Displaying publications 21 - 40 of 52 in total

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  1. Fulltext Malignant Transformation of a Rosette-Forming Glioneuronal Tumor with IDH1 Mutation: A Case Report and Literature Review
    Jayapalan RR, Mun KS, Wong KT, Sia SF
    World Neurosurg X, 2019 Apr;2:100006.
    PMID: 31218281 DOI: 10.1016/j.wnsx.2018.100006
    Background: Rosette-forming glioneuronal tumor (World Health Organization grade I) is considered as a benign tumor with very low potential for progression. The potential for malignant transformation of this tumor is not known and has never been reported before in literature.

    Case Description: We report a 42-year-old man, diagnosed with rosette-forming glioneuronal tumor of the fourth ventricle with a positive isocitrate dehydrogenase 1 mutation, progressed to glioblastoma after 6 years from diagnosis. We discuss the clinical history, radiological findings, and histopathological characteristic with immunohistochemistry findings observed in this unique case.

    Conclusions: Despite being acceptable as benign, based on our observations in this case, there is a potential for malignant transformation of rosette-forming glioneuronal tumor. The role of isocitrate dehydrogenase 1 mutation leading to malignant transformation could not be established as our finding is novel and further prospective studies are required to prove this association.

    Matched MeSH terms: Glioblastoma
  2. Fulltext A dual genetic alteration (mitochondrial and nuclear DNA): first case in Malaysia detected in glioblastoma multiforme
    Abdul Aziz Mohamed Yusoff, Wan Salihah Wan Abdullah, Alarmelu Nithya Ramanathan, Jafri Malin Abdullah, Zamzuri Idris
    Malaysian Journal of Medicine and Health Sciences, 2020;16(2):332-335.
    MyJurnal
    Although the precise etiology of Glioblastoma multiforme (GBM, WHO grade IV) remains unknown, its progression
    is believed to be driven by the accumulation of multiple genetic alterations. Here, we report a case of a patient who
    developed GBM, and associated with dual alterations, particularly 4977-bp deletion in mtDNA (mtDNA4977) and
    p.Arg132His (R132H) mutation in IDH1. A 35-year old Malaysian woman patient who primary diagnosed with astrocytoma WHO grade I and subsequently after four years developed a GBM, was detected with a mtDNA4977. This
    deletion appears to be a sporadic mutation. Additionally, analysis of patient’s tumor tissue also found to harbor a heterozygous IDH1 R132H mutation. This represents the first case report of coexisting mtDNA4977 together with IDH1
    R132H mutation in a Malaysian patient of GBM. The findings of dual alterations could be of therapeutic benefit if
    these alterations were justified to be contributing to GBM growth and aggressiveness.
    Matched MeSH terms: Glioblastoma
  3. Silencing of ZFP36L2 increases sensitivity to temozolomide through G2/M cell cycle arrest and BAX mediated apoptosis in GBM cells
    Che Mat MF, Mohamad Hanif EA, Abdul Murad NA, Ibrahim K, Harun R, Jamal R
    Mol Biol Rep, 2021 Feb;48(2):1493-1503.
