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Journal articles on the topic 'Glioblastoma – therapy'

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

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1

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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2

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Andersen, Rikke Sick, Atul Anand, Dylan Scott Lykke Harwood, and Bjarne Winther Kristensen. "Tumor-Associated Microglia and Macrophages in the Glioblastoma Microenvironment and Their Implications for Therapy." Cancers 13, no. 17 (August 24, 2021): 4255. http://dx.doi.org/10.3390/cancers13174255.

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Glioblastoma is the most frequent and malignant primary brain tumor. Standard of care includes surgery followed by radiation and temozolomide chemotherapy. Despite treatment, patients have a poor prognosis with a median survival of less than 15 months. The poor prognosis is associated with an increased abundance of tumor-associated microglia and macrophages (TAMs), which are known to play a role in creating a pro-tumorigenic environment and aiding tumor progression. Most treatment strategies are directed against glioblastoma cells; however, accumulating evidence suggests targeting of TAMs as a promising therapeutic strategy. While TAMs are typically dichotomously classified as M1 and M2 phenotypes, recent studies utilizing single cell technologies have identified expression pattern differences, which is beginning to give a deeper understanding of the heterogeneous subpopulations of TAMs in glioblastomas. In this review, we evaluate the role of TAMs in the glioblastoma microenvironment and discuss how their interactions with cancer cells have an extensive impact on glioblastoma progression and treatment resistance. Finally, we summarize the effects and challenges of therapeutic strategies, which specifically aim to target TAMs.
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12

Sungarian, Arno, Deus Cielo, Prakash Sampath, Nathaniel Bowling, Peter Moskal, Jack R. Wands, and Suzanne M. de la Monte. "Potential Role of Thymosin-α1 Adjuvant Therapy for Glioblastoma." Journal of Oncology 2009 (2009): 1–11. http://dx.doi.org/10.1155/2009/302084.

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Glioblastomas are high-grade, malignant CNS neoplasms that are nearly always fatal within 12 months of diagnosis. Immunotherapy using proinflammatory cytokines such as IL-2 or IL-12 may prolong survival with glioblastoma. Thymosin-α1 (Talpha1) is a thymic hormone and immunemodulator that increase IL-2 production and T-cell proliferation. We examined potential therapeutic effects of Talpha1 in experimental in vivo glioblastoma, and characterized Talpha1's anti-tumor effects in vitro. Rar 9L cells (104) were implanted into the right frontal lobe of adult Long Evans rats that were subsequently treated with vehicle, BCNU, Talpha1, or Talpha1+BCNU from postoperative day 6. Talpha1+BCNU significantly lowered tumor burdens, and increased cure rates. In vitro experiments demonstrated that Talpha1 had no direct effect on viability or mitochondrial function, and instead, it increased expression of pro-apoptosis genes, including FasL, FasR and TNFα-R1 (65.89%, 44.08%, and 22.18%, resp.), and increased 9L cell sensitivity to oxidative stress. Moreover, Talpha1 enhanced 9L cell sensitivity to both Granzyme B- and BCNU-mediated killing. The findings suggest that Talpha1 enhances BCNUmediated eradication of glioblastoma in vivo, and that Talpha1 mediates its effects by activating pro-apoptosis mechanisms, rendering neoplastic cells more sensitive to oxidative stress and immune-mediated killing by Granzyme B and chemotherapeutic agents.
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13

Mastorakos, Panagiotis, Michael A. Hays, James P. Caruso, Ching-Jen Chen, Dale Ding, Davis G. Taylor, M. Beatriz Lopes, and Mark E. Shaffrey. "Transtentorial dissemination of optic nerve glioblastoma: case report." Journal of Neurosurgery 128, no. 2 (February 2018): 406–13. http://dx.doi.org/10.3171/2016.10.jns161443.

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Optic nerve glioblastoma is a rare entity that usually presents with rapidly progressive vision loss, which eventually results in blindness and, ultimately, death. As with malignant gliomas in other anatomical locations, local recurrence is common. Isolated rapid changes in vision, atypical neuroimaging findings, and the rarity of optic nerve glioblastoma may render diagnosis challenging and, thus, delay treatment. The authors present a case of optic nerve glioblastoma that was treated with subtotal resection followed by adjuvant radiation therapy and temozolomide. One year following the initial diagnosis, the patient developed a right cerebellar lesion, which was histopathologically consistent with glioblastoma. This case represents the first report of transtentorial dissemination of an optic nerve glioblastoma. In addition, the authors reviewed the literature regarding optic nerve glioblastomas. Of the 73 previously reported cases of malignant optic nerve gliomas, 32 were histologically confirmed glioblastomas. The mean age at diagnosis was 62 years, and 56% were male; the median survival was 7 months. A malignant glioma of the optic nerve should be considered in the differential diagnosis of a patient with rapidly progressive visual loss. However, the incidence of optic nerve glioblastoma is exceedingly low.
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14

Babar Khan, Muhammad, Rosamaria Ruggieri, Nhan Tran, Jann Sarkaria, Jennifer MacDiarmid, Himanshu Brahmbhatt, John Boockvar, and Marc Symons. "DDIS-18. NANOCELL-MEDIATED DELIVERY OF MIR-34A COUNTERACTS TEMOZOLOMIDE RESISTANCE IN GLIOBLASTOMA." Neuro-Oncology 21, Supplement_6 (November 2019): vi66—vi67. http://dx.doi.org/10.1093/neuonc/noz175.269.

