Relevant bibliographies by topics / Glioblastoma – therapy

Contents

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

Academic literature on the topic 'Glioblastoma – therapy'

Author: Grafiati
Published: 4 June 2021
Last updated: 4 February 2022

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Journal articles on the topic "Glioblastoma – therapy"

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Kim, Ella L., Maxim Sorokin, Sven Rainer Kantelhardt, Darius Kalasauskas, Bettina Sprang, Julian Fauss, Florian Ringel, et al. "Intratumoral Heterogeneity and Longitudinal Changes in Gene Expression Predict Differential Drug Sensitivity in Newly Diagnosed and Recurrent Glioblastoma." Cancers 12, no. 2 (February 24, 2020): 520. http://dx.doi.org/10.3390/cancers12020520.

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Background: Inevitable recurrence after radiochemotherapy is the major problem in the treatment of glioblastoma, the most prevalent type of adult brain malignancy. Glioblastomas are notorious for a high degree of intratumor heterogeneity manifest through a diversity of cell types and molecular patterns. The current paradigm of understanding glioblastoma recurrence is that cytotoxic therapy fails to target effectively glioma stem cells. Recent advances indicate that therapy-driven molecular evolution is a fundamental trait associated with glioblastoma recurrence. There is a growing body of evidence indicating that intratumor heterogeneity, longitudinal changes in molecular biomarkers and specific impacts of glioma stem cells need to be taken into consideration in order to increase the accuracy of molecular diagnostics still relying on readouts obtained from a single tumor specimen. Methods: This study integrates a multisampling strategy, longitudinal approach and complementary transcriptomic investigations in order to identify transcriptomic traits of recurrent glioblastoma in whole-tissue specimens of glioblastoma or glioblastoma stem cells. In this study, 128 tissue samples of 44 tumors including 23 first diagnosed, 19 recurrent and 2 secondary recurrent glioblastomas were analyzed along with 27 primary cultures of glioblastoma stem cells by RNA sequencing. A novel algorithm was used to quantify longitudinal changes in pathway activities and model efficacy of anti-cancer drugs based on gene expression data. Results: Our study reveals that intratumor heterogeneity of gene expression patterns is a fundamental characteristic of not only newly diagnosed but also recurrent glioblastomas. Evidence is provided that glioblastoma stem cells recapitulate intratumor heterogeneity, longitudinal transcriptomic changes and drug sensitivity patterns associated with the state of recurrence. Conclusions: Our results provide a transcriptional rationale for the lack of significant therapeutic benefit from temozolomide in patients with recurrent glioblastoma. Our findings imply that the spectrum of potentially effective drugs is likely to differ between newly diagnosed and recurrent glioblastomas and underscore the merits of glioblastoma stem cells as prognostic models for identifying alternative drugs and predicting drug response in recurrent glioblastoma. With the majority of recurrent glioblastomas being inoperable, glioblastoma stem cell models provide the means of compensating for the limited availability of recurrent glioblastoma specimens.
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Patrick, Tim. "Glioblastoma Radiation Therapy." Oncology Times 26, no. 3 (February 2004): 6–7. http://dx.doi.org/10.1097/01.cot.0000291725.17913.4a.

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Fahey, Jonathan, and Albert Girotti. "Nitric Oxide Antagonism to Anti-Glioblastoma Photodynamic Therapy: Mitigation by Inhibitors of Nitric Oxide Generation." Cancers 11, no. 2 (February 15, 2019): 231. http://dx.doi.org/10.3390/cancers11020231.

