthermia in Chemotherapy." In Induction Chemotherapy, 59–69. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-18173-3_6.

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Fiorentini, Giammaria, Maurizio Cantore, Francesco Montagnani, Andrea Mambrini, Michelina D’Alessandro, and Stefano Guadagni. "The Role of Hypoxia and Hyperthermia in Chemotherapy." In Induction Chemotherapy, 61–71. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28773-7_6.

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Pereira, Guilherme Luiz Stelko, and Eduardo Saadi Neto. "The Role of Chemotherapy." In Diffuse Gastric Cancer, 65–75. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-95234-5_8.

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Salvatore, Lisa, Federica Zoratto, Fotios Loupakis, and Alfredo Falcone. "The Role of Metronomic Chemotherapy in the Treatment of Metastatic Colorectal Cancer Patients." In Metronomic Chemotherapy, 135–42. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-43604-2_9.

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Trenta, Patrizia, Sara Giovannoni, Emanuela Risi, and Enrico Cortesi. "The Role of Systemic Chemotherapy." In Treatment of Peritoneal Surface Malignancies, 179–94. Milano: Springer Milan, 2015. http://dx.doi.org/10.1007/978-88-470-5711-1_12.

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Chamberlain, Marc C. "Intracranial Ependymoma: Role for Chemotherapy." In Tumors of the Central Nervous System, Volume 8, 331–38. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4213-0_33.

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Brodeur, Garrett M., and Valerie P. Castle. "Role of Apoptosis in Human Neuroblastomas." In Apoptosis and Cancer Chemotherapy, 305–18. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-720-8_20.

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El-Deiry, Wafik S. "The Role of p53 in Chemosensitivity." In Apoptosis and Cancer Chemotherapy, 37–52. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-720-8_3.

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Nuermberger, Eric L. "Chapter 15: The Role of the Mouse Model in the Evaluation of New Antituberculosis Drugs." In Antituberculosis Chemotherapy, 145–52. Basel: KARGER, 2011. http://dx.doi.org/10.1159/000323633.

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Conference papers on the topic "Chemotherapy role"

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Winer, E. "The Evolving Role of Adjuvant Chemotherapy." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-cs1-2.

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Ranchoux, Benoit, Sven Günther, Rozenn Quarck, Marie-Camille Chaumais, Peter Dorfmüller, Fabrice Antigny, Sébastian J. Dumas, et al. "Chemotherapy-induced pulmonary hypertension: Role of alkylating agents." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa581.

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Mansouri, Nahal, Ioanna Keklikoglou, Sina Nassiri, Bruno Torchia, Alan Guichard, and Michele De Palma. "Role of extracellular vesicles in chemotherapy-induced lung metastasis." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.3944.

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Cafforio, Alessia, Brigida Anna Maiorano, Evaristo Maiello, Gennaro Cormio, Ettore Cicinelli, Vera Loizzi, Francesca Arezzo, et al. "EP333/#921 Management of uterine carcinosarcoma: role of adjuvant chemotherapy." In IGCS 2022 Annual Meeting Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/ijgc-2022-igcs.423.

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Levine, M., A. Arnold, L. Kelleher, S. Lord, W. Hryniuk, J. Hrish, and M. Gent. "CANCER CHEMOTHERAPY AND THROMBOSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643203.

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Malignant disease is recognized as a risk factor for venous thromboembolism. A number of recent reports have suggested that cancer chemotherapy may contribute to this risk, but it was not possible to separate the role of chemotherapy from the effects of the malignant disease. We are conducting a randomized trial to determine the optimal duration of adjuvant chemotherapy in women with Stage II breast carcinoma. These ambulatory patients, with negligible tumour burden, receive either 12 weeks of chemo-hormonal therapy (cyclophosphamide, methotrexate, 5 fluorouracil, vincristine, prednisone, adriamycin and tamoxifen) or 36 weeks of chemotherapy (cyclophosphamide, methotrexate, 5 fluorouracil, vincristine and prednisone). This study has provided us with an opportunity to evaluate the thrombogenic effects of chemotherapy since patients in the 12 week group, while off chemotherapy, can be compared directly to the patients in the other group who are still on chemotherapy. This allows the confounding influence of the malignant process to be circumvented. All patients undergo screening tests for thrombosis (impedance plethysmography and Doppler ultrasound) and routine clinical assessments. Suspected venous thrombosis is confirmed by venography and suspected pulmonary embolism by either pulmonary angiography or high probability ventilation perfusion scanning. There have been 11 episodes of venous thromboembolism to date among 191 patients of whom 164 have completed the first 36 weeks of study. There were 3 episodes in each group during the first 12 weeks. During the subsequent 24 weeks there have been no events in the group whose treatment was stopped and 5 events in the group still on treatment (p 0.03). These findings demonstrate that chemotherapy per se is an important risk factor for venous thromboembolism in patients with malignant disease.
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Setton, Ariella Jakobson, Gabriel Levin, Oded Raban, Gad Sabah, Daliah Tsoref, Anat From, Tamar Perri, and Ram Eitan. "EP228/#913 Prognostic role of pathological chemotherapy response score in patients receiving neoadjuvant chemotherapy for epithelial ovarian cancer." In IGCS 2022 Annual Meeting Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/ijgc-2022-igcs.319.

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Tang, Yuan, and Anthony J. McGoron. "The role of temperature increase rate in combinational hyperthermia chemotherapy treatment." In BiOS, edited by Wei R. Chen. SPIE, 2010. http://dx.doi.org/10.1117/12.842587.

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Geng, Hao, Tomasz Beer, Pete Nelson, and David Qian. "Abstract 5775: A novel role for ID1 in prostate cancer chemotherapy." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5775.