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Abstract BACKGROUND Glioblastomas show marked intra- and inter-tumor heterogeneity and are strongly resistant to both radio- and chemo-therapy, which are standard therapeutic modalities for this tumor. MicroRNAs (miRNAs) have the potential to serve as effective therapeutics for glioblastoma as they modulate the activity of multiple signaling pathways. METHODS Glioblastoma cultures were transfected with miR-34a or control miRNA mimics to assess biological function and therapeutic potential in vitro. miR-34a was packaged into bacterially-derived nanocells and administered intravenously for delivery to orthotopic patient-derived glioblastoma xenografts in mice. RESULTS Overexpression of miR-34a strongly reduced the activation status of the three core signaling networks that have been found to be deregulated in the vast majority of glioblastoma tumors, the receptor tyrosine kinase, p53 and Rb networks. miR-34a transfection also inhibited the survival of multiple established glioblastoma cell lines as well as primary patient-derived xenograft cultures representing the proneural, mesenchymal and classical subtypes. Transfection of miR-34a synergized with temozolomide (TMZ) in in vitro cultures of glioblastoma cells with primary TMZ sensitivity, primary TMZ resistance and acquired TMZ resistance. Intravenous administration of bacterially-derived nanocells carrying miR-34a strongly enhanced TMZ sensitivity in an orthotopic patient-derived xenograft mouse model of glioblastoma. CONCLUSIONS miR-34a strongly sensitizes a wide range of glioblastoma cell cultures to TMZ, suggesting that combination therapy of TMZ with miR-34a may serve as a novel therapeutic approach for the treatment of glioblastoma tumors. Bacterially-derived nanocells are an effective vehicle for the delivery of miR-34a to glioblastoma tumors.
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15

Ou, Alexander, W. K. Alfred Yung, and Nazanin Majd. "Molecular Mechanisms of Treatment Resistance in Glioblastoma." International Journal of Molecular Sciences 22, no. 1 (December 31, 2020): 351. http://dx.doi.org/10.3390/ijms22010351.

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Glioblastoma is the most common malignant primary brain tumor in adults and is almost invariably fatal. Despite our growing understanding of the various mechanisms underlying treatment failure, the standard-of-care therapy has not changed over the last two decades, signifying a great unmet need. The challenges of treating glioblastoma are many and include inadequate drug or agent delivery across the blood–brain barrier, abundant intra- and intertumoral heterogeneity, redundant signaling pathways, and an immunosuppressive microenvironment. Here, we review the innate and adaptive molecular mechanisms underlying glioblastoma’s treatment resistance, emphasizing the intrinsic challenges therapeutic interventions must overcome—namely, the blood–brain barrier, tumoral heterogeneity, and microenvironment—and the mechanisms of resistance to conventional treatments, targeted therapy, and immunotherapy.
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16

Trojan, Jerzy, Yuexin X. Pan, Ming X. Wei, Adama Ly, Alexander Shevelev, Maciej Bierwagen, Marie-Yvonne Ardourel, et al. "Methodology for Anti-Gene Anti-IGF-I Therapy of Malignant Tumours." Chemotherapy Research and Practice 2012 (February 14, 2012): 1–12. http://dx.doi.org/10.1155/2012/721873.

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The aim of this study was to establish the criteria for methodology of cellular “anti-IGF-I” therapy of malignant tumours and particularly for glioblastoma multiforme. The treatment of primary glioblastoma patients using surgery, radiotherapy, and chemotherapy was followed by subcutaneous injection of autologous cancer cells transfected by IGF-I antisense/triple helix expression vectors. The prepared cell “vaccines” should it be in the case of glioblastomas or other tumours, have shown a change of phenotype, the absence of IGF-I protein, and expression of MHC-I and B7. The peripheral blood lymphocytes, PBL cells, removed after each of two successive vaccinations, have demonstrated for all the types of tumour tested an increasing level of CD8+ and CD8+28+ molecules and a switch from CD8+11b+ to CD8+11. All cancer patients were supervised for up to 19 months, the period corresponding to minimum survival of glioblastoma patients. The obtained results have permitted to specify the common criteria for “anti-IGF-I” strategy: characteristics sine qua non of injected “vaccines” (cloned cells IGF-I(−) and MHC-I(+)) and of PBL cells (CD8+ increased level).
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17

Kessler, Renate, Michael Fleischer, Christopher Springsguth, Marina Bigl, Jan-Peter Warnke, and Klaus Eschrich. "Prognostic Value of PFKFB3 to PFKFB4 mRNA Ratio in Patients With Primary Glioblastoma (IDH-Wildtype)." Journal of Neuropathology & Experimental Neurology 78, no. 9 (August 1, 2019): 865–70. http://dx.doi.org/10.1093/jnen/nlz067.