    PMID: 33590411 DOI: 10.1007/s11033-021-06144-z
    Despite the advancements in primary brain tumour diagnoses and treatments, the mortality rate remains high, particularly in glioblastoma (GBM). Chemoresistance, predominantly in recurrent cases, results in decreased mean survival of patients with GBM. We aimed to determine the chemosensitisation and oncogenic characteristics of zinc finger protein 36-like 2 (ZFP36L2) in LN18 GBM cells via RNA interference (RNAi) delivery. We conducted a meta-analysis of microarray datasets and RNAi screening using pooled small interference RNA (siRNA) to identify the druggable genes responsive to GBM chemosensitivity. Temozolomide-resistant LN18 cells were used to evaluate the effects of gene silencing on chemosensitisation to the sub-lethal dose (1/10 of the median inhibitory concentration [IC50]) of temozolomide. ZFP36L2 protein expression was detected by western blotting. Cell viability, proliferation, cell cycle and apoptosis assays were carried out using commercial kits. A human apoptosis array kit was used to determine the apoptosis pathway underlying chemosensitisation by siRNA against ZFP36L2 (siZFP36L2). Statistical analyses were performed using one-way analysis of variance; p > 0.05 was considered significant. The meta-analysis and RNAi screening identified ZFP36L2 as a potential marker of GBM. ZFP36L2 knockdown significantly induced apoptosis (p 
    Matched MeSH terms: Glioblastoma/drug therapy*; Glioblastoma/genetics; Glioblastoma/pathology
  4. Fulltext In silico homology modelling and identification of Tousled-Like Kinase 1 Inhibitors for Glioblastoma therapy via high throughput virtual screening proteinligand docking
    Kamariah Ibrahim, Abubakar Danjuma Abdullahi, Nor Azian Abdul Murad, Roslan Harun, Rahman Jamal
    Asia-Pacific Journal of Molecular Medicine, 2018;8(1):1-14.
    MyJurnal
    Glioblastoma multiforme (GBM) is a high-grade brain tumor of which the survival patients remain poor.
    Tousled-like kinase 1 (TLK1), a serine-threonine kinase, was identified to be overexpressed in cancers such
    as GBM. TLK1 plays an important role in controlling survival pathways. To date, there is no structure
    available for TLK1 as well as its inhibitors. We aimed to create a homology model of TLK1 and to identify
    suitable molecular inhibitors that are likely to bind and inhibit TLK1 activity via in silico high-throughput
    virtual screening (HTVS) protein-ligand docking. The 3D homology models of TLK1 were derived from
    various servers. All models were evaluated using Swiss Model QMEAN server. Validation was performed
    using multiple tools. Energy minimization was performed using YASARA. Subsequently, HTVS was
    performed using Molegro Virtual Docker 6.0 and ligands derived from ligand.info database. Drug-like
    molecules were filtered using ADME-Tox filtering program. Best homology model was obtained from the
    Aurora B kinase (PDB ID:4B8M) derived from Xenopus levias structure that share sequence similarity with
    human TLK1. Two compounds were identified from HTVS to be the potential inhibitors as it did not violate
    the Lipinski rule of five and the CNS-based filter as a potential drug-like molecule for GBM
    Matched MeSH terms: Glioblastoma
  5. Fulltext Stearoyl CoA Desaturase Is Essential for Regulation of Endoplasmic Reticulum Homeostasis and Tumor Growth in Glioblastoma Cancer Stem Cells
    Pinkham K, Park DJ, Hashemiaghdam A, Kirov AB, Adam I, Rosiak K, et al.
    Stem Cell Reports, 2019 04 09;12(4):712-727.
    PMID: 30930246 DOI: 10.1016/j.stemcr.2019.02.012
    Inherent plasticity and various survival cues allow glioblastoma stem-like cells (GSCs) to survive and proliferate under intrinsic and extrinsic stress conditions. Here, we report that GSCs depend on the adaptive activation of ER stress and subsequent activation of lipogenesis and particularly stearoyl CoA desaturase (SCD1), which promotes ER homeostasis, cytoprotection, and tumor initiation. Pharmacological targeting of SCD1 is particularly toxic due to the accumulation of saturated fatty acids, which exacerbates ER stress, triggers apoptosis, impairs RAD51-mediated DNA repair, and achieves a remarkable therapeutic outcome with 25%-100% cure rate in xenograft mouse models. Mechanistically, divergent cell fates under varying levels of ER stress are primarily controlled by the ER sensor IRE1, which either promotes SCD1 transcriptional activation or converts to apoptotic signaling when SCD1 activity is impaired. Taken together, the dependence of GSCs on fatty acid desaturation presents an exploitable vulnerability to target glioblastoma.