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Many studies have shown that low flux nitric oxide (NO) produced by inducible NO synthase (iNOS/NOS2) in various tumors, including glioblastomas, can promote angiogenesis, cell proliferation, and migration/invasion. Minimally invasive, site-specific photodynamic therapy (PDT) is a highly promising anti-glioblastoma modality. Recent research in the authors’ laboratory has revealed that iNOS-derived NO in glioblastoma cells elicits resistance to 5-aminolevulinic acid (ALA)-based PDT, and moreover endows PDT-surviving cells with greater proliferation and migration/invasion aggressiveness. In this contribution, we discuss iNOS/NO antagonism to glioblastoma PDT and how this can be overcome by judicious use of pharmacologic inhibitors of iNOS activity or transcription.
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Birzu, Cristina, Pim French, Mario Caccese, Giulia Cerretti, Ahmed Idbaih, Vittorina Zagonel, and Giuseppe Lombardi. "Recurrent Glioblastoma: From Molecular Landscape to New Treatment Perspectives." Cancers 13, no. 1 (December 26, 2020): 47. http://dx.doi.org/10.3390/cancers13010047.

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Glioblastoma is the most frequent and aggressive form among malignant central nervous system primary tumors in adults. Standard treatment for newly diagnosed glioblastoma consists in maximal safe resection, if feasible, followed by radiochemotherapy and adjuvant chemotherapy with temozolomide; despite this multimodal treatment, virtually all glioblastomas relapse. Once tumors progress after first-line therapy, treatment options are limited and management of recurrent glioblastoma remains challenging. Loco-regional therapy with re-surgery or re-irradiation may be evaluated in selected cases, while traditional systemic therapy with nitrosoureas and temozolomide rechallenge showed limited efficacy. In recent years, new clinical trials using, for example, regorafenib or a combination of tyrosine kinase inhibitors and immunotherapy were performed with promising results. In particular, molecular targeted therapy could show efficacy in selected patients with specific gene mutations. Nonetheless, some molecular characteristics and genetic alterations could change during tumor progression, thus affecting the efficacy of precision medicine. We therefore reviewed the molecular and genomic landscape of recurrent glioblastoma, the strategy for clinical management and the major phase I-III clinical trials analyzing recent drugs and combination regimens in these patients.
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Mitrofanov, A. A., D. R. Naskhletashvili, V. A. Aleshin, D. M. Belov, A. Kh Bekyashev, V. B. Karakhan, N. V. Sevyan, E. V. Prozorenko, and K. E. Roshchina. "Causes of drug resistance and glioblastoma relapses." Head and Neck Tumors (HNT) 11, no. 1 (April 24, 2021): 101–8. http://dx.doi.org/10.17650/2222-1468-2021-11-1-101-108.

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Glioblastoma multiform^ is one of the most aggressive malignancies, wich standard of treatment not changed over the past decade, and the average life expectancy from diagnosis to death does not exceed two years in the most optimistic trials. The review examines the features of the glioblastoma microenvironment, its genetic heterogeneity, the development of recurrent glioblastoma, the formation of drug resistance, the influence of the blood-brain barrier and the brain lymphatic system on the development of immunotherapy and targeted therapy. Molecular subgroups of glioblastomas with an assumed prognostic value were analyzed. It was determined that numerous relationships between glioblastoma cells and the microenvironment are aimed at ensuring tumor progression, and also cause a state of reduced effector function of T cells. Data on the development of future molecular-targeted therapies for four types of cancer cells based on their different properties and response to therapy are summarized: primary GSC, RISC cells, and proliferating and postmitotic non-GSC fractions. The penetration of blood-brain barrier with chemotherapeutic drugs and antibodies currently remains the main limitation in the treatment of glioblastoma. The resulting analysis of the causes is reduced to the following conclusions. A detailed understanding of the evolutionary dynamics of tumor progression can provide insight into the related molecular and genetic mechanisms underlying glioblastoma recurrence. The most promising methods of treatment for glioblastoma are combined therapy using immune checkpoint inhibitors in combination with new treatment methods -vaccine therapy, CAR-T-cell therapy and viral therapy. A deeper study of the mechanisms of drug resistance and acquisition resistance, biology and subcloning clonal populations of glioblastoma and its microenvironment, with active consideration of combined trips to the treatment will increase the survival rate of patients, and may lead to stable remission of the disease.
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Yang, Chunzhang, Christopher S. Hong, and Zhengping Zhuang. "Hypoxia and glioblastoma therapy." Aging 7, no. 8 (August 17, 2015): 523–24. http://dx.doi.org/10.18632/aging.100795.

