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Search results for: temozolomide
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for: temozolomide</h1> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">5</span> Anticancer Activity of Edible Coprinus Mushroom (Coprinus comatus) on Human Glioblastoma Cell Lines and Interaction with Temozolomide </h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Maria%20Borawska">Maria Borawska</a>, <a href="https://publications.waset.org/abstracts/search?q=Patryk%20Nowakowski"> Patryk Nowakowski</a>, <a href="https://publications.waset.org/abstracts/search?q=Sylwia%20K.%20Naliwajko"> Sylwia K. Naliwajko</a>, <a href="https://publications.waset.org/abstracts/search?q=Renata%20Markiewicz-Zukowska"> Renata Markiewicz-Zukowska</a>, <a href="https://publications.waset.org/abstracts/search?q=Anna%20Puscion-Jakubik"> Anna Puscion-Jakubik</a>, <a href="https://publications.waset.org/abstracts/search?q=Krystyna%20Gromkowska-Kepka"> Krystyna Gromkowska-Kepka</a>, <a href="https://publications.waset.org/abstracts/search?q=Justyna%20Moskwa"> Justyna Moskwa</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Coprinus comatus (O. F. Müll.) Pers.) should not be confused with the common Ink Cap, which contains coprine and can induce coprine poisoning. We study the possibility of applying coprinus mushroom (Coprinus comatus), available in Poland, as food product supporting the treatment of human glioblastoma cells. The U87MG and T98 glioblastoma cell lines were exposed to water (CW) or ethanol 95° (CE) Cantharellus extracts (50-500 μg/ml), with or without temozolomide (TMZ) during 24, 48 or 72 hours. The cell division was examined by the H³-thymidine incorporation. The statistical analysis was performed using Statistica v. 13.0 software. Significant differences were assumed for p < 0.05. We found that both, CW and CE, administrated alone, had inhibitory effect on cell lines growth, but the CE extract had a higher degree of growth inhibition. The anti-tumor effect of TMZ (50 μM) on U87MG was enhanced by mushroom extracts, and the effect was lower to the effect after using Coprinus comatus extracts (CW and CE) alone. A significant decrease (p < 0.05) in pro-MMP2 (82.61 ± 6.3% of control) secretion in U87MG cells was observed after treated with CE (250 μg/ml). We conclude that extracts of Coprinus comatus, edible mushroom, present cytotoxic properties on U87MG and T98 cell lines and may cooperate with TMZ synergistically enhancing its growth inhibiting activity against glioblastoma U87MG cell line. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=anticancer" title="anticancer">anticancer</a>, <a href="https://publications.waset.org/abstracts/search?q=glioma" title=" glioma"> glioma</a>, <a href="https://publications.waset.org/abstracts/search?q=mushroom" title=" mushroom"> mushroom</a>, <a href="https://publications.waset.org/abstracts/search?q=temozolomide" title=" temozolomide"> temozolomide</a> </p> <a href="https://publications.waset.org/abstracts/104104/anticancer-activity-of-edible-coprinus-mushroom-coprinus-comatus-on-human-glioblastoma-cell-lines-and-interaction-with-temozolomide" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/104104.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">196</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4</span> How OXA GENE Expression is Implicated in the Treatment Resistance and Poor Prognosis in Glioblastoma</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Naomi%20Seidu">Naomi Seidu</a>, <a href="https://publications.waset.org/abstracts/search?q=Edward%20Poluyi"> Edward Poluyi</a>, <a href="https://publications.waset.org/abstracts/search?q=Chibuikem%20Ikwuegbuenyi"> Chibuikem Ikwuegbuenyi</a>, <a href="https://publications.waset.org/abstracts/search?q=Eghosa%20Morgan"> Eghosa Morgan</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The current poor prognosis of glioblastoma has called for the need for an improvement in treatment methods in order to improve its survival rate. Despite the different interventions currently available for this tumor, the average survival is still only a few months. (12-15). The aim is to create a more favorable prognosis and have a reduction in the resistance to treatment currently being experienced, even with surgical interventions