    Matched MeSH terms: Glioblastoma/etiology*; Glioblastoma/metabolism*; Glioblastoma/pathology
  6. Fulltext Overexpression of endothelin B receptor in glioblastoma: a prognostic marker and therapeutic target?
    Vasaikar S, Tsipras G, Landázuri N, Costa H, Wilhelmi V, Scicluna P, et al.
    BMC Cancer, 2018 02 06;18(1):154.
    PMID: 29409474 DOI: 10.1186/s12885-018-4012-7
    BACKGROUND: Glioblastoma (GBM) is the most common malignant brain tumor with median survival of 12-15 months. Owing to uncertainty in clinical outcome, additional prognostic marker(s) apart from existing markers are needed. Since overexpression of endothelin B receptor (ETBR) has been demonstrated in gliomas, we aimed to test whether ETBR is a useful prognostic marker in GBM and examine if the clinically available endothelin receptor antagonists (ERA) could be useful in the disease treatment.

    METHODS: Data from The Cancer Genome Atlas and the Gene Expression Omnibus database were analyzed to assess ETBR expression. For survival analysis, glioblastoma samples from 25 Swedish patients were immunostained for ETBR, and the findings were correlated with clinical history. The druggability of ETBR was assessed by protein-protein interaction network analysis. ERAs were analyzed for toxicity in in vitro assays with GBM and breast cancer cells.

    RESULTS: By bioinformatics analysis, ETBR was found to be upregulated in glioblastoma patients, and its expression levels were correlated with reduced survival. ETBR interacts with key proteins involved in cancer pathogenesis, suggesting it as a druggable target. In vitro viability assays showed that ERAs may hold promise to treat glioblastoma and breast cancer.

    CONCLUSIONS: ETBR is overexpressed in glioblastoma and other cancers and may be a prognostic marker in glioblastoma. ERAs may be useful for treating cancer patients.

    Matched MeSH terms: Glioblastoma/drug therapy; Glioblastoma/genetics*; Glioblastoma/metabolism
  7. Fulltext Anti-neoplastic Potential of Flavonoids and Polysaccharide Phytochemicals in Glioblastoma
    Atiq A, Parhar I
    Molecules, 2020 Oct 23;25(21).
    PMID: 33113890 DOI: 10.3390/molecules25214895
    Clinically, gliomas are classified into four grades, with grade IV glioblastoma multiforme being the most malignant and deadly, which accounts for 50% of all gliomas. Characteristically, glioblastoma involves the aggressive proliferation of cells and invasion of normal brain tissue, outcomes as poor patient prognosis. With the current standard therapy of glioblastoma; surgical resection and radiotherapy followed by adjuvant chemotherapy with temozolomide, it remains fatal, because of the development of drug resistance, tumor recurrence, and metastasis. Therefore, the need for the effective therapeutic option for glioblastoma remains elusive. Previous studies have demonstrated the chemopreventive role of naturally occurring pharmacological agents through preventing or reversing the initiation phase of carcinogenesis or arresting the cancer progression phase. In this review, we discuss the role of natural phytochemicals in the amelioration of glioblastoma, with the aim to improve therapeutic outcomes, and minimize the adverse side effects to improve patient's prognosis and enhancing their quality of life.
    Matched MeSH terms: Glioblastoma/drug therapy*
  8. Fulltext Anticancer Mechanism of Curcumin on Human Glioblastoma
    Wong SC, Kamarudin MNA, Naidu R
    Nutrients, 2021 Mar 16;13(3).
