Academic literature on the topic 'Glioblastoma multiform (GBM)'
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Journal articles on the topic "Glioblastoma multiform (GBM)"
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Yahya, Farah, DJIMRABEYE Alngar, TOUATI Lina, et al. "Cystic glioblastoma mimicking toxoplasmosis in a young adult: A case report." World Journal of Advanced Research and Reviews 19, no. 3 (2023): 585–88. https://doi.org/10.5281/zenodo.11668458.
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Glioblastoma multiform it is most frequent brain tumor which highly malignancy, also there is rare cases presentation for solitary cystic glioblastoma (GBM) form which is mimicking infection, especially toxoplasmosis. In our case report highlighted the gold stone of the clinical feature identifying of cystic GBM to ensure early diagnosis and treatment.
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Ashing, Liz, Ashley Nelson, Zefanias Ngove, and Aundrea Crain. "Bavachin Suppresses Cell Growth and Enhances Temozolomide Efficacy in U-87 MG Glioblastoma Cells." American Journal of Undergraduate Research 21, no. 3 (2024): 63–71. https://doi.org/10.33697/ajur.2024.126.
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Glioblastoma multiform (GBM) is a lethal cancer affecting the central nervous system. Existing treatment methods for GBM include chemotherapy, radiation, and surgery. Temozolomide is a common chemotherapy treatment for GBM but causes unwanted side effects, as do most chemotherapy treatments. To decrease the harmful side effects of chemotherapy, research has turned to exploring natural compounds to treat cancer. In this study, the natural compound bavachin was investigated to determine cytotoxicity in GBM cells. Bavachin has been tested in many cell lines but not glioblastoma. A sulforhodamine B (SRB) assay, trypan blue counting, and a tumorsphere assay were used to test the hypothesis in this study. It was found that bavachin suppressed glioblastoma cell and tumorsphere viability, had a synergistic interaction with temozolomide, and ornithine decarboxylase was identified as a potential target in silico. This study demonstrated the ability of bavachin to suppress the growth of U-87 MG glioblastoma cells and enhance temozolomide efficacy. These findings demonstrated that bavachin is a potential treatment for GBM based on its ability to suppress cell growth. KEYWORDS: Glioblastoma Multiforme; Temozolomide; Bavachin; Flavonoid; Tumorspheres; Cell Viability; Cancer; Apoptosis; Psoralea corylifolia
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Yahya Farah, Alngar DJIMRABEYE, Lina TOUATI, et al. "Cystic glioblastoma mimicking toxoplasmosis in a young adult: A case report." World Journal of Advanced Research and Reviews 19, no. 3 (2023): 585–88. http://dx.doi.org/10.30574/wjarr.2023.19.3.1595.
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Glioblastoma multiform it is most frequent brain tumor which highly malignancy, also there is rare cases presentation for solitary cystic glioblastoma (GBM) form which is mimicking infection, especially toxoplasmosis. In our case report highlighted the gold stone of the clinical feature identifying of cystic GBM to ensure early diagnosis and treatment.
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K, Tanti Ajoe, and Martin M. "Medical Rehabilitation of Glioblastoma Multiform: Case Report." Indonesian Journal of Physical Medicine & Rehabilitation 7, no. 01 (2019): 36. http://dx.doi.org/10.36803/ijpmr.v7i01.132.
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Introduction: Glioblastoma Multiform (GBM) is the most common malignant primary brain tumor. Early rehabilitation program is needed to increasing the independency and the quality of life.Methods: Case presentation of a woman, age 31 years, diagnosed with GBM. Subject has chronic headache by visual analog scale (VAS) was 5 to 6 and progressive of vision loss (0/0), short and intermediate memory loss, the average of limb strength by manual muscle test were four, and immobilization on bedsince one and half year. The first day after craniotomy, patient has Rehabilitation Program; cryotherapy for decreased the pain, therapeutic exercise, and cognitive stimulation exercise for 5 week.Results: After 5 weeks of rehabilitation program, patient has reduced the pain measured by VAS was 0, improved the memory, and be able to ambulationConclusion: Patient post GBM post craniotomy need to have comprehensive rehabilitation program to reduce pain, improve memory and ambulation.Keywords: Glioblastoma Multiform, Rehabilitation Medicine Program
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Yazıcı, Emine, Aleyna Gezen, Ece Oylumlu, and Gamze Tanrıöver. "Glioblastoma multiform tedavisindeki birincil engel: Kan beyin bariyeri." Ege Tıp Dergisi 64, no. 1 (2025): 184–92. https://doi.org/10.19161/etd.1621826.
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Dünya Sağlık Örgütü tarafından derece 4 astrositom olarak sınıflandırılan Glioblastoma Multiform (GBM), merkezi sinir sisteminin en agresif ve yaygın görülen primer beyin tümörüdür. Klinikteki GBM hastaları için mevcut tedavi; rezeksiyonun ardından eş zamanlı uygulanan radyoterapi ve kemoterapiyi içermektedir. Glioblastoma Multiform tedavisindeki bu yaklaşımların etkinliği; tümör heterojenliği, glioma kök hücreleri, DNA hasar onarım mekanizmaları ve kan-beyin bariyeri gibi faktörler nedeniyle yetersiz kalmaktadır. Temozolomid, lipofilik bir ajan olması nedeniyle kan-beyin bariyerini kolaylıkla geçebilmekte ve bu özelliği sayesinde glioma tedavisinde etkili bir ajan olarak kullanılmaktadır. Bununla birlikte, hastaların büyük bir kısmında nüks meydana gelmekte ve bu hastalar Temozolomid’e uzun süre maruz kaldığı için tedaviye direnç geliştirmektedir. Günümüzde, nüks eden GBM hastaları için farklı bir tedavi yaklaşımı söz konusu değildir. Bu yüzden, hasta sağkalımını uzatacak yeni ajanların araştırılması son derece önemlidir. Terapötik ajanların merkezi sinir sistemine iletimi, kan-beyin bariyeri tarafından engellenmekte ve beyindeki hedeflenen bölgelere erişim, GBM için yeni ilaçların geliştirilmesinde en büyük zorluklardan birini oluşturmaktadır. Beyin tümörleri tedavisinde kan-beyin bariyerinin ilaç geçirgenliği heterojen bir yapı sergilemektedir. Sonuç olarak, bu bariyer geçirgenliğinin modüle edilmesi ve ilaç biyoyararlanımını artırmayı hedefleyen çeşitli stratejiler geliştirilmelidir. Kan-beyin bariyerinin aşılması, hedefe yönelik tedavi yaklaşımlarında dikkate alınması gereken önemli bir konudur. Bu derleme, kan-beyin bariyerinin GBM ile ilişkisini inceleyerek, konuya dair güncel bilgileri ayrıntılı bir şekilde sunmayı amaçlamaktadır.