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Strebe, Joslyn K., Jonathan A. Lubin, and John S. Kuo. "“Tag Team” Glioblastoma Therapy." Neurosurgery 79, no. 6 (December 2016): N18—N20. http://dx.doi.org/10.1227/01.neu.0000508605.38694.fd.

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Chiocca, E. Antonio, Manish Aghi, and Giulia Fulci. "Viral Therapy for Glioblastoma." Cancer Journal 9, no. 3 (May 2003): 167–79. http://dx.doi.org/10.1097/00130404-200305000-00005.

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Wen, Patrick, and Timothy F. Cloughesy. "Viral Therapy for Glioblastoma." Oncology Times 42, no. 5 (March 2020): 18–19. http://dx.doi.org/10.1097/01.cot.0000657760.45429.bd.

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Gerstner, Elizabeth R., and Tracy T. Batchelor. "Antiangiogenic Therapy for Glioblastoma." Cancer Journal 18, no. 1 (2012): 45–50. http://dx.doi.org/10.1097/ppo.0b013e3182431c6f.

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Dissertations / Theses on the topic "Glioblastoma – therapy"

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Setua, Sonali. "Development of targeted nanomedicine for glioblastoma therapy." Thesis, University of Cambridge, 2014. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708268.

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Kegelman, Timothy P. "MDA-9/Syntenin: From Glioblastoma Pathogenesis to Targeted Therapy." VCU Scholars Compass, 2014. http://scholarscompass.vcu.edu/etd/4676.

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The most common malignant glioma, glioblastoma multiforme (GBM), remains an intractable tumor despite advances in therapy. Its proclivity to infiltrate surrounding brain tissue contributes greatly to its treatment failure and the grim prognosis of patients. Radiation is a staple in modern therapeutic regimens, though cells surviving radiation become more aggressive and invasive. Consequently, it is imperative to define further the cellular mechanisms that control GBM invasion and identify promising novel therapeutic targets. Melanoma differentiation associated gene-9 (MDA-9/Syntenin) is a highly conserved PDZ domain-containing scaffolding protein that promotes invasion and metastasis in human melanoma models. We show that MDA-9/Syntenin is robustly expressed in GBM cell lines and patient samples, and expression increases by tumor grade. These findings are confirmed through database analysis, which revealed MDA-9/Syntenin expression correlates with shorter survival times and patient tumors high in MDA-9/Syntenin have a worse prognosis when undergoing radiotherapy. Modulating MDA-9/Syntenin levels produced changes in invasion, angiogenesis, and signaling, indicating MDA-9/Syntenin enhances glioma pathogenesis. Overexpression of MDA-9/Syntenin enhances invasion, while knockdown inhibits invasion, migration, and anchorage-independent growth in soft agar. MDA-9/Syntenin increases activation of c-Src, P38MAPK, and NF-kB, leading to elevated MMP2 expression and IL-8 secretion. Through an orthotopic tumor model, we show that shmda-9 tumor cells formed smaller tumors and had a less invasive phenotype in vivo. Knockdown of MDA-9/Syntenin radiosensitizes GBM cells and significantly reduces post-radiation invasion gains through abrogation of radiation-induced Src and EphA2 activity. In efforts to pharmacologically inhibit MDA-9/Syntenin, we describe the effects of a novel small molecule, PDZ1i, which targets the PDZ1 domain of MDA-9/Syntenin and successfully reduces invasion gains in GBM cells following radiation. While it does not effect astrocyte radiosensitivity, PDZ1i radiosensitizes GBM cells. PDZ1i inhibits crucial GBM signaling including FAK and mutant EGFR, EGFRvIII, and can negate gains in secreted proteases, such as MMP2 and MMP9, following radiation. In a model of glioma, PDZ1i treatment combined with radiation results in less invasive tumors and extends survival. Our findings indicate that MDA-9/Syntenin is a novel and important mediator of GBM pathogenesis, and further identify it as a targetable protein that enhances radiotherapy for treatment in glioma.
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Gao, Yi. "Development of a novel hTERTC27 based cancer : gene therapy /." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/HKUTO/record/B39557790.