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Abstract A hallmark of glioblastoma is the high level of aerobic glycolysis. PFKFB3 and PFKFB4 are regulatory glycolytic enzymes, which are overexpressed in glioblastomas. Selective inhibition of these enzymes has emerged as a new approach in tumor therapy. We investigated the ratios of PFKFB3 to PFKFB4 mRNA expression in 66 astrocytic tumors of different malignancy grades. PFKFB3 mRNA levels were considerably higher than those of PFKFB4 in all analyzed tumors. IDH-wildtype glioblastomas showed lower PFKFB3 to PFKFB4 mRNA ratios (7.7:1) than IDH-mutant low-grade astrocytomas (36.5:1), indicating a dependency of the ratio on malignancy grade. In IDH-wildtype glioblastomas exhibiting loss of heterozygosity (LOH) of the PFKFB3 gene locus, the decrease of PFKFB3 mRNA levels was accompanied by lower PFKFB4 mRNA levels, but the PFKFB3 to PFKFB4 mRNA ratio did not differ between tumors with or without PFKFB3 LOH. IDH-wildtype primary glioblastoma patients with high PFKFB3 to PFKFB4 mRNA ratios above the average of 7.7:1 had a significantly longer overall survival time (14 months) than patients with lower ratios (9 months). Our results indicate that low PFKFB3 to PFKFB4 expression ratio is a poor prognostic factor in patients with IDH-wildtype primary glioblastoma and that PFKFB3 and PFKFB4 might represent promising targets for astrocytoma and glioblastoma treatment.
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Lee, Dong Hoon, Hyun-Wook Ryu, Hye-Rim Won, and So Hee Kwon. "Advances in epigenetic glioblastoma therapy." Oncotarget 8, no. 11 (January 12, 2017): 18577–89. http://dx.doi.org/10.18632/oncotarget.14612.

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19

R Hooper, Malcolm. "Glioblastoma & Hyperbaric Oxygen Therapy." Alzheimer’s & Neurodegenerative Diseases 6, no. 2 (June 30, 2020): 1–4. http://dx.doi.org/10.24966/and-9608/100044.

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20

Goh, Jia Jun, Siew Ju See, Emily Ang, and Wai Hoe Ng. "Vanishing glioblastoma after corticosteroid therapy." Journal of Clinical Neuroscience 16, no. 9 (September 2009): 1226–28. http://dx.doi.org/10.1016/j.jocn.2008.10.029.

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21

Mehta, Nalini, Johnathan G. Lyon, Ketki Patil, Nassir Mokarram, Christine Kim, and Ravi V. Bellamkonda. "Bacterial Carriers for Glioblastoma Therapy." Molecular Therapy - Oncolytics 4 (March 2017): 1–17. http://dx.doi.org/10.1016/j.omto.2016.12.003.

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22

Bartek, Jiri, Kimberly Ng, Jiri Bartek, Walter Fischer, Bob Carter, and Clark C. Chen. "Key concepts in glioblastoma therapy." Journal of Neurology, Neurosurgery & Psychiatry 83, no. 7 (March 6, 2012): 753–60. http://dx.doi.org/10.1136/jnnp-2011-300709.

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23

Colman, Howard. "Future Directions in Glioblastoma Therapy." American Society of Clinical Oncology Educational Book, no. 32 (June 2012): 108–11. http://dx.doi.org/10.14694/edbook_am.2012.32.49.

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Overview: The standard of care for both newly diagnosed and recurrent glioblastoma (GBM) patients has changed significantly in the past 10 years. Surgery followed by radiation and concurrent and adjuvant temozolomide is now the well-established standard treatment for newly diagnosed GBM. More recently, bevacizumab has become a mainstay of treatment for recurrent GBM. However, despite these advances and significant improvements in patient outcomes, the management and treatment of GBM patients remains a challenging and frustrating endeavor. Difficulties in interpretation of imaging changes after initial treatment, as well as the effects of antiangiogenic agents like bevacizumab on MRI characteristics, can make even the determination of disease progression complicated in multiple situations. Although a high percentage of patients benefit from antiangiogenic therapy in terms of radiographic response and progression-free survival, the effects of bevacizumab on prolonging overall survival remain controversial. Furthermore, tumor progression after treatment with antiangiogenic agents carries a particularly poor prognosis and there is a general lack of effective therapies for this group of patients. These limitations in terms of standard treatments contrast with a relative wealth of new information regarding the molecular underpinnings of GBM. Data from several large-scale efforts to molecularly profile GBM tumors including The Cancer Genome Atlas (TCGA) project have helped define specific molecular subtypes of GBM with distinct biology and clinical outcomes. These findings are helping to refine our understanding of the molecular heterogeneity and pathogenesis of these tumors and provide a basis for the future development of rational and targeted therapies for specific tumor subtypes.
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Royer-Perron, Louis, Ahmed Idbaih, Marc Sanson, Jean-Yves Delattre, Khê Hoang-Xuan, and Agusti Alentorn. "Precision medicine in glioblastoma therapy." Expert Review of Precision Medicine and Drug Development 1, no. 5 (September 2, 2016): 451–68. http://dx.doi.org/10.1080/23808993.2016.1241128.