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Goodarzi, Arash, Mehdi Khanmohammadi, Arman Ai, et al. "Simultaneous impact of atorvastatin and mesenchymal stem cells for glioblastoma multiform suppression in rat glioblastoma multiform model." Molecular Biology Reports 47, no. 10 (2020): 7783–95. http://dx.doi.org/10.1007/s11033-020-05855-z.
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Abstract Glioblastoma multiform (GBM) is known as an aggressive glial neoplasm. Recently incorporation of mesenchymal stem cells with anti-tumor drugs have been used due to lack of immunological responses and their easy accessibility. In this study, we have investigated the anti-proliferative and apoptotic activity of atorvastatin (Ator) in combination of mesenchymal stem cells (MSCs) on GBM cells in vitro and in vivo. The MSCs isolated from rats and characterized for their multi-potency features. The anti-proliferative and migration inhibition of Ator and MSCs were evaluated by MTT and scratch migration assays. The annexin/PI percentage and cell cycle arrest of treated C6 cells were evaluated until 72 h incubation. The animal model was established via injection of C6 cells in the brain of rats and subsequent injection of Ator each 3 days and single injection of MSCs until 12 days. The growth rate, migrational phenotype and cell cycle progression of C6 cells decreased and inhibited by the interplay of different factors in the presence of Ator and MSCs. The effect of Ator and MSCs on animal models displayed a significant reduction in tumor size and weight. Furthermore, histopathology evaluation proved low hypercellularity and mitosis index as well as mild invasive tumor cells for perivascular cuffing without pseudopalisading necrosis and small delicate vessels in Ator + MSCs condition. In summary, Ator and MSCs delivery to GBM model provides an effective strategy for targeted therapy of brain tumor.
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Litak, Jakub, Wiesława Grajkowska, Justyna Szumiło, et al. "PD-L1 Expression Correlated with p53 Expression in Pediatric Glioblastoma Multiforme." Brain Sciences 11, no. 2 (2021): 262. http://dx.doi.org/10.3390/brainsci11020262.
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High-grade gliomas are infrequent in the pediatric population compared to adults, nevertheless, mortality and morbidity caused by malignant gliomas in this group of patients remain significant. PD-L1 and PD-1 Immune checkpoints (IC) molecules maintain immunological balance between activation and suppression. Eighteen patients with a histopathological diagnosis of pediatric glioblastoma multiforme (GBM, WHO IV) were studied. In total, PD-L1 expression was detected in 8 patients (44%). The molecular aspect of IC and immunotherapy targeted on PD-1/PD-L1 axis in pediatric population may be a promising adjuvant therapy in pediatric glioblastoma multiform treatment, however, this subject requires further investigation.
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Naveenkumr., R., A. Nagarathna., and V. K. Prathiba. "A Review of Glioblastoma Tumor Image Segmentation Techniques." Journal of Medical Surgical Nursing Practice and Research 2, no. 2 (2020): 20–24. https://doi.org/10.5281/zenodo.3750733.
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The heterogeneous and persistent growth of tumor cells in glioblastoma multiform is an intricate confrontation for brain tumor treatment. The advanced therapies with improved precision are effective in mapping the tumor cells and helpful in combating the brain tumor. The multimodality image processing has become more popular in brain tumor quantification; it includes image segmentation as essential step adopted for standard treatment plans. To reduce the manual segmentation procedure and to optimization in targeted treatments are major key issues are still needs to focus for effective image segmentation. This paper highlights the primary clinical therapies applied for different stage of glioblastoma multiform and processing of multimodal information. The recent glioblastoma multiform segmentation techniques are discussed with key features of mapping probability and prediction capabilities.
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Alshabi, Ali Mohamed, Basavaraj Vastrad, Ibrahim Ahmed Shaikh, and Chanabasayya Vastrad. "Identification of Crucial Candidate Genes and Pathways in Glioblastoma Multiform by Bioinformatics Analysis." Biomolecules 9, no. 5 (2019): 201. http://dx.doi.org/10.3390/biom9050201.
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The present study aimed to investigate the molecular mechanisms underlying glioblastoma multiform (GBM) and its biomarkers. The differentially expressed genes (DEGs) were diagnosed using the limma software package. The ToppGene (ToppFun) was used to perform pathway and Gene Ontology (GO) enrichment analysis of the DEGs. Protein-protein interaction (PPI) networks, extracted modules, miRNA-target genes regulatory network and TF-target genes regulatory network were used to obtain insight into the actions of DEGs. Survival analysis for DEGs was carried out. A total of 590 DEGs, including 243 up regulated and 347 down regulated genes, were diagnosed between scrambled shRNA expression and Lin7A knock down. The up-regulated genes were enriched in ribosome, mitochondrial translation termination, translation, and peptide biosynthetic process. The down-regulated genes were enriched in focal adhesion, VEGFR3 signaling in lymphatic endothelium, extracellular matrix organization, and extracellular matrix. The current study screened the genes in the PPI network, extracted modules, miRNA-target genes regulatory network, and TF-target genes regulatory network with higher degrees as hub genes, which included NPM1, CUL4A, YIPF1, SHC1, AKT1, VLDLR, RPL14, P3H2, DTNA, FAM126B, RPL34, and MYL5. Survival analysis indicated that the high expression of RPL36A and MRPL35 were predicting longer survival of GBM, while high expression of AP1S1 and AKAP12 were predicting shorter survival of GBM. High expression of RPL36A and AP1S1 were associated with pathogenesis of GBM, while low expression of ALPL was associated with pathogenesis of GBM. In conclusion, the current study diagnosed DEGs between scrambled shRNA expression and Lin7A knock down samples, which could improve our understanding of the molecular mechanisms in the progression of GBM, and these crucial as well as new diagnostic markers might be used as therapeutic targets for GBM.
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Berthier, Sylvie, Louis Larrouquère, Pierre Champelovier, et al. "A New Patient-Derived Metastatic Glioblastoma Cell Line: Characterisation and Response to Sodium Selenite Anticancer Agent." Cancers 11, no. 1 (2018): 12. http://dx.doi.org/10.3390/cancers11010012.