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Frixa, Christophe. "Boronated tetraphenylporphyrins for use in boron neutron capture therapy of cancer." Thesis, University of Bath, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268747.

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Heywood, Richard Martyn. "NG2/CSPG4 promotes progression of glioblastoma multiforme by enhancing proliferation and resistance to therapy." Thesis, University of Cambridge, 2014. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.707912.

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Gao, Yi, and 高毅. "Development of a novel hTERTC27 based cancer: gene therapy." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39557790.

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Pikhartova-Martinkova, Eva. "Combination of ellipticine chemotherapy and alpha5beta1 integrin-targeted therapy in human glioblastoma." Strasbourg, 2010. https://publication-theses.unistra.fr/restreint/theses_doctorat/2010/PIKHARTOVA-MARTINKOVA_Eva_2010.pdf.

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Les glioblastomes sont des tumeurs cérébrales agressives pour lesquelles les thérapies classiques se révèlent souvent inefficaces. Les intégrines peuvent aussi réguler l’angiogénèse, l’embryogenèse, la prolifération, la différentiation, la migration et la survie. Nous avons proposé l`intégrine α5β1 comme un cible thérapeutique pour les glioblastomes, comme elle est surexprimée dans les gliomes en fonction du grade tumoral et comme les travaux récents l`indiquent ayant un rôle central dans un réseau fonctionnel de la cellule tumoral. Les deux lignées cellulaires de glioblastome testés (U87MG et U373) ont été sensibles à l`ellipticine. Dans le contexte de la protéine p53 fonctionnelle (U87MG), l`ellipticine induit la sénescence, alors que dans U373 (p53mt), il induit l'apoptose. Les deux lignées cellulaires expriment des enzymes générant les métabolites de l'ellipticine connus pour se lier de façon covalente à l’ADN. Ensuite, nous montrons que en inhibant l'intégrine α5β1 avec ses deux ligands sélectifs (SJ749 et K34c) diminue la sénescence induite par la chimiothérapie et facilite l'apoptose dans un contexte p53 fonctionnelle. Lorsque la p53 est muté et inactif, la chimiothérapie provoque de l'apoptose p53-indépendante au lieu de la sénescence, ce qui n'a pas été améliorée par les antagonistes des intégrines. Les antagonistes de l'intégrine α5β1 modulent la p53 signalisation chimio-induite. Ce travail fournit des nouvelles preuves des avantages de la combinaison de la chimiothérapie conventionnelle avec la thérapie ciblée sur l'intégrine α5β1 sous-tendent l'importance de connaître les caractéristiques de base de la tumeur pour estimer le bénéfit de la thérapie finale
Gliomas are highly aggressive and resistant brain tumors difficult to cure with conventional therapies. Therefore, targeted therapies are needed. Integrins are implicated in angiogenesis, cell proliferation, differentiation, migration and survival. We have identified the α5β1 integrin as a promising therapeutic target as its expression correlates with tumor grade and recent studies predispose it to play a key role in tumor cell functional network. Ellipticine was shown to be brain tumor specific. Its pharmacological efficiency and/or genotoxic side effects are dependent on its enzymatic activation. U87MG and U373 glioblastoma cell lines are sensitive to ellipticine. P53 plays an important role in their response to it. In the context of functional p53 (U87MG), ellipticine induced senescence, whereas in U373 (p53mt) it induced apoptosis. Both cell lines express enzymes generating ellipticine metabolites known to covalently bind to DNA. We next investigated whether blocking α5β1 integrin concomitantly with chemotherapy may impact the response to chemotherapy of human glioblastoma. Inhibiting α5β1 integrin with two selective ligands (SJ749 and K34c) decreases drug-induced senescence and facilitates cell apoptosis in a functional p53 background. When p53 is mutated and/or inactive, chemotherapy provoked cell apoptosis instead of senescence, which was not improved by integrin antagonists. Results were confirmed using multiple models. In summary, this work provides novel evidences of profitability of combining conventional chemotherapy with α5β1 integrin-targeted therapy underlying the importance of knowing basic tumor characteristics to may estimate the final therapy outcome
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Haseley, Amy M. "The Effect of the Tumor Microenvironment on Oncolytic Virus Therapy for Glioblastoma." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1350413344.