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Junck, L. "Bevacizumab antiangiogenic therapy for glioblastoma." Neurology 76, no. 5 (February 1, 2011): 414–15. http://dx.doi.org/10.1212/wnl.0b013e31820a0d7e.

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Whitley, R. J., and J. M. Markert. "Viral therapy of glioblastoma multiforme." Proceedings of the National Academy of Sciences 110, no. 29 (July 8, 2013): 11672–73. http://dx.doi.org/10.1073/pnas.1310253110.

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Weller, Michael, Roger Stupp, Monika Hegi, and Wolfgang Wick. "Individualized Targeted Therapy for Glioblastoma." Cancer Journal 18, no. 1 (2012): 40–44. http://dx.doi.org/10.1097/ppo.0b013e318243f6c9.

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Festuccia, Claudio, Assunta Leda Biordi, Vincenzo Tombolini, Akira Hara, and David Bailey. "Targeted Molecular Therapy in Glioblastoma." Journal of Oncology 2020 (January 14, 2020): 1–3. http://dx.doi.org/10.1155/2020/5104876.

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Guo, Dongsheng, Baofeng Wang, Fuxin Han, and Ting Lei. "RNA interference therapy for glioblastoma." Expert Opinion on Biological Therapy 10, no. 6 (April 23, 2010): 927–36. http://dx.doi.org/10.1517/14712598.2010.481667.

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Le Rhun, Emilie, Matthias Preusser, Patrick Roth, David A. Reardon, Martin van den Bent, Patrick Wen, Guido Reifenberger, and Michael Weller. "Molecular targeted therapy of glioblastoma." Cancer Treatment Reviews 80 (November 2019): 101896. http://dx.doi.org/10.1016/j.ctrv.2019.101896.

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Tirapelli, Daniela Pretti da Cunha, Isis Lacrose Lustosa, Sarah Bomfim Menezes, Indira Maynart Franco, Andressa Romualdo Rodrigues, Fernanda Maris Peria, Alexandre Magno da Nóbrega Marinho, Luciano Neder Serafini, Carlos Gilberto Carlotti Jr, and Luís Fernando Tirapelli. "High expression of XIAP and Bcl-2 may inhibit programmed cell death in glioblastomas." Arquivos de Neuro-Psiquiatria 75, no. 12 (December 2017): 875–80. http://dx.doi.org/10.1590/0004-282x20170156.

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ABSTRACT Glioblastoma (GBM) is the most malignant glioma and represents 29% of all brain tumors. Tumorigenesis is intimately connected with characteristics acquired in the physiologic pathway of cellular death. Objective: In the present study, the expression of anti-apoptotic (XIAP and Bcl-2) and apoptotic (cytochrome C, caspase 9, APAF-1), caspase 3 and the Smac/DIABLO genes related to the apoptosis pathway were evaluated in 30 samples of glioblastoma. Methods: The gene expression was evaluated in 30 glioblastomas (WHO grade IV) and compared to 10 white matter control samples with real-time PCR. Results and Conclusion: There were higher expressions of XIAP (p = 0.0032) and Bcl-2 (p = 0.0351) in the glioblastoma samples compared to the control samples of normal brain. These results raise the question of whether Bcl-2 and XIAP genes can be responsible for the inhibition of programmed cell death in glioblastomas. Moreover, they provide additional information capable of allowing the development of new target therapy strategies.
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Stragliotto, Giuseppe, Mattia Russel Pantalone, Afsar Rahbar, and Cecilia Söderberg-Nauclér. "Valganciclovir as Add-On to Standard Therapy in Secondary Glioblastoma." Microorganisms 8, no. 10 (September 24, 2020): 1471. http://dx.doi.org/10.3390/microorganisms8101471.

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Patients with glioblastoma have a very poor prognosis despite aggressive therapeutic strategies. Cytomegalovirus has been detected in >90% of glioblastoma tumors. This virus can affect tumor progression and may represent a novel glioblastoma therapy target. We report, here, a retrospective survival analysis of patients with secondary glioblastoma who were treated with the anti-viral drug valganciclovir at Karolinska University Hospital in Stockholm. We performed survival analyses of eight patients with secondary glioblastoma who were treated with a standard dose of valganciclovir as an add-on to second-line therapy after their disease progression to glioblastoma. Thirty-six patients with secondary glioblastoma admitted during the same time period who received similar treatment and care served as contemporary controls. The patients treated with valganciclovir showed an increased median overall survival after progression to glioblastoma compared with controls (19.1 versus 12.7 months, p = 0.0072). This result indicates a potential positive effect of valganciclovir in secondary glioblastoma, which is in agreement with our previous observation that valganciclovir treatment improves the outcomes of patients with newly diagnosed glioblastoma. Larger randomized studies are warranted to prove this hypothesis.
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Bredel, M., J. Renfrow, A. Yadav, A. Alvarez, D. Lin, D. Scholtens, X. He, J. Chandler, A. Scheck, and G. Harsh. "Role of IκBα as a negative regulator of EGFR and a molecular determinant of prognosis in glioblastoma multiforme." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): 2028. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.2028.