    PMID: 33809462 DOI: 10.3390/nu13030950
    Glioblastoma (GBM) is the most malignant brain tumor and accounts for most adult brain tumors. Current available treatment options for GBM are multimodal, which include surgical resection, radiation, and chemotherapy. Despite the significant advances in diagnostic and therapeutic approaches, GBM remains largely resistant to treatment, with a poor median survival rate between 12 and 18 months. With increasing drug resistance, the introduction of phytochemicals into current GBM treatment has become a potential strategy to combat GBM. Phytochemicals possess multifarious bioactivities with multitarget sites and comparatively marginal toxicity. Among them, curcumin is the most studied compound described as a potential anticancer agent due to its multi-targeted signaling/molecular pathways properties. Curcumin possesses the ability to modulate the core pathways involved in GBM cell proliferation, apoptosis, cell cycle arrest, autophagy, paraptosis, oxidative stress, and tumor cell motility. This review discusses curcumin's anticancer mechanism through modulation of Rb, p53, MAPK, P13K/Akt, JAK/STAT, Shh, and NF-κB pathways, which are commonly involved and dysregulated in preclinical and clinical GBM models. In addition, limitation issues such as bioavailability, pharmacokinetics perspectives strategies, and clinical trials were discussed.
    Matched MeSH terms: Glioblastoma/drug therapy*
  9. Fulltext The radiobiological effects of He, C and Ne ions as a function of LET on various glioblastoma cell lines
    Chew MT, Bradley DA, Suzuki M, Matsufuji N, Murakami T, Jones B, et al.
    J Radiat Res, 2019 Mar 01;60(2):178-188.
    PMID: 30624699 DOI: 10.1093/jrr/rry099
    The effects of the charged ion species 4He, 12C and 20Ne on glioblastoma multiforme (GBM) T98G, U87 and LN18 cell lines were compared with the effects of 200 kVp X-rays (1.7 keV/μm). These cell lines have different genetic profiles. Individual GBM relative biological effectiveness (RBE) was estimated in two ways: the RBE10 at 10% survival fraction and the RBE2Gy after 2 Gy doses. The linear quadratic model radiosensitivity parameters α and β and the α/β ratio of each ion type were determined as a function of LET. Mono-energetic 4He, 12C and 20Ne ions were generated by the Heavy Ion Medical Accelerator at the National Institute of Radiological Sciences in Chiba, Japan. Colony-formation assays were used to evaluate the survival fractions. The LET of the various ions used ranged from 2.3 to 100 keV/μm (covering the depth-dose plateau region to clinically relevant LET at the Bragg peak). For U87 and LN18, the RBE10 increased with LET and peaked at 85 keV/μm, whereas T98G peaked at 100 keV/μm. All three GBM α parameters peaked at 100 keV/μm. There is a statistically significant difference between the three GBM RBE10 values, except at 100 keV/μm (P < 0.01), and a statistically significant difference between the α values of the GBM cell lines, except at 85 and 100 keV/μm. The biological response varied depending on the GBM cell lines and on the ions used.
    Matched MeSH terms: Glioblastoma/radiotherapy*
  10. Fulltext Knockdown of Tousled‑like kinase 1 inhibits survival of glioblastoma multiforme cells
    Ibrahim K, Abdul Murad NA, Harun R, Jamal R
    Int J Mol Med, 2020 Aug;46(2):685-699.
    PMID: 32468002 DOI: 10.3892/ijmm.2020.4619
    Glioblastoma multiforme (GBM) is an aggressive type of brain tumour that commonly exhibits resistance to treatment. The tumour is highly heterogenous and complex kinomic alterations have been reported leading to dysregulation of signalling pathways. The present study aimed to investigate the novel kinome pathways and to identify potential therapeutic targets in GBM. Meta‑analysis using Oncomine identified 113 upregulated kinases in GBM. RNAi screening was performed on identified kinases using ON‑TARGETplus siRNA library on LN18 and U87MG. Tousled‑like kinase 1 (TLK1), which is a serine/threonine kinase was identified as a potential hit. In vitro functional validation was performed as the role of TLK1 in GBM is unknown. TLK1 knockdown in GBM cells significantly decreased cell viability, clonogenicity, proliferation and induced apoptosis. TLK1 knockdown also chemosensitised the GBM cells to the sublethal dose of temozolomide. The downstream pathways of TLK1 were examined using microarray analysis, which identified the involvement of DNA replication, cell cycle and focal adhesion signalling pathways. In vivo validation of the subcutaneous xenografts of stably transfected sh‑TLK1 U87MG cells demonstrated significantly decreased tumour growth in female BALB/c nude mice. Together, these results suggested that TLK1 may serve a role in GBM survival and may serve as a potential target for glioma.