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Glioblastoma multiform (GBM) tumors are very heterogeneous, organized in a hierarchical pattern, including cancer stem cells (CSC), and are responsible for development, maintenance, and cancer relapse. Therefore, it is relevant to establish new GBM cell lines with CSC characteristics to develop new treatments. A new human GBM cell line, named R2J, was established from the cerebro-spinal fluid (CSF) of a patient affected by GBM with leptomeningeal metastasis. R2J cells exhibits an abnormal karyotype and form self-renewable spheres in a serum-free medium. Original tumor, R2J, cultured in monolayer (2D) and in spheres showed a persistence expression of CD44, CD56 (except in monolayer), EGFR, Ki67, Nestin, and vimentin. The R2J cell line is tumorigenic and possesses CSC properties. We tested in vitro the anticancer effects of sodium selenite (SS) compared to temozolomide TMZ. SS was absorbed by R2J cells, was cytotoxic, induced an oxidative stress, and arrested cell growth in G2M before inducing both necrosis and apoptosis via caspase-3. SS also modified dimethyl-histone-3-lysine-9 (H3K9m2) levels and decreased histone deacetylase (HDAC) activity, suggesting anti-invasiveness potential. This study highlights the value of this new GBM cell line for preclinical modeling of clinically relevant, patient specific GBM and opens a therapeutic window to test SS to target resistant and recurrent GBM.
Dissertations / Theses on the topic "Glioblastoma multiform (GBM)"
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Aljohani, Hashim M. B. S. "Signaling Pathways Associated with Gefitinib Resistance in Glioblastoma Multiforme (GBM)." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1406900804.
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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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Alowaidi, Faisal A. N. "Functional Identification of Cripto-1 (TDGF1) Role in Glioblastoma Multiforme." Thesis, Griffith University, 2015. http://hdl.handle.net/10072/366238.
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Glioblastoma multiforme (GBM) is one of the most aggressive tumours and has poor survival rate. The expression of the embryonic stem cell factor Crypto-1 has been documented in most cancer types. More specifically, Cripto-1 expression has recently been correlated with low survival rate of young glioblastoma patients. It has been demonstrated that Cripto-1 controls cell survival and stemness, as well as proliferation and epithelial to mesenchymal transition (EMT). The contribution of Cripto-1 to tumour vascularisation was also reported. Even though Cripto-1 expression and signalling in most cancers has been well characterised, its involvement in controlling glioblastoma cells is poorly studied. The aim of this thesis was to interrogate the contribution of Cripto-1 to multiple processes mediating gliomagenesis and further to understand the underlying signalling pathways impacted upon by Cripto-1. The findings of the current study are in line with those reported for other tumour models. Moreover, this study provides further evidence on the important roles Cripto-1 plays in tumourigenesis, particularly, its role in de-differentiating cancer cells. This was shown by confirming its effect on the activation of factors known to maintain cancer cells in an undifferentiated state like OCT4, NANOG and SOX2. Most significantly, this study has unravelled for the first time the positive effect of ectopic Cripto-1 expression on CD44, a cell surface marker known for its involvement in maintaining GBM stem like cells in their undifferentiated phenotype. We also show that Cripto-1 is indispensable in controlling the infiltrative phenotype of glioma cells via regulating EMT. Ectopic Cripto-1 expression also regulates the proliferation of this GBM cell model by increasing levels of the proliferation markers Ki-67 and cyclin D1. This led to a significant increase in cellular growth rate over time. These findings suggest that Cripto-1 might control cellular proliferation in GBM.<br>Thesis (PhD Doctorate)<br>Doctor of Philosophy (PhD)<br>School of Medical Science<br>Griffith Health<br>Full Text
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Jilesen, Zachary Keavin. "Discovery and Application of Neoepitopes in an Oncolytic Rhabdovirus Vaccine Approach to Treat Glioblastoma Multiforme." Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/39688.
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Glioblastoma multiforme is the most common and lethal primary brain tumour in adults. Its aggressive and invasive phenotype makes it resistant to current standards of care, with a patient median survival following treatment of only 14 months. Potent and safe therapeutics are necessary to improve patient prognosis. Globally, efforts are being made in immunotherapies to combat such deleterious tumours. Preliminary work in the Stojdl lab has developed a novel oncolytic virus platform for brain cancer therapy that is non-toxic and exhibits potent anti-tumour efficacy. This platform is based on the rhabdovirus Farmington, identified for its potent oncolytic properties and engineering malleability. Herein, we begin to show our capability to discover and vaccinate against immunogenic neoepitopes derived from a mouse cancer mutanome. Engineering Farmington virus to express neoepitopes, allows for robust tumour specific immune proliferation following a prime vaccination. Overcoming problems of targeting self-antigen and antigen loss variants, a multi-neoepitope vaccine, presented here, is one of many alternative approaches to help combat cancer resistance. Despite achieving robust anti-tumour immunity by vaccination, selectivity of the tumour microenvironment remains an enormous challenge. Cumulative efforts in immunotherapy research will help drive novel therapeutics, like Farmington, into clinic and, ultimately, improve patient’s prognosis and quality of life.
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Xie, Yuan. "Modeling glioblastoma heterogeneity to decipher its biology." Doctoral thesis, Uppsala universitet, Institutionen för immunologi, genetik och patologi, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-278529.
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Glioblastoma multiforme (GBM) is the most common and lethal form of primary brain tumor that mainly affects adults. GBM displays remarkable intra- and inter-tumoral heterogeneity and contains a subpopulation of cells named glioma stem cells that is believed to be responsible for tumor maintenance, progression and recurrence. We have established and characterized a biobank of 48 cell lines derived from GBM patients. The cells were explanted and maintained as adherent cultures in serum-free, defined neural stem cell medium. These GBM cells (GCs) displayed NSC marker expression in vitro, had orthotopic tumor initiating capability in vivo, harboured genomic alterations characteristic of GBM and represented all four TCGA molecular subtypes. Our newly established biobank is also connected with a database (www.hgcc.se) that provides all molecular and clinical data. This resource provides a valuable platform of valid in vitro and in vivo models for basic GBM research and drug discovery. By using RCAS/tv-a mouse models for glioma, we found that GBMs originating from a putative NSC origin caused more tumorigenic GCs that had higher self-renewal abilities than those originating from putative glial precursor cell origin. By transcriptome analysis a mouse cell origin (MCO) gene signature was generated to cluster human GCs and GBM tissue samples and a functional relationship between the differentiation state of the initially transformed cell and the phenotype of GCs was discovered, which provides the basis for a new predictive MCO-based patient classification. LGR5 was found to be highly expressed in the most malignant mouse GC lines of putative NSC origin and also enriched in proneural GBMs characterized by PDGFRA alterations and OLIG2 up-regulation. By overexpressing or depleting LGR5 we discovered that high LGR5 expression in proneural GC lines increased the tumorigenicity, self-renewal and invasive capacities of the cells and could potentiate WNT signalling through its ligand RSPO1. Through transcriptome analysis we identified the candidate genes CCND2, PDGFRA, OLIG2, DKK1 that were found to be regulated by LGR5. In the last study, we found that mouse OPCs could initiate both astrocytic and oligdendroglial gliomas, which indicated that oncogenic signalling is dominant to cell of origin in affecting the histology of gliomas.