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Carroll, Molly J., Leora Nusblat, and Charles M. Roth. "Role of inflammatory pathway and cells on glioma cell response to chemotherapy." In 2012 38th Annual Northeast Bioengineering Conference (NEBEC). IEEE, 2012. http://dx.doi.org/10.1109/nebc.2012.6207060.

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Zakir, Mohammad Z. Mohammad, Pritam Chatterjee, and R. Ravikumar. "To Study Role of Intra-arterial Chemotherapy in Treatment of Intraocular Retinoblastoma." In Presentation Abstracts. Thieme Medical and Scientific Publishers Pvt. Ltd., 2021. http://dx.doi.org/10.1055/s-0041-1740837.

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Reports on the topic "Chemotherapy role"

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Paget, Christophe, Helene Duret, and Mark J. Smyth. Role of Natural Killer T Cells In Immunogenic Chemotherapy for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada571626.

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Paget, Christophe, Helene Duret, and Mark J. Smyth. Role of Natural Killer T Cells in Immunogenic Chemotherapy for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada595285.

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Krosky, Daniel J. Rational Inhibitors of DNA Base Excision Repair Enzymes: New Tools for Elucidating the Role of BER in Cancer Chemotherapy. Fort Belvoir, VA: Defense Technical Information Center, May 2006. http://dx.doi.org/10.21236/ada456909.

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Krosky, Daniel J., and James T. Stivers. Rational Inhibitors of DNA Base Excision (BER) Enzymes: New Tools for Elucidating the Role of BER in Cancer Chemotherapy. Fort Belvoir, VA: Defense Technical Information Center, May 2004. http://dx.doi.org/10.21236/ada424155.

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Krosky, Daniel J. Rational Inhibitors of DNA Base Excision Repair Enzymes: New Tools for Elucidating the Role of BER in Cancer Chemotherapy. Addendum. Fort Belvoir, VA: Defense Technical Information Center, November 2006. http://dx.doi.org/10.21236/ada502370.

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Krosky, Daniel J. Rational Inhibitors of DNA Base Excision Repair (BER) Enzymes: New Tools for Elucidating the Role of the BER in Cancer Chemotherapy. Fort Belvoir, VA: Defense Technical Information Center, May 2005. http://dx.doi.org/10.21236/ada437740.

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Sordillo, Lorraine, Don Wojchowski, Gary Perdew, Arthur Saran, and Gabriel Leitner. Identification of Staphylococcus aureaus Virulence Factors Associated with Bovine Mastitis. United States Department of Agriculture, February 2001. http://dx.doi.org/10.32747/2001.7574340.bard.

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Staphylococcus aureus is a major cause of mastitis in dairy cattle. The organism is able to adhere to and penetrate mammary epithelium, forming deep seated abscesses that result in chronic infections. This study was based on the observation that certain genotypes of S. aureus are isolated more frequently from field cases of bovine mastitis than others and the most prevalent genotypes of S. aureus have an increased ability to resist neutrophil phagocytosis and killing compared to the rare variants. It was hypothesized that these predominating genotypes differentially express virulence factors that allow them to overcome or suppress essential host defense mechanisms and successfully colonize mammary parenchyma. The overall objective of this study was to determine the mechanisms by which predominating S. aureus genotypes were able to resist mammary gland defense mechanisms. The following specific aims were accomplished to address the overall objectives of this project: 1. Analyze and compare cell surface and secreted protein profiles of common and rare S. aureus genotypes isolated from field cases of bovine mastitis. 2. Purify and sequence selectively synthesized proteins unique to the most prevalent genotypes of S. aureus . 3. Determine the in vitro effects of isolated proteins on essential host defense mechanisms. Results from each specific aim showed that these redominating genotypes differentially express factors that may allow them to overcome or suppress essential host defense mechanisms and successfully colonize mammary parenchyma. Using complementary approaches, both the US and Israeli teams identified differentially expressed S. aureus factors that were positively correlated with virulence as determined by the ability to modify host immune cell responses and increase disease pathogenesis. Several candidate virulence factors have ben identified at both the molecular (US team) and protein (Israeli team) levels. Components of the phosphotransferase system were shown to be differentially expressed in prevalent strains of S. aureus and to modify the growth potential of these strains in a milk microenvironment. Evidence provided by both the Israeli and US teams also demonstrated a potential role of Staphylococcal enterotoxins in the pathogenesis of mastitis. Certain enterotoxins were shown to directly affect neutrophil bactericidal activities which can profoundly affect the establishment of new intramammary infections. Other evidence suggests that S. aureus superantigens can suppress mammary defenses by enhancing lymphoid suppressor cell activity. Collectively, these data suggest that unique factors are associated with predominating S. aureus genotypes that can affect in vitro and in vivo virulence as related to the pathogenesis of bovine mastitis. The potential development of a subunit mastitis vaccine which incorporates only relevant antigenic determinants has not been investigated in depth. Experiments outlined in this proposal has identified putative virulence factors which contribute to the pathogenesis of S. aureus mastitis and which may be used to formulate an efficacious subunit mastitis vaccine. Results from these studies may lead to the development of new methods to prevent this costly disease, providing a viable alternative to less effective mastitis control procedures based on chemotherapy.
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The role of systemic chemotherapy in penile cancer. BJUI Knowledge, November 2018. http://dx.doi.org/10.18591/bjuik.0198.

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Is there a role for systemic chemotherapy in upper tract urothelial carcinoma? BJUI Knowledge, May 2017. http://dx.doi.org/10.18591/bjuik.0123.

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