    Matched MeSH terms: Glioblastoma/genetics; Glioblastoma/metabolism*
  11. Silencing of PROS1 induces apoptosis and inhibits migration and invasion of glioblastoma multiforme cells
    Che Mat MF, Abdul Murad NA, Ibrahim K, Mohd Mokhtar N, Wan Ngah WZ, Harun R, et al.
    Int J Oncol, 2016 Dec;49(6):2359-2366.
    PMID: 27840905 DOI: 10.3892/ijo.2016.3755
    Glioblastoma multiforme (GBM) is an aggressive brain tumor and most patients have poor prognosis. Despite many advances in research, there has been no significant improvement in the patient survival rate. New molecular therapies are being studied and RNA interference (RNAi) therapy is one of the promising approaches to improve prognosis and increase survival in patients with GBM. We performed a meta‑analysis of five different microarray datasets and identified 460 significantly upregulated genes in GBM. Loss‑of‑function screening of these upregulated genes using LN18 cells was performed to identify the significant target genes for glioma. Further investigations were performed using siRNA in LN18 cells and various functional assays were carried out on the selected candidate gene to understand further its role in GBM. We identified PROS1 as a candidate gene for GBM from the meta‑analysis and RNAi screening. Knockdown of PROS1 in LN18 cells significantly induced apoptosis compared to siPROS1‑untreated cells (p<0.05). Migration in cells treated with siPROS1 was reduced significantly (p<0.05) and this was confirmed with wound-healing assay. PROS1 knockdown showed substantial reduction in cell invasion up to 82% (p<0.01). In addition, inhibition of PROS1 leads to decrease in cellular proliferation by 18%. Knockdown of PROS1 in LN18 cells caused activation of both of the extrinsic and intrinsic apoptotic pathways. It caused major upregulation of FasL which is important for death receptor signaling activation and also downregulation of GAS6 and other members of TAM family of receptors. PROS1 may play an important role in the development of GBM through cellular proliferation, migration and invasion as well as apoptosis. Targeting PROS1 in GBM could be a novel therapeutic strategy in GBM treatment.
    Matched MeSH terms: Glioblastoma/genetics*; Glioblastoma/pathology
  12. Association of p53 tumor suppressor gene with paraclinical and clinical modalities of gliomas patients in Malaysia
    Yusoff AA, Abdullah J, Abdullah MR, Mohd Ariff AR, Isa MN
    Acta Neurochir (Wien), 2004 Jun;146(6):595-601.
    PMID: 15168228
    Alteration of the tumor suppressor gene p53 is considered to be a critical step in the development of human cancer. Changes in this gene have been detected in a wide range of human tumours, including gliomas. In glioma, the presence of p53 gene alterations has been associated with worse prognosis.
    Matched MeSH terms: Glioblastoma/diagnosis; Glioblastoma/genetics*; Glioblastoma/surgery
  13. Fulltext Gliosarcoma of a brain: a challenging diagnosis
    Nornazirah Azizan, Nor Haizura Ab Rani, Ahmad Toha Samsudin, Fadhli Mustaffa, Firdaus Hayati
    Borneo Journal of Medical Sciences, 2020;14(3):39-44.
    MyJurnal
    Gliosarcoma is a rare primary malignant tumour of the central nervous system. A 28-year-old radiographer without a history of neurological disorder, malignancy or trauma presented with unprovoked seizures. He was symptom-free for 3 years but developed relapsed. Computed tomography of the brain was consistent with anaplastic convexity meningioma which was identical via intraoperative findings. However, the final histology revealed gliosarcoma of the brain. He recovered well postoperatively without any neurological deficit and had completed adjuvant chemo-radiotherapy. He was asymptomatic during follow up with no tumour recurrence. Gliosarcoma with predominant sarcomatous component mimicking a meningioma has prolonged survival as compared to a case with predominant glioblastoma component. Hence, the discordance between clinical, radiological, intraoperative and histopathological findings is a challenge in establishing a diagnosis of gliosarcoma.