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2028 Background: Glioblastoma multiforme is a complex disease that involves the deregulation of overlapping signaling pathways. Constitutive activation of the transcription factor nuclear factor-κB (NF-κB) has been broadly associated with various human cancers, including glioblastomas, and their therapy resistance and may be due to cross-coupling with other oncogenic pathways, such as epidermal growth factor signaling. Methods: Multidimensional analysis involving gene and transcript data for the endogenous NF-κB modulator IκBα/NFKBIA and clinical patient profiles of 482 glioblastomas/high-grade gliomas from multiple institutions in the United States and The Cancer Genome Atlas Pilot Project. Functional analyses using LN229, U87, and U118 glioblastoma cells, and human embryonic kidney 293T cells with transgene phenotypes for IκBα. IκBα promoter and coding sequence and promoter methylation analyses in a resistance model of 15 glioblastomas cell lines with in vitro and/or in vivo resistance to O6-alkylating agents. Results: We have identified a regulatory circuit between NF-κB and EGFR signaling in glioblastomas, where IκBα binds to EGFR and attenuates EGFR signaling by immobilizing its kinase domain into an inactive conformation. We found the NFKBIA gene at 14q13.2 deleted in 25% of glioblastomas and its occurrence mutually exclusive with EGFR amplification. Loss of NFKBIA associates independently with patient survival. Functional analyses uncover a bona fide tumor suppressor role for IκBα in glioblastoma cells, where it functions to constrain tumorigenic and migratory potential, and induce spontaneous cellular senescence, and apoptosis in response to treatment. IκBα expression is an independent predictor of patient prognosis in multiple glioblastoma populations. Glioblastomas with initially high IκBα expression significantly repress IκBα upon tumor recurrence, suggesting an acquired mechanism to evade its tumor-suppressive and/or chemo-sensitizing effects during tumor progression. Conclusions: IκBα is a molecular determinant of biological tumor behavior and patient survival in glioblastoma multiforme. Deletion of NFKBIA could present an alternate mechanism to activate EGFR signaling in EGFR non-amplified glioblastomas. No significant financial relationships to disclose.
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Wesseling, Pieter, Jeroen A. W. M. van der Laak, Henk de Leeuw, Dirk J. Ruiter, and Peter C. Burger. "Quantitative immunohistological analysis of the microvasculature in untreated human glioblastoma multiforme." Journal of Neurosurgery 81, no. 6 (December 1994): 902–9. http://dx.doi.org/10.3171/jns.1994.81.6.0902.

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✓ Because histologically prominent microvascular proliferation is frequently present in glioblastoma multiforme, it has been hypothesized that this neoplasm is particularly dependent on neovascularization for its continued growth and that antiangiogenic therapy might be especially useful. To quantify the histological aspects of microvascular proliferation in glioma, a feasible and reproducible method was developed for computer-assisted image analysis of the visualized microvasculature in glial tissue. This method was used to compare several vascular parameters in histological whole-tumor sections of untreated human glioblastoma multiforme with those in histologically normal cerebral cortex and white matter. There was a significant increase in mean number, area, and perimeter of blood vessels per microscopic field in glioblastoma multiforme compared to normal cerebral white matter. In a substantial number of tumor fields, however, the vascular density was in the same range as that of normal cerebral white matter. The striking heterogeneity of the microvasculature within glioblastoma multiforme was illustrated by the significantly higher standard deviation for the vascular parameters in tumor tissue. The results of this study suggest that many regions of glioblastomas multiforme are not overtly angiogenesis dependent and may be difficult to treat by antiangiogenic therapy alone.
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Liebelt, Brandon D., Takashi Shingu, Xin Zhou, Jiangong Ren, Seul A. Shin, and Jian Hu. "Glioma Stem Cells: Signaling, Microenvironment, and Therapy." Stem Cells International 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/7849890.

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Glioblastoma remains the most common and devastating primary brain tumor despite maximal therapy with surgery, chemotherapy, and radiation. The glioma stem cell (GSC) subpopulation has been identified in glioblastoma and likely plays a key role in resistance of these tumors to conventional therapies as well as recurrent disease. GSCs are capable of self-renewal and differentiation; glioblastoma-derived GSCs are capable ofde novotumor formation when implanted in xenograft models. Further, GSCs possess unique surface markers, modulate characteristic signaling pathways to promote tumorigenesis, and play key roles in glioma vascular formation. These features, in addition to microenvironmental factors, present possible targets for specifically directing therapy against the GSC population within glioblastoma. In this review, the authors summarize the current knowledge of GSC biology and function and the role of GSCs in new vascular formation within glioblastoma and discuss potential therapeutic approaches to target GSCs.
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Catacuzzeno, Luigi, Bernard Fioretti, and Fabio Franciolini. "Expression and Role of the Intermediate-Conductance Calcium-Activated Potassium Channel KCa3.1 in Glioblastoma." Journal of Signal Transduction 2012 (May 17, 2012): 1–11. http://dx.doi.org/10.1155/2012/421564.