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Skog, Johan. "The quest for new improved adenovirus gene therapy vectors against glioma tumours." Doctoral thesis, Umeå : Umeå University, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-624.

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Agliardi, Giulia. "Development of a Chimeric Antigen Receptor (CAR)-based T cell therapy for glioblastoma." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/10025011/.

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High grade gliomas are aggressive brain tumours for which treatment is highly challenging due to the location within the central nervous system (CNS), which may reduce access of cytotoxic chemotherapy, and their infiltrative growth, which precludes complete surgical resection. Current treatment includes surgical removal – wherever possible - followed by radiotherapy and chemotherapy. However, recurrence is common, resulting in a survival of only 12 to 15 months after diagnosis. This highlights the need for new therapies. Chimeric antigen receptors (CARs) are synthetic molecules which combine the specificity of an antibody to the signalling domains of a T cell receptor (TCR), allowing T cells to directly recognise tumour antigens with no need for co-stimulation. CAR-T cells have shown promising responses in the treatment of haematological malignancies, inducing complete and durable responses in patients with chemo-refractory disease treated with CD19-redirected T cells. This therapeutic approach may be highly suitable for high grade gliomas as T cells have the ability to track to distant tumour sites. However, translation of this technology to solid tumours is proving more difficult, due to several challenges, including: requirement for an effective infiltration of CAR-T cells within the tumour and the immunosuppressive environment provided by solid malignancies. In this work, we developed an immunocompetent animal model of glioma, to study kinetics of migration and infiltration of CAR-T cells and the interplay between CAR-T cells, the tumour and the endogenous immune system to inform the design of T cell immunotherapy for this brain tumours. The tumour specific variant III of the epidermal growth factor receptor (EGFRvIII) – a mutation found in 30% of glioblastomas – was used as model antigen. A murine CAR was constructed based on the single chain fragment variant (ScFv) of EGFRvIII-specific antibody MR1.1 linked with a CD8 stalk to CD28-CD3ζ activation domains. A murine marker gene (truncated CD34) was co-expressed to allow for ex vivo analysis as well as firefly luciferase for in vivo tracking of CAR T-cells. The mouse glioma cell line GL261 was modified to express the mouse version of EGFRvIII and used to establish orthotopic tumours. After validation of function and specificity in vitro, efficacy of CAR-T cells was tested in vivo. Both bioluminescence imaging (BLI) and flow cytometry demonstrated that CAR T cells accumulated within the tumour in an antigen-dependent manner. MRI demonstrated that CAR T cells delayed tumour growth and increased survival. However, tumours were not consistently eradicated. Both immunohistochemistry and BLI indicated lack of long term persistence of T cells within the tumour. Analysis of tumour infiltrating lymphocytes (TILs) phenotype suggested that decreased functionality of CAR-T cells could be a result of their exhaustion in situ. We hypothesised that additional strategies were required to improve efficacy and persistence of CAR-T cells. We postulated that CAR-T cell fitness may be prolonged by: - Incorporation of 41BB as additional co-stimulatory domain in the CAR to provide a pro-survival signal. - Combination therapy with PD1 blockade to overcome T cell exhaustion (both on CAR and endogenous T cells) in situ. While the employment of third-generation CAR did not significantly improve survival and showed increased toxicity, combination therapy of CAR-T cells and PD-1 blockade promoted complete clearance of tumours resulting in long term survival. Immunohistochemistry and flow cytometry analysis suggested that combination therapy may increase persistence of CAR-T cells, leading to a more rapid and consistent tumour eradication compared to CAR-T cell administration alone. However, data presented here did not demonstrate a synergistic effect of CAR-T cell therapy and PD1 blockade, as an effect of PD1 blockade alone was also observed. Therefore, additional experiments are required to examine this further.
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Books on the topic "Glioblastoma – therapy"