    Matched MeSH terms: Glioblastoma
  14. Fulltext o-Vanillin Derived Schiff Bases and Their Organotin(IV) Compounds: Synthesis, Structural Characterisation, In-Silico Studies and Cytotoxicity
    Yusof ENM, Latif MAM, Tahir MIM, Sakoff JA, Simone MI, Page AJ, et al.
    Int J Mol Sci, 2019 Feb 15;20(4).
    PMID: 30781445 DOI: 10.3390/ijms20040854
    Six new organotin(IV) compounds of Schiff bases derived from S-R-dithiocarbazate [R = benzyl (B), 2- or 4-methylbenzyl (2M and 4M, respectively)] condensed with 2-hydroxy-3-methoxybenzaldehyde (oVa) were synthesised and characterised by elemental analysis, various spectroscopic techniques including infrared, UV-vis, multinuclear (¹H, 13C, 119Sn) NMR and mass spectrometry, and single crystal X-ray diffraction. The organotin(IV) compounds were synthesised from the reaction of Ph₂SnCl₂ or Me₂SnCl₂ with the Schiff bases (S2MoVaH/S4MoVaH/SBoVaH) to form a total of six new organotin(IV) compounds that had a general formula of [R₂Sn(L)] (where L = Schiff base; R = Ph or Me). The molecular geometries of Me₂Sn(S2MoVa), Me₂Sn(S4MoVa) and Me₂Sn(SBoVa) were established by X-ray crystallography and verified using density functional theory calculations. Interestingly, each experimental structure contained two independent but chemically similar molecules in the crystallographic asymmetric unit. The coordination geometry for each molecule was defined by thiolate-sulphur, phenoxide-oxygen and imine-nitrogen atoms derived from a dinegative, tridentate dithiocarbazate ligand with the remaining positions occupied by the methyl-carbon atoms of the organo groups. In each case, the resulting five-coordinate C₂NOS geometry was almost exactly intermediate between ideal trigonal-bipyramidal and square-pyramidal geometries. The cytotoxic activities of the Schiff bases and organotin(IV) compounds were investigated against EJ-28 and RT-112 (bladder), HT29 (colon), U87 and SJ-G2 (glioblastoma), MCF-7 (breast) A2780 (ovarian), H460 (lung), A431 (skin), DU145 (prostate), BE2-C (neuroblastoma) and MIA (pancreatic) cancer cell lines and one normal breast cell line (MCF-10A). Diphenyltin(IV) compounds exhibited greater potency than either the Schiff bases or the respective dimethyltin(IV) compounds. Mechanistic studies on the action of these compounds against bladder cancer cells revealed that they induced the production of reactive oxygen species (ROS). The bladder cancer cells were apoptotic after 24 h post-treatment with the diphenyltin(IV) compounds. The interactions of the organotin(IV) compounds with calf thymus DNA (CT-DNA) were experimentally explored using UV-vis absorption spectroscopy. This study revealed that the organotin(IV) compounds have strong DNA binding affinity, verified via molecular docking simulations, which suggests that these organotin(IV) compounds interact with DNA via groove-binding interactions.
    Matched MeSH terms: Glioblastoma
  15. Fulltext Synthesis and Characterization of Diosgenin Encapsulated Poly-ε-Caprolactone-Pluronic Nanoparticles and Its Effect on Brain Cancer Cells
    Rabha B, Bharadwaj KK, Baishya D, Sarkar T, Edinur HA, Pati S
    Polymers (Basel), 2021 Apr 18;13(8).