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Glioblastomas are characterized by altered expression of several ion channels that have important consequences in cell functions associated with their aggressiveness, such as cell survival, proliferation, and migration. Data on the altered expression and function of the intermediate-conductance calcium-activated K (KCa3.1) channels in glioblastoma cells have only recently become available. This paper aims to (i) illustrate the main structural, biophysical, pharmacological, and modulatory properties of the KCa3.1 channel, (ii) provide a detailed account of data on the expression of this channel in glioblastoma cells, as compared to normal brain tissue, and (iii) critically discuss its major functional roles. Available data suggest that KCa3.1 channels (i) are highly expressed in glioblastoma cells but only scantly in the normal brain parenchima, (ii) play an important role in the control of glioblastoma cell migration. Altogether, these data suggest KCa3.1 channels as potential candidates for a targeted therapy against this tumor.
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Shinoura, Nobusada, Lin Chen, Maqsood A. Wani, Young Gyu Kim, Jeffrey J. Larson, Ronald E. Warnick, Matthias Simon, Anil G. Menon, Wan Li Bi, and Peter J. Stambrook. "Protein and messenger RNA expression of connexin43 in astrocytomas: implications in brain tumor gene therapy." Journal of Neurosurgery 84, no. 5 (May 1996): 839–45. http://dx.doi.org/10.3171/jns.1996.84.5.0839.

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✓ The expression of connexin43, the primary gap-junction constituent of glial cells, was evaluated at the messenger RNA and protein levels in different grades of astrocytoma to investigate the relevance of gap junctions in herpes simplex virus—thymidine kinase (HSV-tk)—mediated gene therapy of brain tumors. Transduction of the retroviral-mediated HSV-tk gene into tumor cells with subsequent administration of ganciclovir has recently been used as an experimental therapeutic strategy for treatment of brain tumors. One aspect of this approach is the bystander effect, which augments the efficacy of this therapeutic approach. Glioblastoma cells with minimum levels of connexin43 protein were transfected with a connexin43 complementary DNA. These cells manifested a marked increase in the in vitro bystander effect, supporting the contention that the in vitro bystander effect is a consequence of metabolic cooperation between cells mediated by gap junctions. To assess relative levels of gap-junction protein expression in the relevant tumor type, we examined primary astrocytomas, primary astrocytoma cell cultures, and glioblastoma cell lines. Although most astrocytoma tumor samples expressed connexin43, they differed in the level of expression, with the greatest variation exhibited in high-grade astrocytomas. Primary glioblastoma cell cultures and established glioblastoma cell lines also displayed some variability in connexin43 levels. In aggregate, our results anticipate that glioblastomas will have a varied bystander effect during HSV-tk gene therapy depending on the level of connexin43 expression.
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KOTELNIKOVA, EKATERINA, ANTON YURYEV, ILYA MAZO, and NIKOLAI DARASELIA. "COMPUTATIONAL APPROACHES FOR DRUG REPOSITIONING AND COMBINATION THERAPY DESIGN." Journal of Bioinformatics and Computational Biology 08, no. 03 (June 2010): 593–606. http://dx.doi.org/10.1142/s0219720010004732.

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Heterogeneous high-throughput biological data become readily available for various diseases. The amount of data points generated by such experiments does not allow manual integration of the information to design the most optimal therapy for a disease. We describe a novel computational workflow for designing therapy using Ariadne Genomics Pathway Studio software. We use publically available microarray experiments for glioblastoma and automatically constructed ResNet and ChemEffect databases to exemplify how to find potentially effective chemicals for glioblastoma — the disease yet without effective treatment. Our first approach involved construction of signaling pathway affected in glioblastoma using scientific literature and data available in ResNet database. Compounds known to affect multiple proteins in this pathway were found in ChemEffect database. Another approach involved analysis of differential expression in glioblastoma patients using Sub-Network Enrichment Analysis (SNEA). SNEA identified angiogenesis-related protein Cyr61 as the major positive regulator upstream of genes differentially expressed in glioblastoma. Using our findings, we then identified breast cancer drug Fulvestrant as a major inhibitor of glioblastoma pathway as well as Cyr61. This suggested Fulvestrant as a potential treatment against glioblastoma. We further show how to increase efficacy of glioblastoma treatment by finding optimal combinations of Fulvestrant with other drugs.
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Appolloni, Irene, Francesco Alessandrini, Laura Menotti, Elisa Avitabile, Daniela Marubbi, Noemi Piga, Davide Ceresa, Francesca Piaggio, Gabriella Campadelli-Fiume, and Paolo Malatesta. "Specificity, Safety, Efficacy of EGFRvIII-Retargeted Oncolytic HSV for Xenotransplanted Human Glioblastoma." Viruses 13, no. 9 (August 24, 2021): 1677. http://dx.doi.org/10.3390/v13091677.