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Anand, Monika. "FUNCTION AND REGULATION OF MATRIX METALLOPROTEINASE-1 IN GLIOBLASTOMA MULTIFORME." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/2214.
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Glioblastoma Multiforme (GBM) is an aggressive and fatal cancer of the brain. It is characterized with augmented morbidity and elusion to therapies due in part to the incessant infiltration and spread of tumor cells in normal brain. We investigated the function of Matrix metalloproteinase-1, an important enzyme noted to be responsible for invasion in other cancers, in GBM and its regulation by epidermal growth factor receptor (EGFR) signaling. Previous studies from our laboratory demonstrated elevated levels of MMP-1 in GBM. Further studies indicated the involvement of MMP-1 in GBM invasion. The GBM cell lines T98G, U251MG and U87MG were used for this study. In T98G cell lines, inhibition of MMP-1 by siRNA significantly suppressed basal in vitro invasion without impacting cell viability. The over-expression of MMP-1 was accomplished in U251MG and U87MG using the mammalian expression vector, pIRES, encoding full length MMP-1 cDNA. The MMP-1 over-expressing U251MG and U87MG cells exhibited significantly enhanced invasion in vitro with no modification in the cell proliferation rates. A majority of GBM patients present defective EGFR signaling due to over-expression, amplification or mutation in the receptor. MMP-1 is known to be up-regulated by various stimulatory agents including growth factors. We examined the regulation of MMP-1 by EGFR activation and observed the induction of MMP-1 after EGF treatment. Inhibition of the receptor by pharmaceutic inhibitor treatment and genetic approaches led to reduction in MMP-1 levels. We also observed that this regulation is primarily mediated by the downstream MAPK pathway. Inhibition of MAPK and not PI3K pathway resulted in diminished MMP-1 protein levels even in the presence of EGF. These studies demonstrate the importance of the EGFR-MAPK signaling pathway in the induction of MMP-1 in glioma cell lines. In addition, MMP-1 plays a role in glioma cell invasion in vitro. These results along with the reports of MMP-1 over-expression in GBM warrant future studies examining the function of MMP-1 in vivo.
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Waters, Michael R. "RelB acts as a molecular switch to drive chronic inflammation in glioblastoma multiforme (GBM)." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4958.
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Inflammation is a homeostatic response to tissue injury or infection, which is normally short- lived and quickly resolves to limit tissue damage. In contrast, chronic inflammation has been linked to a variety of human diseases, including cancers such as glioblastoma multiforme (GBM). GBMs are very aggressive tumors with very low patient survival rates, which have not improved in several decades. GBM tumors are characterized by necrosis and profound inflammation; with cytokines secreted by both GBM cells and the tumor microenvironment. The mechanisms by which chronic inflammation develops and persists in GBM regardless of multiple anti-inflammatory feedback loops remain elusive. This project identifies a molecular switch which promotes chronic inflammation in GBM, but not primary human astrocytes.
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Mazumdar, Tapati. "ROLE AND REGULATION OF MYC IN GLIOBLASTOMA MULTIFORME CELL DIFFERENTIATION: IMPLICATION IN TUMOR FORMATION." [Kent, Ohio] : Kent State University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=kent1214366273.
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Thesis (Ph.D.)--Kent State University, 2008.<br>Title from PDF t.p. (viewed Sept. 28, 2009). Advisor: Saikh Jaharul Haque. Keywords: GBM; Differentiation; Myc; Stat3; GFAP. Includes bibliographical references (p. 153-189).
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BUTTA, VALENTINA. "Studio dei potenziali effetti antineoplastici del pioglitazone su cellule staminali tumorali da Glioblastoma Multiforme." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2014. http://hdl.handle.net/10281/54504.
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Il glioblastoma multiforme (GBM) è un astrocitoma di IV grado, è il più comune tra i tumori maligni cerebrali. La sopravvivenza media dei pazienti trattati è inferiore a 16 mesi e non è significativamente migliorata in questi ultimi decenni, sottolineando le difficoltà nell’efficace caratterizzazione e trattamento di questo tipo di tumore. L’alta frequenza di recidiva del GBM, il suo elevato potere infiltrante e la resistenza alla radio e chemioterapia rendono urgente lo sviluppo di strategie di trattamento maggiormente efficaci per la cura di questo tumore.
La resistenza ai trattamenti convenzionali è legata alla presenza di una sottopopolazione di cellule tumorali con caratteristiche staminali definite glioma stem cells (GSCs), in grado di sostenere la propagazione del tumore e di guidarne la recidiva.
Interessanti evidenze preliminari suggeriscono che pazienti diabetici con GBM, trattati con agonisti di PPARɤ (peroxisome proliferator-activated receptor gamma) mostrano una sopravvivenza media maggiore rispetto a pazienti riceventi la terapia standard per il trattamento del GBM. Da qui nasce l’interesse di uno studio più approfondito sui potenziali effetti antineoplastici di un agonista di PPARɤ, il Pioglitazone, farmaco insulino-sensibilizzante, attualmente impiegato in clinica per il trattamento del diabete di tipo II. Inoltre, in diversi studi condotti su diversi tipi di cellule di glioma, è stato dimostrato un effetto Pioglitazone nella riduzione della proliferazione cellulare, nell’invasività e nell’induzione della morte cellulare per apoptosi.
Lo scopo di questo studio è stato dunque quello di verificare se il Pioglitazone possa avere gli stessi effetti antineoplastici anche su linee di cellule staminali tumorali da GBM utilizzate nel nostro laboratorio e già precedentemente caratterizzate e pubblicate (GBM2, G179, G166, G144, Glins2 e GBM04) al fine di individuare nuove potenziali strategie terapeutiche.
Sono state condotte diverse analisi tra cui saggi di vitalità (MTT e Trypan Blue) e valutazione dell’indice mitotico, analisi morfologica e di immunofluorescenza, analisi di espressione tramite RT-PCR e saggio di invasione cellulare. Tutte queste analisi hanno messo in luce l’estrema variabilità di risposta di queste linee a conferma dell’ eterogeneità che caratterizza questo tipo di tumore. Dai risultati ottenuti si possono suddividere le linee in base alla loro sensibilità/resistenza al trattamento con Pioglitazone o alla possibile attivazione di vie indipendenti dal recettore di PPARɤ attivate da questo farmaco.
Questo studio rappresenta un inizio di valutazione dei potenziali effetti antineoplastici del Pioglitazone e ci ha permesso di identificare tra le nostre linee in esame quelle più o meno responsive al trattamento farmacologico, per poter procedere con studi futuri più specifici e selettivi.