    PMID: 33919483 DOI: 10.3390/polym13081322
    Diosgenin encapsulated PCL-Pluronic nanoparticles (PCL-F68-D-NPs) were developed using the nanoprecipitation method to improve performance in brain cancer (glioblastoma) therapy. The nanoparticles were characterized by dynamic light scattering (DLS)/Zeta potential, Fourier-transform infrared (FTIR) spectra, X-ray diffraction (XRD), Field Emission Scanning Electron Microscopy (FESEM), and Transmission electron microscopy (TEM). The encapsulation efficiency, loading efficiency, and yield were calculated. The in vitro release rate was determined, and the kinetic model of diosgenin release was plotted and ascertained. The cytotoxicity was checked by MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide)assay against U87-MG cells (glioblastoma cell lines). The obtained nanoparticles demonstrated good size distribution, stability, morphology, chemical, and mechanical properties. The nanoparticles also possessed high encapsulation efficiency, loading efficiency, and yield. The release rate of Diosgenin was shown in a sustained manner. The in vitro cytotoxicity of PCL-F68-D-NPs showed higher toxicity against U87-MG cells than free Diosgenin.
    Matched MeSH terms: Glioblastoma
  16. Fulltext Reflux of Endoplasmic Reticulum proteins to the cytosol inactivates tumor suppressors
    Sicari D, Centonze FG, Pineau R, Le Reste PJ, Negroni L, Chat S, et al.
    EMBO Rep, 2021 May 05;22(5):e51412.
    PMID: 33710763 DOI: 10.15252/embr.202051412
    In the past decades, many studies reported the presence of endoplasmic reticulum (ER)-resident proteins in the cytosol. However, the mechanisms by which these proteins relocate and whether they exert cytosolic functions remain unknown. We find that a subset of ER luminal proteins accumulates in the cytosol of glioblastoma cells isolated from mouse and human tumors. In cultured cells, ER protein reflux to the cytosol occurs upon ER proteostasis perturbation. Using the ER luminal protein anterior gradient 2 (AGR2) as a proof of concept, we tested whether the refluxed proteins gain new functions in the cytosol. We find that refluxed, cytosolic AGR2 binds and inhibits the tumor suppressor p53. These data suggest that ER reflux constitutes an ER surveillance mechanism to relieve the ER from its contents upon stress, providing a selective advantage to tumor cells through gain-of-cytosolic functions-a phenomenon we name ER to Cytosol Signaling (ERCYS).
    Matched MeSH terms: Glioblastoma
  17. Fulltext Zika Virus as Oncolytic Therapy for Brain Cancer: Myth or Reality?
    Su KY, Balasubramaniam VRMT
    Front Microbiol, 2019;10:2715.
    PMID: 31824472 DOI: 10.3389/fmicb.2019.02715
    The ability of self-replicating oncolytic viruses (OVs) to preferentially infect and lyse cancer cells while stimulating anti-tumor immunity of the host strongly indicates its value as a new field of cancer therapeutics to be further explored. The emergence of Zika virus (ZIKV) as a global health threat due to its recent outbreak in Brazil has caught the attention of the scientific community and led to the discovery of its oncolytic potential for the treatment of glioblastoma multiforme (GBM), the most common and fatal brain tumor with poor prognosis. Herein, we evaluate the neurotropism of ZIKV relative to the receptor tyrosine kinase AXL and its ligand Gas6 in viral entry and the RNA-binding protein Musashi-1 (MSI1) in replication which are also overexpressed in GBM, suggesting its potential for specific targeting of the tumor. Additionally, this review discusses genetic modifications performed to enhance safety and efficacy of ZIKV as well as speculates future directions for the OV therapy.
    Matched MeSH terms: Glioblastoma
  18. Fulltext Distribution pattern of brain tumour in a tertiary hospital in East Coast, Malaysia
    Nurul Balqis Md Dzali, Mohd Nizam Zahary, Nor Hidayah Abu Bakar, Hasnan Jaafar, Wan Rohani Wan Taib
    Malaysian Journal of Public Health Medicine, 2017;17 Special(2):41-48.