and chemotherapy. From the available literature, there is a relationship between the presence of HOX genes (Homeobox genes) and glioblastoma, which could be attributable to the increasing treatment resistance. Hence silencing these genes can be a key to improving survival rates of glioblastoma. A series of studies have highlighted the role that HOX genes play in glioblastoma prognosis. Promotion of human glioblastoma initiation, aggressiveness, and resistance to Temozolomide has been associated with HOXA9. The role of HOX gene expression in cancer stem cells should be studied as it could provide a means of designing CSC-targeted therapies, as CSCs play a part in the initiation and progression of solid tumors. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=GBM-%20%20glioblastoma" title="GBM- glioblastoma">GBM- glioblastoma</a>, <a href="https://publications.waset.org/abstracts/search?q=HOXA%20gene-%20homeobox%20genes%20cluster" title=" HOXA gene- homeobox genes cluster"> HOXA gene- homeobox genes cluster</a>, <a href="https://publications.waset.org/abstracts/search?q=signaling%20pathways" title=" signaling pathways"> signaling pathways</a>, <a href="https://publications.waset.org/abstracts/search?q=temozolomide" title=" temozolomide"> temozolomide</a> </p> <a href="https://publications.waset.org/abstracts/153813/how-oxa-gene-expression-is-implicated-in-the-treatment-resistance-and-poor-prognosis-in-glioblastoma" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/153813.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">106</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3</span> COX-2 Inhibitor NS398 Counteracts Chemoresistance to Temozolomide in T98G Glioblastoma Cell Line</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Francesca%20Lombardi">Francesca Lombardi</a>, <a href="https://publications.waset.org/abstracts/search?q=Francesca%20Rosaria%20Augello"> Francesca Rosaria Augello</a>, <a href="https://publications.waset.org/abstracts/search?q=Benedetta%20Cinque"> Benedetta Cinque</a>, <a href="https://publications.waset.org/abstracts/search?q=Maria%20Grazia%20Cifone"> Maria Grazia Cifone</a>, <a href="https://publications.waset.org/abstracts/search?q=Paola%20Palumbo"> Paola Palumbo</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Glioblastoma multiforme (GBM) is a high-grade primary brain tumor refractory to current forms of treatment. The survival benefits of patients with GBM remain unsatisfactory due to the intrinsic or acquired resistance to temozolomide (TMZ), an alkylating agent, used as the first-line chemotherapeutic drug to treat GBM patients. Its cytotoxic effect is visualized by the induction of O6-methylguanine (O6MeG) within DNA. Cyclooxygenase-2 (COX-2), an inflammation-associated enzyme, has been implicated in tumorigenesis and progression of GBM, its inhibition shows anticancer activities. In the present study, it was verified if the combination of a COX-2 selective inhibitor, NS398, with TMZ could counteract the TMZ resistance. In particular, the effect of NS398 mixed with TMZ was investigated in the GBM TMZ-resistant cell line, T98G. Cells were pretreated with NS398 (100µM, 24 hours) and then exposed to TMZ alone (200µM), NS398 alone, or both for 72 hours, after which cell growth rate and cycle phases, as well as apoptosis level, were evaluated. Coadministration of NS398 and TMZ caused a significant decrease in cell growth and a progressive increase of dead cells detected by trypan blue staining. Moreover, a significant level of apoptotic cell percentage and alteration of cell cycle phases were observed in T98G treated with TMZ-NS398 combination when compared to untreated cells or TMZ-treated cells. TMZ-resistant tumors, as GBM, express elevated levels of DNA repair enzyme O6-methylguanine-DNA methyltransferase (MGMT). The mixture drastically reduced MGMT expression in the TMZ-resistant cell line T98G, known to express high levels of MGMT basically. Moreover, while TMZ alone did not influence the COX-2 protein expression, the combination successfully reduced it. In conclusion, these results demonstrated that NS398 enhanced the efficacy of TMZ through cell number reduction, apoptosis induction, and decreased MGMT levels, suggesting the ability of drug combination to reduce the chemoresistance. This drug combination deserves attention and could be considered as a promising therapeutic strategy for GBM patients. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=COX-2" title="COX-2">COX-2</a>, <a href="https://publications.waset.org/abstracts/search?q=COX-2%20inhibitor" title=" COX-2 inhibitor"> COX-2 inhibitor</a>, <a href="https://publications.waset.org/abstracts/search?q=glioblastoma" title=" glioblastoma"> glioblastoma</a>, <a href="https://publications.waset.org/abstracts/search?q=NS398" title=" NS398"> NS398</a>, <a href="https://publications.waset.org/abstracts/search?q=T98G" title=" T98G"> T98G</a>, <a href="https://publications.waset.org/abstracts/search?q=temozolomide" title=" temozolomide"> temozolomide</a> </p> <a href="https://publications.waset.org/abstracts/129238/cox-2-inhibitor-ns398-counteracts-chemoresistance-to-temozolomide-in-t98g-glioblastoma-cell-line" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/129238.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">153</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">2</span> Bionaut™: A Microrobotic Drug-Device Platform for the Local Treatment of Brainstem Gliomas</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Alex%20Kiselyov">Alex Kiselyov</a>, <a href="https://publications.waset.org/abstracts/search?q=Suehyun%20Cho"> Suehyun Cho</a>, <a href="https://publications.waset.org/abstracts/search?q=Darrell%20Harrington%3B%20Florent%20Cros"> Darrell Harrington; Florent Cros</a>, <a href="https://publications.waset.org/abstracts/search?q=Olin%20Palmer"> Olin Palmer</a>, <a href="https://publications.waset.org/abstracts/search?q=John%20Caputo"> John Caputo</a>, <a href="https://publications.waset.org/abstracts/search?q=Michael%20Kardosh"> Michael Kardosh</a>, <a href="https://publications.waset.org/abstracts/search?q=Eran%20Oren"> Eran Oren</a>, <a href="https://publications.waset.org/abstracts/search?q=William%20Loudon"> William Loudon</a>, <a href="https://publications.waset.org/abstracts/search?q=Michael%20Shpigelmacher"> Michael Shpigelmacher</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Despite the most aggressive surgical and adjuvant therapeutic strategies, treatment of both pediatric and adult brainstem tumors remains problematic. Novel strategies, including targeted biologics, immunotherapy, and specialized delivery systems such as convection-enhanced delivery (CED), have been proposed. While some of these novel treatments are entering phase I trials, the field is still in need of treatment(s) that exhibits dramatically enhanced potency with optimal therapeutic ratio. Bionaut Labs has developed a modular microrobotic platform for performing localized delivery of diverse therapeutics in vivo. Our biocompatible particles (Bionauts™) are externally propelled and visualized in real-time. Bionauts™ are specifically designed to enhance the effect of radiation therapy via anatomically precise delivery of a radiosensitizing agent, as exemplified by temozolomide (TMZ) and Avastin™ to the brainstem gliomas of diverse origin. The treatment protocol is designed to furnish a better therapeutic outcome due to the localized (vs systemic) delivery of the drug to the neoplastic lesion(s) for use as a synergistic combination of radiation and radiosensitizing agent. In addition, the procedure is minimally invasive and is expected to be appropriate for both adult and pediatric patients. Current progress, including platform optimization, selection of the lead radiosensitizer as well as in vivo safety studies of the Bionauts™ in large animals, specifically the spine and the brain of porcine and ovine models, will be discussed. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=Bionaut" title="Bionaut">Bionaut</a>, <a href="https://publications.waset.org/abstracts/search?q=brainstem" title=" brainstem"> brainstem</a>, <a href="https://publications.waset.org/abstracts/search?q=glioma" title=" glioma"> glioma</a>, <a href="https://publications.waset.org/abstracts/search?q=local%20delivery" title=" local delivery"> local delivery</a>, <a href="https://publications.waset.org/abstracts/search?q=micro-robot" title=" micro-robot"> micro-robot</a>, <a href="https://publications.waset.org/abstracts/search?q=radiosensitizer" title=" radiosensitizer"> radiosensitizer</a> </p> <a href="https://publications.waset.org/abstracts/131922/bionaut-a-microrobotic-drug-device-platform-for-the-local-treatment-of-brainstem-gliomas" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/131922.