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Chen, Clark C. Advances in the biology, imaging and therapies for glioblastoma. Rijeka: InTech, 2011.

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Glioblastoma: Molecular mechanisms of pathogenesis and current therapeutic strategies. Dordrecht: Springer, 2010.

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Irons, Howard S. Rae of hope. Charlotte Harbor, FL: Tabby House, 1994.

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Ray, Swapan K. Glioblastoma : : Molecular Mechanisms of Pathogenesis and Current Therapeutic Strategies. Springer, 2011.

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Ray, Swapan K. Glioblastoma : : Molecular Mechanisms of Pathogenesis and Current Therapeutic Strategies. Springer, 2014.

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Huntoon, Kristin, and J. Bradley Elder. High-Grade Gliomas. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190696696.003.0001.

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Glioblastoma is the most common primary malignant brain tumor. This chapter discusses the clinical presentation and initial workup for a patient with a suspected glioblastoma, as well as the optimal treatment strategy and prognosis. Diagnosis is typically made using magnetic resonance imaging. Optimal treatment involves maximal safe surgical resection followed by adjuvant chemotherapy and radiation therapy. Surgical adjuncts including intraoperative imaging modalities and brain mapping techniques help improve neurologic morbidity associated with surgery. Despite maximal treatment, virtually all patients with glioblastoma will experience recurrence of their tumor and may be considered for clinical trials or second-line therapy. This chapter highlights important pearls associated with management of patients with glioblastoma and written for those who are interested in neuro-oncology, neurosurgery, and the field of brain tumors.
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Book chapters on the topic "Glioblastoma – therapy"

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Hingtgen, Shawn. "Glioblastoma Therapy." In Encyclopedia of Cancer, 1–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_7171-5.

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Hingtgen, Shawn. "Glioblastoma Therapy." In Encyclopedia of Cancer, 1911–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_7171.

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Moon, Dominic H., and Timothy M. Zagar. "Glioblastoma." In Hypofractionated and Stereotactic Radiation Therapy, 117–25. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-92802-9_8.

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Puduvalli, Vinay K. "Aberrations of the Epigenome in Gliomas: Novel Targets for Therapy." In Glioblastoma, 185–202. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0410-2_9.

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Barani, Igor J., and David A. Larson. "Radiation Therapy of Glioblastoma." In Cancer Treatment and Research, 49–73. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-12048-5_4.

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Dillman, Robert O. "Biological therapy of glioblastoma." In Principles of Cancer Biotherapy, 723–32. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-2289-9_30.

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Yamamoto, Tetsuya, Kei Nakai, and Hiroaki Kumada. "Glioblastoma: Boron Neutron Capture Therapy." In Tumors of the Central Nervous System, Volume 2, 229–39. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-0618-7_24.

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Yamamoto, Tetsuya, and Akira Matsumura. "External Beam BNCT for Glioblastoma Multiforme." In Neutron Capture Therapy, 377–88. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-31334-9_20.

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Matsutani, Masao, Tadayoshi Matsuda, Takeshi Kohno, Tadashi Nagashima, Akio Asai, and Takamitsu Fujimaki. "Intraoperative radiation therapy for glioblastoma multiforme." In Biology of Brain Tumour, 269–75. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2297-9_36.