    Brain tumour occurrence in Malaysia demonstrates an increasing trend from year to year among adults and the second most common cancer among children. Thus, the expansion of numerous research for novel therapy and treatment are necessary. The distribution of brain tumour in a specific population is important to provide substantial information about the current trends for developing new diagnostic technique and research. Consequently, this study is opted to provide descriptive data of brain tumour in Hospital Universiti Sains Malaysia (USM). 217 brain tumour cases were collected from the hospital record between 2011 and 2014. The brain tumour cases were confirmed by pathologists according to WHO classification and grading. Descriptive analysis was evaluated by using Microsoft Excel and IBM SPSS version 22. Gender preponderance in this study shows very little difference. The most common adult primary brain tumour in this study was meningioma (32.7%) followed by glioblastoma (7.8%), a type of diffuse astrocytic tumour. According to age factor, brain tumour distribution pattern shows an increasing trend as the age increases and meningioma is the most common among the elder patients. Secondary tumour takes more than 10% from overall percentage of brain tumour cases. In conclusion, the descriptive data presentation in this study is very helpful to provide baseline information on the current brain tumour occurrence in this region.
    Matched MeSH terms: Glioblastoma
  19. Fulltext A rare case of paediatric pontine glioblastoma presenting as a cerebellopontine angle otogenic abscess
    Rasalingam K, Abdullah JM, Idris Z, Pal HK, Wahab N, Omar E, et al.
    Malays J Med Sci, 2008 Jan;15(1):44-8.
    PMID: 22589615
    We describe rare case of a 9-year old boy who presented with a two-week history of right ear discharge and mild fever. Contrast enhanced CT scan of the brain showed a lesion in the right cerebellopontine angle with mild enhancement mimicking early abscess formation. Involvement of the mastoid air cells pointing towards a radiological diagnosis of mastoiditis reinforced the diagnosis of an abscess. A magnetic resonance imaging (MRI) was planned for the patient but his conscious level deteriorated and patient slipped into coma warranting immediate surgical intervention. Intraoperatively, about 90% of the tumour was removed and the appearance of the tumour resembled that of an acoustic schwannoma but histopathology confirmed the diagnosis of a glioblastoma multiforme (GBM). MRI done post operatively showed lesion in the pons confirming the diagnosis of an exophytic pontine glioblastoma multiforme.
    Matched MeSH terms: Glioblastoma
  20. Fulltext Advancing towards Effective Glioma Therapy: MicroRNA Derived from Umbilical Cord Mesenchymal Stem Cells' Extracellular Vesicles
    Ngadiono E, Hardiany NS
    Malays J Med Sci, 2019 Jul;26(4):5-16.
    PMID: 31496889 DOI: 10.21315/mjms2019.26.4.2
    A glioma, especially a grade IV glioblastoma, is a malignant tumour with a poor prognosis despite growing medical advancements. Researchers have been looking for better and more effective treatments targeting the molecular pathways of gliomas due to glioblastomas' ability to develop resistance to chemotherapies. Moreover, glioma stem cells (GSC) contribute to maintaining the glioma population, which benefits from its ability to self-renew and differentiate. Recent research has reported that through the introduction of umbilical cord mesenchymal stem cells (UCMSC) into glioma cells, the growth and development of the glioma cells can be downregulated. It has more currently been found out that UCMSC release extracellular vesicles (EVs) containing miRNA that are responsible for this phenomenon. Therefore, this review analyses literature to discuss all possible miRNAs contained within the UCMSC's EVs and to elaborate on their molecular mechanisms in halting gliomas and GSC growth. This review will also include the challenges and limitations, to account for which more in vivo research is suggested. In conclusion, this review highlights how miRNAs contained within UCMSC's EVs are able to downregulate multiple prominent pathways in the survival of gliomas.
    Matched MeSH terms: Glioblastoma
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