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MONGIARDI, MARIA PATRIZIA. "Inhibition of telomerase and hypoxia-inducible factor-1 in human glioblastoma multiforme." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2009. http://hdl.handle.net/2108/985.
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Il glioblastoma multiforme (GBM), il più comune e aggressivo dei tumori gliali, è composto da una popolazione eterogenea di cellule tumorali astrocitarie scarsamente differenziate. Questi tumori possono svilupparsi dall’evoluzione maligna di un astrocitoma di più basso grado (grado WHO I o II) o da un astrocitoma anaplastico (grado WHO III), ma più frequentemente si manifestano de novo, senza alcuna evidenza di una neoplasia precedente.
Il GBM è un tumore paradigmatico nella capacità di indurre neo-angiogenesi, processo necessario per la crescita dei tumori solidi. Le cellule endoteliali del GBM hanno la peculiarità di riattivare la telomerasi, enzima deputato al mantenimento dei telomeri. Questa riattivazione della telomerasi da parte delle cellule endoteliali è una caratteristica esclusiva delle cellule endoteliali tumorali: l’attività telomerasica, infatti, non è stata mai osservata in cellule endoteliali che proliferano in contesti di neoangiogenesi non neoplastica.
Uno dei regolatori piu' importanti dei processi angiogenetici è il fattore di trascrizione HIF-1, che coordina la risposta cellulare all’ipossia. Sebbene HIF-1 sia universalmente riconosciuto come un fattore chiave nell’induzione della neo-angiogenesi come risposta all’ipossia, le conseguenze di una sua inibizione nello sviluppo dei tumori solidi non sono ancora del tutto chiare.
Lo scopo dei miei studi di dottorato è stato quello di esplorare le conseguenze dell’inibizione dell’angiogenesi sullo sviluppo del GBM umano. A tale scopo, ho deciso di seguire due strategie parallele: l’inibizione della telomerasi nelle cellule endoteliali del tumore e l’inibizione di HIF-1 nelle cellule tumorali gliali.
Tramite un modello di angiogenesi neoplastica in vivo, messo a punto nel nostro laboratorio, siamo stati in grado di dimostrare che le cellule endoteliali umane primarie HUVEC, indipendentemente dall’espressione di attività telomerasica, non crescono e non sopravvivono se iniettate nel sottocute murino. Al contrario, se le stesse cellule sono coiniettate insieme al GBM nel sottocute del topo, si evidenzia un significativo aumento della loro sopravvivenza. Inoltre, in questo modello sperimentale, le HUVEC collaborano con le cellule endoteliali dell’ospite per formare i neovasi associati al tumore. Questo effetto è amplificato nel caso in cui le cellule HUVEC esprimono alti livelli di telomerasi. Al contrario, cellule HUVEC in cui, tramite RNAi, è impedita la riattivazione dell’espressione della telomerasi non sopravvivono nemmeno se co-iniettate insieme al GBM.
Tramite l’utilizzo della tecnica dell’RNAi siamo andati poi ad inibire il pathway di HIF nelle cellule di GBM umano. In vitro, mediante curve di crescita e saggi di proliferazione, abbiamo dimostrato che il tasso proliferativo delle cellule in cui HIF-1 è inibito non si presenta alterato. Invece in co-coltura, dopo molte replicazioni cellulari, il numero delle cellule wild type è maggiore rispetto alla controparte con l’espressione di HIF-1 inibita. In modelli di tumorigenesi in vivo in topi nudi, mediante iniezione nel sottocute murino, abbiamo poi dimostrato che la tumorigenicità dei due gruppi è comparabile. Al contrario, inaspettatamente, co-iniettando le due popolazioni cellulari si ottenevano tumori misti con caratteristiche di aggressività accresciute, sia in termini di percentuale di attecchimento dello xenotrapianto, sia in termini di dimensioni raggiunte dal tumore. Questo dato suggerisce che l’eterogeneità della popolazione cellulare nella capacità di rispondere all’ipossia può promuovere l’aggressività tumorale.<br>Glioblastoma Multiforme (GBM) is the most common and the most aggressive glial tumor. It is composed by a heterogeneous tumor cell population, poorly differentiated. GBM (WHO grade IV) develop from low grade astrocytoma (WHO grade I or II) or anaplastic astrocytoma (WHO grade III), but more frequently they arise de novo.
GBM tumors are paradigmatic in their ability to induce neo-angiogenesis, a fundamental process in the growth of solid tumors. Of note, endothelial cells of GBM have the peculiarity to reactivate telomerase, the enzyme necessary to maintain telomere length. Telomerase reactivation is a characteristic feature of tumor endothelial cells, since it was not observed in endothelial cells proliferating in non neoplastic contexts.
One of the most important regulators of angiogenic processes is the transcriptional factor HIF-1, which orchestrates cellular response to hypoxia. Although HIF-1 is universally recognized as a key factor in inducing neo-angiogenesis as a response to reduced oxygen levels, the consequences of HIF-1 inhibition on the growth of solid tumors are not fully elucidated.
The aim of my PhD studies was to explore the consequences of targeting angiogenesis on the development of human GBM. To address this purpose, I selected two parallel strategies: inhibition of telomerase expression in tumor endothelial cells and inhibition of HIF-1 in glial tumor cells.
We developed a controlled in vivo assay of tumor angiogenesis in which primary human umbilical vascular endothelial cells (HUVECs) were subcutaneously grafted with or without human GBM cells in immunocompromised mice as Matrigel implants. We found that primary HUVECs did not survive in Matrigel implants, and that telomerase up regulation had little effect on HUVEC survival. In the presence of GBM cells, however, the grafted HUVECs not only survived in Matrigel implants but developed tubule structures that integrated with murine microvessels. Telomerase up regulation in HUVECs enhanced such effect. More importantly, inhibition of telomerase in HUVECs completely abolished tubule formation and greatly reduced survival of these cells in the tumor xenografts.
In the second part of this study, we investigated the consequence of downregulating HIF-1 function in a human GBM cell line on cell proliferation in vitro and tumor growth in vivo. RNA interference targeting the O2-regulated HIF-1α subunit efficiently reduced HIF-1α expression and transcriptional induction of HIF-1α responsive genes. In vitro proliferation rate of HIF-1 α - inhibited cells was not altered. Conversely long term co-cultures of wild type and HIF-1 α - inhibited GBM cells resulted in the overgrowth of the wild type cells. Subcutaneous grafting in nude mice of wild type and HIF-1 α - inhibited GBM cells lead to comparable tumor formation and growth. Surprisingly, co-grafting of HIF-1-positive and HIF1-negative GBM cells resulted in more aggressive tumors, both in terms of tumor appearance and tumor growth. This suggests that heterogeneity of the cellular populations in their ability to mount a response to hypoxia may promote tumor aggressiveness.