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Glioblastoma is a lethal primary brain tumor lacking effective therapy. The secluded onset site, combined with the infiltrative properties of this tumor, require novel targeted therapies. In this scenario, the use of oncolytic viruses retargeted to glioblastoma cells and able to spread across the tumor cells represent an intriguing treatment strategy. Here, we tested the specificity, safety and efficacy of R-613, the first oncolytic HSV fully retargeted to EGFRvIII, a variant of the epidermal growth factor receptor carrying a mutation typically found in glioblastoma. An early treatment with R-613 on orthotopically transplanted EGFRvIII-expressing human glioblastoma significantly increased the median survival time of mice. In this setting, the growth of human glioblastoma xenotransplants was monitored by a secreted luciferase reporter and showed that R-613 is able to substantially delay the development of the tumor masses. When administered as late treatment to a well-established glioblastomas, R-613 appeared to be less effective. Notably the uninfected tumor cells derived from the explanted tumor masses were still susceptible to R-613 infection ex vivo, thus suggesting that multiple treatments could enhance R-613 therapeutic efficacy, making R-613 a promising oncolytic HSV candidate for glioblastoma treatment.
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Hau, Peter, Roger Stupp, and Monika E. Hegi. "MGMT Methylation Status: The Advent of Stratified Therapy in Glioblastoma?" Disease Markers 23, no. 1-2 (2007): 97–104. http://dx.doi.org/10.1155/2007/159242.

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Glioblastomas are the most malignant gliomas with median survival times of only 15 months despite modern therapies. All standard treatments are palliative. Pathogenetic factors are diverse, hence, stratified treatment plans are warranted considering the molecular heterogeneity among these tumors. However, most patients are treated with "one fits all" standard therapies, many of them with minor response and major toxicities. The integration of clinical and molecular information, now becoming available using new tools such as gene arrays, proteomics, and molecular imaging, will take us to an era where more targeted and effective treatments may be implemented.A first step towards the design of such therapies is the identification of relevant molecular mechanisms driving the aggressive biological behavior of glioblastoma. The accumulation of diverse aberrations in regulatory processes enables tumor cells to bypass the effects of most classical therapies available. Molecular alterations underlying such mechanisms comprise aberrations on the genetic level, such as point mutations of distinct genes, or amplifications and deletions, while others result from epigenetic modifications such as aberrant methylation of CpG islands in the regulatory sequence of genes. Epigenetic silencing of theMGMTgene encoding a DNA repair enzyme was recently found to be of predictive value in a randomized clinical trial for newly diagnosed glioblastoma testing the addition of the alkylating agent temozolomide to standard radiotherapy. Determination of the methylation status of theMGMTpromoter may become the first molecular diagnostic tool to identify patients most likely to respond that will allow individually tailored therapy in glioblastoma.To date, the test for theMGMT-methylation status is the only tool available that may direct the choice for alkylating agents in glioblastoma patients, but many others may hopefully become part of an arsenal to stratify patients to respective targeted therapies within the next years.
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Chavda, Vishal, Vimal Patel, Dhananjay Yadav, Jigar Shah, Snehal Patel, and Jun-O. Jin. "Therapeutics and Research Related to Glioblastoma: Advancements and Future Targets." Current Drug Metabolism 21, no. 3 (June 25, 2020): 186–98. http://dx.doi.org/10.2174/1389200221666200408083950.

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Glioblastoma, the most common primary brain tumor, has been recognized as one of the most lethal and fatal human tumors. It has a dismal prognosis, and survival after diagnosis is less than 15 months. Surgery and radiotherapy are the only available treatment options at present. However, numerous approaches have been made to upgrade in vivo and in vitro models with the primary goal of assessing abnormal molecular pathways that would be suitable targets for novel therapeutic approaches. Novel drugs, delivery systems, and immunotherapy strategies to establish new multimodal therapies that target the molecular pathways involved in tumor initiation and progression in glioblastoma are being studied. The goal of this review was to describe the pathophysiology, neurodegeneration mechanisms, signaling pathways, and future therapeutic targets associated with glioblastomas. The key features have been detailed to provide an up-to-date summary of the advancement required in current diagnosis and therapeutics for glioblastoma. The role of nanoparticulate system graphene quantum dots as suitable therapy for glioblastoma has also been discussed.
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Kobayashi, Yusuke, Takashi Kon, Katsuyoshi Shimizu, Daisuke Tanioka, Yosuke Satou, and Tohru Mizutani. "COT-18 TWO CASES OF GLIOBLASTOMA WITH ASYMPTOMATIC PULMONARY ARTERY EMBOLISM AND DEEP VEIN THROMBOSIS FROM ADMISSION TO HOSPITAL." Neuro-Oncology Advances 1, Supplement_2 (December 2019): ii43—ii44. http://dx.doi.org/10.1093/noajnl/vdz039.198.