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">195</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">1</span> Targeting Glucocorticoid Receptor Eliminate Dormant Chemoresistant Cancer Stem Cells in Glioblastoma</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Aoxue%20Yang">Aoxue Yang</a>, <a href="https://publications.waset.org/abstracts/search?q=Weili%20Tian"> Weili Tian</a>, <a href="https://publications.waset.org/abstracts/search?q=Yonghe%20Wu"> Yonghe Wu</a>, <a href="https://publications.waset.org/abstracts/search?q=Haikun%20Liu"> Haikun Liu</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Brain tumor stem cells (BTSCs) are resistant to therapy and give rise to recurrent tumors. These rare and elusive cells are likely to disseminate during cancer progression, and some may enter dormancy, remaining viable but not increasing. The identification of dormant BTSCs is thus necessary to design effective therapies for glioblastoma (GBM) patients. Little progress has been made in therapeutic treatment of glioblastoma in the last decade despite rapid progress in molecular understanding of brain tumors1. Here we show that the stress hormone glucocorticoid is essential for the maintenance of brain tumor stem cells (BTSCs), which are resistant to conventional therapy. The glucocorticoid receptor (GR) regulates metabolic plasticity and chemoresistance of the dormant BTSC via controlling expression of GPD1 (glycerol-3-phosphate dehydrogenase 1), which is an essential regulator of lipid metabolism in BTSCs. Genomic, lipidomic and cellular analysis confirm that GR/GPD1 regulation is essential for BTSCs metabolic plasticity and survival. We further demonstrate that the GR agonist dexamethasone (DEXA), which is commonly used to control edema in glioblastoma, abolishes the effect of chemotherapy drug temozolomide (TMZ) by upregulating GPD1 and thus promoting tumor cell dormancy in vivo, this provides a mechanistic explanation and thus settle the long-standing debate of usage of steroid in brain tumor patient edema control. Pharmacological inhibition of GR/GPD1 pathway disrupts metabolic plasticity of BTSCs and prolong animal survival, which is superior to standard chemotherapy. Patient case study shows that GR antagonist mifepristone blocks tumor progression and leads to symptomatic improvement. This study identifies an important mechanism regulating cancer stem cell dormancy and provides a new opportunity for glioblastoma treatment. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=cancer%20stem%20cell" title="cancer stem cell">cancer stem cell</a>, <a href="https://publications.waset.org/abstracts/search?q=dormancy" title=" dormancy"> dormancy</a>, <a href="https://publications.waset.org/abstracts/search?q=glioblastoma" title=" glioblastoma"> glioblastoma</a>, <a href="https://publications.waset.org/abstracts/search?q=glycerol-3-phosphate%20dehydrogenase%201" title=" glycerol-3-phosphate dehydrogenase 1"> glycerol-3-phosphate dehydrogenase 1</a>, <a href="https://publications.waset.org/abstracts/search?q=glucocorticoid%20receptor" title=" glucocorticoid receptor"> glucocorticoid receptor</a>, <a href="https://publications.waset.org/abstracts/search?q=dexamethasone" title=" dexamethasone"> dexamethasone</a>, <a href="https://publications.waset.org/abstracts/search?q=RNA-sequencing" title=" RNA-sequencing"> RNA-sequencing</a>, <a href="https://publications.waset.org/abstracts/search?q=phosphoglycerides." title=" phosphoglycerides."> phosphoglycerides.</a> </p> <a href="https://publications.waset.org/abstracts/150825/targeting-glucocorticoid-receptor-eliminate-dormant-chemoresistant-cancer-stem-cells-in-glioblastoma" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/150825.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">85</span> </span> </div> </div> </div> </main> <footer> <div id="infolinks" class="pt-3 pb-2"> <div class="container"> <div style="background-color:#f5f5f5;" class="p-3"> <div class="row"> <div class="col-md-2"> <ul class="list-unstyled"> About <li><a href="https://waset.org/page/support">About Us</a></li> <li><a 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