Book chapters on the topic "Glioblastoma multiform (GBM)"
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Quinones, Addison, and Anne Le. "The Multifaceted Glioblastoma: From Genomic Alterations to Metabolic Adaptations." In The Heterogeneity of Cancer Metabolism. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_4.
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AbstractGlioblastoma multiforme (GBM) develops on glial cells and is the most common as well as the deadliest form of brain cancer. As in other cancers, distinct combinations of genetic alterations in GBM subtypes induce a diversity of metabolic phenotypes, which explains the variability of GBM sensitivity to current therapies targeting its reprogrammed metabolism. Therefore, it is becoming imperative for cancer researchers to account for the temporal and spatial heterogeneity within this cancer type before making generalized conclusions about a particular treatment’s efficacy. Standard therapies for GBM have shown little success as the disease is almost always lethal; however, researchers are making progress and learning how to combine therapeutic strategies most effectively. GBMs can be classified initially into two subsets consisting of primary and secondary GBMs, and this categorization stems from cancer development. GBM is the highest grade of gliomas, which includes glioma I (low proliferative potential), glioma II (low proliferative potential with some capacity for infiltration and recurrence), glioma III (evidence of malignancy), and glioma IV (GBM) (malignant with features of necrosis and microvascular proliferation). Secondary GBM develops from a low-grade glioma to an advanced-stage cancer, while primary GBM provides no signs of progression and is identified as an advanced-stage glioma from the onset. The differences in prognosis and histology correlated with each classification are generally negligible, but the demographics of individuals affected and the accompanying genetic/metabolic properties show distinct differentiation [3].
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Lukiw, Walter J., and Frank Culicchia. "Genetic Signaling in Glioblastoma Multiforme (GBM): A Current Overview." In Neurochemical Mechanisms in Disease. Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-7104-3_24.
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Gentilal, Nichal, Ricardo Salvador, and Pedro Cavaleiro Miranda. "A Thermal Study of Tumor-Treating Fields for Glioblastoma Therapy." In Brain and Human Body Modeling 2020. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-45623-8_3.
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AbstractTumor-treating fields (TTFields) is an antimitotic cancer treatment technique used for glioblastoma multiforme (GBM) and malignant pleural mesothelioma. Although the frequency used is not as high as in hyperthermia, temperature increases due to the Joule effect might be meaningful given the necessary time that these fields should be applied for. Post hoc analysis of the EF-11 clinical trial showed higher median overall survival in patients whose compliance was at least 18 h per day. To quantify these temperature increases and predict the thermal impact of TTFields delivery to the head, we used a realistic model created from MR images segmented in five tissues: scalp, skull, CSF, gray matter (GM), and white matter (WM). Through COMSOL Multiphysics, we solved Laplace’s equation for the electric field and Pennes’ equation for the temperature distribution. To mimic the therapy as realistically as possible, we also considered complete current shutdown whenever any transducer reached 41 °C to allow transducers and tissues’ temperature to decrease. Our results indicate an intermittent operation of Optune due to this necessary current shutdown. Localized temperature increases were seen, especially underneath the regions where the transducers were placed. Maximum temperature values were around 41.5 °C on the scalp and 38 °C on the brain. According to the literature, significant thermal impact is only predicted for the brain where the rise in temperature may lead to an increased BBB permeability and variation in the blood flow and neurotransmitter concentration. Additionally, our results showed that if the injected current is reduced by around 25% compared to Optune’s standard way of operating, then uninterrupted treatment might be attainable. These predictions might be used to improve TTFields delivery in real patients and to increase awareness regarding possible thermal effects not yet reported elsewhere.
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Siddiqui, Ehraz Mehmood, Andleeb Khan, Sidharth Mehan, and Rakesh Sahu. "Green Nanoparticles: A Hope for Targeted Delivery of Natural Therapeuticals for the Management of Glioblastoma Multiforme (GBM)." In Polyphenols-based Nanotherapeutics for Cancer Management. Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-4935-6_12.
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Gentilal, Nichal, Ariel Naveh, Tal Marciano, et al. "The Impact of Scalp’s Temperature in the Predicted LMiPD in the Tumor During TTFields Treatment for Glioblastoma Multiforme." In Brain and Human Body Modelling 2021. Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-15451-5_1.
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AbstractTumor Treating Fields (TTFields) is a cancer treatment technique used for glioblastoma multiforme (GBM). It consists in the application of an electric field (EF) in two perpendicular directions alternately by placing transducer arrays on the patient’s scalp. In-vitro studies showed that the higher the electric field in the tumor, the better are the outcomes of the therapy. Therefore, these arrays are strategically placed in positions that can optimize the EF, based on the results of computational simulations. However, due to the required daily usage of this technique, at least 18 hours per day, the temperature of head tissues increases inevitably. To ensure patient’s safety, the temperature of the scalp is monitored and kept around 39.5 °C by changing the injected current, which consequently changes the EF in the tumor. In this work, we studied the impact that accounting for the temperature of the scalp might have in the choice of which layout should be used during TTFields planning. We used both a simplified and a realistic head model in our studies. We solved Laplace’s equation for the electric potential and Pennes’ equation for the temperature distribution using COMSOL Multiphysics. The electric field in the tumor was evaluated using the local minimum power density (LMiPD) both when the temperature of the scalp was considered in treatment planning and when it was not. We concluded that the values of the LMiPD significantly decrease when the temperature is considered. Furthermore, layouts in which two pairs of different arrays are very close to each other lead to the appearance of a common temperature hotspot, and consequently to the most significant variations in the predicted LMiPD values. In future, TTFields treatment planning studies, considering the temperature of the scalp might be beneficial to improve the predictions of treatment effectiveness.
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Sims, Eliot, and Kathryn Tarver. "Glioblastoma multiforme (GBM)." In Challenging Concepts in Oncology. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199688883.003.0020.
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Roy Morgan, Lee, Branko Jursic, Marcus Ware, and Roy S. Weiner. "New Approaches in the Treatment of Glioblastoma Multiforme." In Glioblastoma - Current Evidences [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.105886.