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Abstract Patients with malignant tumors are susceptible to concurrent venous thromboembolism. We report two cases of glioblastomas that showed asymptomatic pulmonary embolism and deep vein thrombosis on admission. The first case was a 77-year-old male. He was referred to our clinic for a tumor found in the left temporal lobe on computed tomography scan performed when he suffered pneumonia. On admission,he had a Karnofsky performance status (KPS) score of 50 and an elevated D-dimer level (16.46 μg/ml). Pulmonary embolism and deep vein thrombosis were noted on detailed examination. Direct oral anticoagulant (DOAC) therapy resulted in the disappearance of pulmonary embolism. On biopsy,the tumor was diagnosed as glioblastoma. The patient underwent radiation therapy in combination with chemotherapy. The second case was a 71-year-old female. She developed a disorder of consciousness and was admitted to a clinic. Brain magnetic resonance imaging (MRI) revealed a high T2 signal area in the left temporal lobe. The patient was initially diagnosed with encephalitis. Though the consciousness disorder improved quickly,she was referred to our clinic after a hyperintense area was observed on MRI. On admission,she had a KPS score of 100,and an elevated D-dimer level (7.59μg/ml),revealing pulmonary embolism and deep vein thrombosis. She was started on a DOAC and underwent surgical removal of the tumor via craniotomy. She was diagnosed with glioblastoma and underwent radiation therapy in combination with chemotherapy. Approximately 20% of the patients with glioblastomas suffer concurrent symptomatic venous thromboembolism. The incidence of venous thromboembolism is further elevated in patients with a poor KPS score or elderly people. Many patients with glioblastomas suffer asymptomatic venous thromboembolism. In this report,asymptomatic venous thromboembolism was noted in patients with a good KPS score. In glioblastoma patients,it is necessary to test for venous thromboembolism by measuring D-dimer levels before surgery.
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43

Dimberg, Anna. "The glioblastoma vasculature as a target for cancer therapy." Biochemical Society Transactions 42, no. 6 (November 17, 2014): 1647–52. http://dx.doi.org/10.1042/bst20140278.

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Glioblastoma is characterized by microvascular proliferation and a highly abnormal dysfunctional vasculature. The glioblastoma vessels differ significantly from normal brain vessels morphologically, functionally and molecularly. The present review provides a brief overview of the current understanding of the formation, functional abnormalities and specific gene expression of glioblastoma vessels and the consequences of vascular abnormalization for the tumour microenvironment.
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Zhu, Jianhong, and Junjie Zhong. "Engineered T Cells for glioblastoma therapy." Glioma 1, no. 4 (2018): 125. http://dx.doi.org/10.4103/glioma.glioma_26_18.

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Kwiatkowska, Aneta, Mohan Nandhu, Prajna Behera, E. Chiocca, and Mariano Viapiano. "Strategies in Gene Therapy for Glioblastoma." Cancers 5, no. 4 (October 23, 2013): 1271–305. http://dx.doi.org/10.3390/cancers5041271.

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46

&NA;. "Gene therapy potential in glioblastoma multiforme." Inpharma Weekly &NA;, no. 1046 (July 1996): 11. http://dx.doi.org/10.2165/00128413-199610460-00018.

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Popescu, Alisa Madalina, Stefana Oana Purcaru, Oana Alexandru, and Anica Dricu. "New perspectives in glioblastoma antiangiogenic therapy." Współczesna Onkologia 2 (2016): 109–18. http://dx.doi.org/10.5114/wo.2015.56122.

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48

Ferrarelli, Leslie K. "A link closer to glioblastoma therapy." Science Signaling 10, no. 473 (April 4, 2017): eaan3515. http://dx.doi.org/10.1126/scisignal.aan3515.

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Fan, Qiwen, Zhenyi An, Robyn A. Wong, Xujun Luo, Edbert D. Lu, Albert Baldwin, Manasi K. Mayekar, et al. "Betacellulin drives therapy resistance in glioblastoma." Neuro-Oncology 22, no. 4 (November 3, 2019): 457–69. http://dx.doi.org/10.1093/neuonc/noz206.

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Abstract Background The transcription factor signal transducer and activator of transcription 3 (STAT3) drives progression in glioblastoma (GBM), suggesting STAT3 as a therapeutic target. Surprisingly however, GBM cells generally show primary resistance to STAT3 blockade. Methods Human glioblastoma cell lines LN229, U87, SF767, and U373, and patient-derived xenografts (PDXs) GBM8 and GBM43 were used to evaluate epidermal growth factor receptor (EGFR) activation during STAT3 inhibition. Protein and gene expression experiments, protein stability assays, cytokine arrays, phospho-tyrosine arrays and EGFR-ligand protein arrays were performed on STAT3 inhibitor–treated cells. To evaluate antitumor activity, we administered a betacellulin (BTC)-neutralizing antibody alone and in combination with STAT3 inhibition. BTC is an EGFR ligand. We therefore treated mice with orthotopic xenografts using the third-generation EGFR inhibitor osimertinib, with or without STAT3 knockdown. Results We demonstrate that both small-molecule inhibitors and knockdown of STAT3 led to expression and secretion of the EGFR ligand BTC, resulting in activation of EGFR and subsequent downstream phosphorylation of nuclear factor-kappaB (NF-κB). Neutralizing antibody against BTC abrogated activation of both EGFR and NF-κB in response to inhibition of STAT3; with combinatorial blockade of STAT3 and BTC inducing apoptosis in GBM cells. Blocking EGFR and STAT3 together inhibited tumor growth, improving survival in mice bearing orthotopic GBM PDXs in vivo. Conclusion These data reveal a feedback loop among STAT3, EGFR, and NF-κB that mediates primary resistance to STAT3 blockade and suggest strategies for therapeutic intervention.
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Balasubramaniyan, Veerakumar, and Krishna Bhat. "Targeting pyrimidine metabolism for glioblastoma therapy." Neuro-Oncology 22, no. 2 (December 21, 2019): 169–70. http://dx.doi.org/10.1093/neuonc/noz239.

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