Displaying publications 81 - 100 of 149 in total

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  1. Seow P, Narayanan V, Hernowo AT, Wong JHD, Ramli N
    Neuroimage Clin, 2018;20:531-536.
    PMID: 30167373 DOI: 10.1016/j.nicl.2018.08.003
    Objectives: This study maps the lipid distributions based on magnetic resonance imaging (MRI) in-and opposed-phase (IOP) sequence and correlates the findings generated from lipid map to histological grading of glioma.

    Methods: Forty histologically proven glioma patients underwent a standard MRI tumour protocol with the addition of IOP sequence. The regions of tumour (solid enhancing, solid non-enhancing, and cystic regions) were delineated using snake model (ITK-SNAP) with reference to structural and diffusion MRI images. The lipid distribution map was constructed based on signal loss ratio (SLR) obtained from the IOP imaging. The mean SLR values of the regions were computed and compared across the different glioma grades.

    Results: The solid enhancing region of glioma had the highest SLR for both Grade II and III. The mean SLR of solid non-enhancing region of tumour demonstrated statistically significant difference between the WHO grades (grades II, III & IV) (mean SLRII = 0.04, mean SLRIII = 0.06, mean SLRIV = 0.08, & p 

    Matched MeSH terms: Brain Neoplasms/metabolism
  2. 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: Brain Neoplasms/drug therapy*
  3. Foo LS, Yap WS, Hum YC, Manan HA, Tee YK
    J Magn Reson, 2020 01;310:106648.
    PMID: 31760147 DOI: 10.1016/j.jmr.2019.106648
    Chemical exchange saturation transfer (CEST) magnetic resonance imaging (MRI) holds great potential to provide new metabolic information for clinical applications such as tumor, stroke and Parkinson's Disease diagnosis. Many active research and developments have been conducted to translate this emerging MRI technique for routine clinical applications. In general, there are two CEST quantification techniques: (i) model-free and (ii) model-based techniques. The reliability of these quantification techniques depends heavily on the experimental conditions and quality of the collected data. Errors such as noise may lead to misleading quantification results and thus inaccurate diagnosis when CEST imaging becomes a standard or routine imaging scan in the future. This paper investigates the accuracy and robustness of these quantification techniques under different signal-to-noise (SNR) levels and magnetic field strengths. The quantified CEST effect before and after adding random Gaussian White Noise using model-free and model-based quantification techniques were compared. It was found that the model-free technique consistently yielded larger average percentage error across all tested parameters compared to its model-based counterpart, and that the model-based technique could withstand SNR of about 3 times lower than the model-free technique. When applied on noisy brain tumor, ischemic stroke, and Parkinson's Disease clinical data, the model-free technique failed to produce significant differences between normal and abnormal tissue whereas the model-based technique consistently generated significant differences. Although the model-free technique was less accurate and robust, its simplicity and thus speed would still make it a good approximate when the SNR was high (>50) or when the CEST effect was large and well-defined. For more accurate CEST quantification, model-based techniques should be considered. When SNR was low (<50) and the CEST effect was small such as those acquired from clinical field strength scanners, which are generally 3T and below, model-based techniques should be considered over model-free counterpart to maintain an average percentage error of less than 44% even under very noisy condition as tested in this work.
    Matched MeSH terms: Brain Neoplasms/diagnosis
  4. Kong PL, Cheah PL, Mun KS, Chiew SF, Lau TP, Koh CC, et al.
    Malays J Pathol, 2020 Dec;42(3):369-376.
    PMID: 33361717