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Central nervous system (CNS) malignancies are rare, but commonly fatal and glioblastoma (GBM) is the most common of the primary brain tumors. In contrast to metastatic malignancies involving the CNS, which have external blood supplies that develop when the malignant cells penetrate the blood-brain-barrier (BBB), GBM generates its own intracerebral neovascular support system. Thus, the therapeutic issues as discussed herein review the development of drugs and therapeutics that will penetrate the BBB and are cytotoxic to GBM and other brain tumors. Since GBM is a CNS malignancy with minimal effective therapeutic options available, designing drugs and therapeutics as treatment for this malignancy that penetrate, but do not disrupt the BBB is the goal of this chapter. 4-Demethylcholesteryl-4-penclomedine (DM-CHOC-PEN) was designed and developed because of its lipophilic properties that would potentiate crossing the BBB and penetrate brain tumors. The drug has now completed Phase I/II clinical trial in humans with primary brain malignancies demonstrating objective responses in GBM. In addition, preliminary experiences with naturally occurring polyphenols—curcumin, quercetin, catechins and phloretin and derivatives—are reviewed as potential naturally occurring anti-glioblastoma agents.
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Tiwari, Meenakshi, Lokendra Kumar Sharma, and Ajit Kumar Saxena. "Potential Role of Cancer Stem Cells in Glioblastoma: A Therapeutic Aspect." In Glioblastoma - Current Evidences [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.106332.
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High-grade glioma (HGG) such as glioblastoma multiforme (GBM) is an aggressive brain tumor that is still associated with poor prognosis. With the discovery and advancement in understanding of cancer stem cells (CSC) in glioma, these cells have emerged as seed cells for tumor growth and recurrence and appear as a potential target for therapeutics. Glioma stem cells (GSCs) demonstrate capacity of self-renewal, proliferation, and differentiation into multiple cell types and can contribute to tumor heterogeneity. Their role is established in tumorigenesis, metastasis, chemo- and radio-resistance and appears as a major cause for tumor recurrence. Thus, targeting GSCs by various therapeutics may improve effectiveness of the drugs in use alone or in combination to significantly improve patient survival outcome in GBM cases. In this chapter, we have discussed various mechanisms that drive GSC including signaling pathways and tumor microenvironment. We have also discussed the mechanism behind resistance of GSCs toward therapeutics and the pathways that can be targeted to improve the outcome of the patients.
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Kulavi, Sohini, Debajit Dhar, Karan Iyer, Arnab Kumar Ghosh, and Jaya Bandyopadhyay. "Unveiling the Potentials of Withania somnifera (L.) Dunal as a Precise Therapeutic Intervention Against Glioblastoma Multiforme." In Life as Basic Science: An Overview and Prospects for the Future [Volume: 1]. International Academic Publishing House (IAPH), 2024. http://dx.doi.org/10.52756/lbsopf.2024.e01.007.
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Glioblastoma multiforme (GBM) is the most severe and fatal form of brain tumor, leading to a poor survival rate in patients and making a significant contribution to cancer-related deaths. The typical approaches to treating GBM involve surgical procedures followed by chemotherapy, targeting molecular pathways involving receptors like Epidermal Growth Factor Receptor (EGFR, EGFRvIII) and Vascular Endothelial Growth Factor Receptor (VEGFR) to modulate various cell signaling pathways. However, the effectiveness of current GBM treatments is notably constrained. Withania somnifera (WS) (L.) Dunal, commonly known as Ashwagandha, has a history spanning over 3,000 years in Ayurvedic and traditional medicine. This medicinal plant has diverse properties, encompassing anti-inflammatory, anticancer and antioxidant attributes. Recent advancements in the field of herbal and traditional medicines have explored its potential in managing deadly diseases like cancer. Ashwagandha or W. somnifera, mostly found in dry, sub-tropical regions of the world including India, is a well-known source of traditional and herbal medicines, and has many specific phytochemicals, viz. Withaferin A, Withanolide etc. This review discusses the potential of W. somnifera, supported by several research reports dealing with the extracts and phytochemicals from different parts of the plant, showing effectiveness against
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Applebaum, Allison J., and William S. Breitbart. "MCP-C Sample Case." In Meaning-Centered Psychotherapy for Cancer Caregivers. Oxford University PressNew York, 2024. http://dx.doi.org/10.1093/med/9780197640777.003.0010.
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Abstract A case example is provided to bring the material of Meaning-Centered Psychotherapy for Cancer Caregivers (MCP-C) to life and to assist therapists using the manual to elicit themes of meaning and caregiving with their own patients. The case presents the experience of Elliot, a 32-year-old Indian American cis man who engaged in MCP-C six months after Leo, his husband, was diagnosed with glioblastoma multiforme (GBM). An in-depth description of each of session is provided, with a focus on Elliot’s responses to the experiential exercise questions. The case example covers all four sources of meaning, and highlights how discussions of attitude and creativity can engender a sense of pride in caregivers despite the profound limitations they face.
Conference papers on the topic "Glioblastoma multiform (GBM)"
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Al Mamlook, Rabia Emhamed, Ahmad Nasayreh, Hasan Gharaibeh, and Sujeet Shrestha. "Classification Of Cancer Genome Atlas Glioblastoma Multiform (TCGA-GBM) Using Machine Learning Method." In 2023 IEEE International Conference on Electro Information Technology (eIT). IEEE, 2023. http://dx.doi.org/10.1109/eit57321.2023.10187283.
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Patel, Heet. "Cellular Metabolism Therapy Slowing Growth Rate of Glioblastomas." In 27th Annual Rowan-Virtua Research Day. Rowan University Libraries, 2023. https://doi.org/10.31986/issn.2689-0690_rdw.stratford_research_day.137_2023.
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Glioblastoma Multiforme (GBM), more commonly known as glioblastomas, are a form of specialized brain tumors called gliomas. Glioblastomas most commonly occur in glial cells of the central nervous system and the average age of diagnosis is 64. Treatment methods implemented currently are surgery of the removable masses followed by courses of chemotherapy and radiotherapy. These methods can only prolong the life span by a few months and as such, new research focused on tumor cell metabolism is being conducted to determine its impact on the progression of this tumor. Tumor masses, such as Glioblastomas, modify their metabolism via the Warburg Effect. This effect states that ATP production via the inefficient processing of carbon-based compounds into lactate is employed by tumors. Some avenues used to target this weakness are keto diets and glycolysis inhibitors. Keto diets restrict the intake of carbohydrates and move cellular metabolism towards fat and protein catabolism. This has shown some promise in restricting growth and in reducing the speed of tumor progression. In addition, targeted drug therapies with Lonidamine and Azaserine are shown to be effective in disrupting hexokinase-2 and glutaminase activity, respectively. Overall, these new mechanisms may hold the key to prolonging the lifespan and to treating individuals suffering from glioblastomas.
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Lan, Xiaoyang, Mona Meyer, Jüri Reimand, et al. "Abstract B29: Defining subclonal signaling heterogeneity in glioblastoma multiforme (GBM)." In Abstracts: Third AACR International Conference on Frontiers in Basic Cancer Research - September 18-22, 2013; National Harbor, MD. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.fbcr13-b29.