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Matsutani, M., O. Nakamura, T. Nagashima, Y. Tanaka, and T. Matsuda. "Intraoperative Radiation Therapy for Glioblastoma — Indications and Treatment Results." In Cancer Therapy, 49–57. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74683-3_7.

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Conference papers on the topic "Glioblastoma – therapy"

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Lee, Pui Mun, Xi Tian, and John S. Ho. "Wireless Power Transfer for Glioblastoma Photodynamic Therapy." In 2019 IEEE Biomedical Circuits and Systems Conference (BioCAS). IEEE, 2019. http://dx.doi.org/10.1109/biocas.2019.8918760.

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Mallidi, Srivalleesha, Huang-Chiao Huang, Joyce Liu, Zhiming Mai, and Tayyaba Hasan. "Towards image-guided photodynamic therapy of Glioblastoma." In SPIE BiOS, edited by David H. Kessel and Tayyaba Hasan. SPIE, 2013. http://dx.doi.org/10.1117/12.2010684.

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Ozturk, Mehmet S., Vivian K. Lee, Guohao Dai, and Xavier Intes. "Longitudinal Volumetric Assessment of Glioblastoma Brain Tumors in 3D Bio-Printed Environment by Mesoscopic Fluorescence Molecular Tomography." In Cancer Imaging and Therapy. Washington, D.C.: OSA, 2016. http://dx.doi.org/10.1364/cancer.2016.jm3a.46.

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Fitzel, R., H. Strobel, T. Baisch, VJ Herbener, G. Karpel-Massler, M.-E. Halatsch, K.-M. Debatin, and M.-A. Westhoff. "Combining Autophagy Inhibition and Temozolomide in Glioblastoma Therapy." In 28th Annual Meeting of the working group “Experimental Neuro-Oncology”. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1696333.

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Orsila, Lasse, Visa Kaivosoja, Jukka-Pekka Alanko, and Toomas Uibu. "Photodynamic therapy platform for glioblastoma and intrabronchial tumors." In Clinical and Translational Neurophotonics 2018, edited by Steen J. Madsen and Victor X. D. Yang. SPIE, 2018. http://dx.doi.org/10.1117/12.2297229.

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Keir, Stephen T., Lloyd Gray, and Henry S. Friedman. "Abstract LB-76: Mibefradil, a novel therapy for glioblastoma: An interlaced therapy approach." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-lb-76.

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Strobel, H., VJ Herbener, T. Baisch, R. Fitzel, G. Karpel-Massler, M.-E. Halatsch, K.-M. Debatin, and M.-A. Westhoff. "Re-assessing the Role of Temozolomide in Glioblastoma Therapy." In 28th Annual Meeting of the working group “Experimental Neuro-Oncology”. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1696332.

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Dupont, Clément, Fabienne Lecomte, Pascal Deleporte, Gregory Baert, Serge R. Mordon, Nicolas Reyns, and Maximilien Vermandel. "DOSINDYGO: DOSe finding for INtraoperative photoDYnamic therapy of GliOblastoma." In 17th International Photodynamic Association World Congress, edited by Tayyaba Hasan. SPIE, 2019. http://dx.doi.org/10.1117/12.2524949.

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Kattner, P., L. Nonnenmacher, K. Buljovcic, S. Bartholomä, K. Zeiler, G. Karpel-Massler, ME Halatsch, MA Westhoff, and KM Debatin. "Combination therapy as a potential strategy in Glioblastoma treatment." In 27th Annual Meeting of the working group “Experimental Neuro-Oncology”. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1675273.

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Lenz, Gabriela Spies, Juliana Hofstätter Azambuja, Roselena Silvestri Schuh, Luana Roberta Michels, Nicolly Espindola Gelsleichter, Liziane Raquel Beckenkamp, Gabriela Goncalves Roliano, et al. "Abstract B058: CD73 siRNA therapy regulates glioblastoma immune microenvironment." In Abstracts: AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics; October 26-30, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1535-7163.targ-19-b058.

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