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Castro, Natasha Kuromoto de, Luisa Oliveira Wey Rossettini, and Mirto Nelso Prandini. "The future in glioblastoma treatment." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.081.
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Introduction: Glioblastoma multiforme (GBM) is the most aggressive tumor that affects humans. Surgical treatment based on cytoreduction presents serious limitations. Consequently, treatments that use selective measures, in order to define relevant antigens that retard growth and recurrences, acquire a prominent position. The complex tumor microenvironment and the infiltration into adjacent tissues make surgical therapies, radiotherapy and chemotherapy, approaches still unsatisfactory when the increase in survival rate is evaluated. Studies on central nervous system immunovigilance have found the presence of lymphatic vessels and the perivascular system that allows the presentation of antigens to T4 cells bringing with it great relevance of immunotherapy, and the creation of active immune responses, recruiting the immune system itself to fight the tumor locally or systemically. Objectives: Determine the effectiveness of combining immunotherapy with conventional therapies of treatments in order to prolong the survival of patients with GBM. Methodology: Databases of Springer Link, Oxford academic, PubMed, Biblioteca USP. Results: For an active immunotherapy to be well-defined, it is necessary to have a strong and efficient antigen presentation breaking the state of tumor immune tolerance and activating effector lymphocytes. The use of dendritic cells for this presentation may be a good strategy. Finally, the antitumor response requires coordination between various local and systemic components. Conclusion: The use of immunotherapy in the treatment of GBM continues to expand. Despite several problems, due to immunosuppression mediated by the tumor itself, the immunotherapy brings a hope regarding to the possibility of to increase the immunogenicity and, thus, prolonging patient survival.
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Mess, Griffin, Rasika Thombre, Max Kerensky, et al. "Designing a Murine Model of Human Glioblastoma Brain Tumor: Development of a Platform for Validation Using Ultrasound Elastography." In 2022 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2022. http://dx.doi.org/10.1115/dmd2022-1025.
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Abstract Glioblastoma Multiforme (GBM) is a malignant brain cancer with low overall survival. Therefore, researchers are looking to augment its current therapeutic regimen, which includes surgical tumor resection, chemotherapy and radiation. A promising treatment modality, focused ultrasound, has been used as a non-invasive treatment for GBM through multiple approaches such as thermal ablation, immunomodulation, and blood brain barrier disruption. In order to develop these treatments for clinical trials, testing in animal models needs to be performed to investigate the efficacy of the treatment in complex biological environments, as well as to evaluate any side-effects. The more biologically relevant the animal model is to human anatomy, the more applicable the results will be for translation to clinical trials. Here, we report a human GBM rat model, which utilizes an IDH-wildtype, EGFRvIII mutant patient-derived xenograft in athymic rats. The in vivo tumor growth rate was assessed over a period of 20 days to evaluate reproducibility and to develop the model for future testing of FUS in the treatment of GBM.
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Ahmad, Fahim, and Ellora Sen. "Abstract A08: Telomerase inhibition brings metabolic compromises in glioblastoma multiforme (GBM)." In Abstracts: Fourth AACR International Conference on Frontiers in Basic Cancer Research; October 23-26, 2015; Philadelphia, PA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.fbcr15-a08.
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Sharma, Puja, Brian Koons, and Amrinder S. Nain. "Blebbing Dynamics, Single Cell Force Measurements, and the Influence of Cytochalasin D on Glioblastoma Multiforme Cells Using STEP Fibers." In ASME 2013 2nd Global Congress on NanoEngineering for Medicine and Biology. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/nemb2013-93105.
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Classified as a grade IV tumor of the central nervous system, Glioblastoma multiforme (GBM) arises from the glia. A poor understanding of tumor metastasis and limited treatment options have led to increase in deaths of patients suffering from GBM. Studying glioma behavior using aligned structures that mimic native glioblastoma metastatic path is challenging. In this study, we utilize a previously described non-electrospinning platform to manufacture aligned 3D structures called STEP nanonets that not only allows the study of individual cell-nanofiber interaction, but also allows the calculation of migratory forces using beam mechanics. In particular, the blebbing dynamics, force generation, and the effect of an actin disruptor, Cytochalasin D have been investigated on a glioma cell line (DBTRG, Denver Based Tumor Research Group). It was observed that cell pulled onto the nanofibers causing measurable deflections when they were in spread and non-blebbing conditions. In non-spread configurations while attached to fibers, the cells acquired spherical configurations and resumed blebbing. The average migratory force generated by cells exposed to DMSO (control, 1:1000 dilution) using nanonets of 2μm by 400nm fibers was 0.58±0.06nN. Actin disruptor, Cytochalasin D severely compromised the ability of the glioma cells to migrate causing no deflection of the fibers. Forces exerted by tumor cells on their native microenvironment affects their ability to metastasize, invade and proliferate. While the result presents actin disruptor as a potential target to minimize metastasis, the influence of other cytoskeleton disruptors can also be studied using the platform. Moreover, the results obtained from the study can be utilized to better understand the individual cell – nanofibers interaction which can shed light on how cells interact with their native environment during metastasis.
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Wesley, Umadevi V., Paul Clark, Jacob Jaeger, John Kuo, and Robert Dempsey. "Abstract 4300: Cell cycle pathway gene regulation in glioblastoma multiforme (GBM) and GBM derived stem cells: Implicating Pentraxin 3 upregulation." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4300.
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Gonzalez, Oscar A., Darren Seals, and Waldemar Debinski. "Abstract LB-115: EphA2/ephrinA1 system may regulate invadopodia formation of glioblastoma multiforme (GBM) cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-lb-115.
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Ma, Liang, Lei Gao, Yichen Luo, et al. "Flow Analysis of a Porous Polymer-Based Three-Dimensional Cell Culture Device for Drug Screening." In ASME 2018 13th International Manufacturing Science and Engineering Conference. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/msec2018-6313.
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A porous polymer-based three-dimensional (3D) cell culture device has been developed as an in vitro tissue model system for the cytotoxicity of anticancer drug test. The device had two chambers connected in tandem, each loaded with a 3D scaffold made of highly biocompatible poly (lactic acid) (PLA). Hepatoma cells (HepG2) and glioblastoma multiforme (GBM) cancer cells were cultured in the two separate porous scaffolds. A peristaltic pump was adopted to realize a perfusion cell culture. In this study, we focus on cell viability inside the 3D porous scaffolds under flow-induced shear stress effects. A flow simulation was conducted to predict the shear stress based on a realistic representation of the porous structure. The simulation results were correlated to the cell variability measurements at different flow rates. It is shown that the modeling approach presented in this paper can be useful for shear stress predication inside porous scaffolds and the computational fluid dynamics model can be an effective way to optimize the operation parameters of perfused 3D cell culture devices.