    Together with isocitrate dehydrogenase (IDH) mutation, co-deletion of 1p19q (1p19q codel) is a prerequisite for diagnosis of oligodendroglioma, making it imperative that histopathology laboratories introduce testing for 1p19q codel. To date there is still no consensus reference range and cut-offs that confirm deletion of 1p or 19q. We embarked on determining our reference range in 11 formalinfixed, paraffin-embedded non-neoplastic brain tissue using fluorescence in situ hybridisation (FISH) with the Vysis 1p36/1q25 and 19q13/19p13 FISH Probe Kit (Abbott Molecular Inc., USA). At same time we attempted to validate our methodology in 13 histologically-confirmed IDH-mutant oligodendrogliomas. For 1p, percentage cells with deletion (range=8-23%; mean±SD = 15.73±5.50%) and target: control (1p36:1q25) ratio (range = 0.89-0.96; mean±SD = 0.92±0.03) in non-neoplastic brain, differed significantly (p<0.000) from oligodendroglioma (percentage cells with deletion: range = 49-100%; mean±SD = 82.46±15.21%; target:control ratio range:0.50-0.76; mean±SD = 0.59±0.08). For 19q, percentage cells with deletion (range = 7-20%; mean±SD = 12.00±3.49%) and target:control (19q13/19p13) ratio (range:0.90-0.97; mean±SD = 0.94±0.02) in non-neoplastic brain also differed significantly from oligodendroglioma (percentage cells with deletion: range = 45-100%; mean±SD = 82.62±18.13%; target:control ratio range:0.50-0.78; mean±SD = 0.59±0.09). Using recommended calculation method, for diagnosis of 1p deletion, percentage of cells showing deletion should be >32-33% and/or target:control ratio <0.83. For 19q, percentage of cells showing deletion should be >22% and target:control ratio <0.88. Using these cut-offs all 13 oligodendroglioma demonstrated 1p19q codel.
    Matched MeSH terms: Brain Neoplasms/genetics*
  5. Sheikh Abdullah SN, Bohani FA, Nayef BH, Sahran S, Al Akash O, Iqbal Hussain R, et al.
    Comput Math Methods Med, 2016;2016:8603609.
    PMID: 27516807 DOI: 10.1155/2016/8603609
    Brain magnetic resonance imaging (MRI) classification into normal and abnormal is a critical and challenging task. Owing to that, several medical imaging classification techniques have been devised in which Learning Vector Quantization (LVQ) is amongst the potential. The main goal of this paper is to enhance the performance of LVQ technique in order to gain higher accuracy detection for brain tumor in MRIs. The classical way of selecting the winner code vector in LVQ is to measure the distance between the input vector and the codebook vectors using Euclidean distance function. In order to improve the winner selection technique, round off function is employed along with the Euclidean distance function. Moreover, in competitive learning classifiers, the fitting model is highly dependent on the class distribution. Therefore this paper proposed a multiresampling technique for which better class distribution can be achieved. This multiresampling is executed by using random selection via preclassification. The test data sample used are the brain tumor magnetic resonance images collected from Universiti Kebangsaan Malaysia Medical Center and UCI benchmark data sets. Comparative studies showed that the proposed methods with promising results are LVQ1, Multipass LVQ, Hierarchical LVQ, Multilayer Perceptron, and Radial Basis Function.
    Matched MeSH terms: Brain Neoplasms/physiopathology
  6. Wastie NL, Chawla JC
    Med J Malaysia, 1973 Jun;27(4):271-4.
    PMID: 4270784
    Matched MeSH terms: Brain Neoplasms/radiography*
  7. Soo YS, Ang AH
    Med J Malaya, 1971 Mar;25(3):168-74.
    PMID: 4253242
    Matched MeSH terms: Brain Neoplasms/radiography
  8. Mishra A, Mishra PS, Bandopadhyay R, Khurana N, Angelopoulou E, Paudel YN, et al.
    Molecules, 2021 Oct 26;26(21).
    PMID: 34770864 DOI: 10.3390/molecules26216456
    Chrysin, a herbal bioactive molecule, exerts a plethora of pharmacological effects, including anti-oxidant, anti-inflammatory, neuroprotective, and anti-cancer. A growing body of evidence has highlighted the emerging role of chrysin in a variety of neurological disorders, including Alzheimer's and Parkinson's disease, epilepsy, multiple sclerosis, ischemic stroke, traumatic brain injury, and brain tumors. Based on the results of recent pre-clinical studies and evidence from studies in humans, this review is focused on the molecular mechanisms underlying the neuroprotective effects of chrysin in different neurological diseases. In addition, the potential challenges, and opportunities of chrysin's inclusion in the neurotherapeutics repertoire are critically discussed.
    Matched MeSH terms: Brain Neoplasms/drug therapy*
  9. Seow P, Wong JHD, Ahmad-Annuar A, Mahajan A, Abdullah NA, Ramli N
    Br J Radiol, 2018 Dec;91(1092):20170930.
    PMID: 29902076 DOI: 10.1259/bjr.20170930
    OBJECTIVE:: The diversity of tumour characteristics among glioma patients, even within same tumour grade, is a big challenge for disease outcome prediction. A possible approach for improved radiological imaging could come from combining information obtained at the molecular level. This review assembles recent evidence highlighting the value of using radiogenomic biomarkers to infer the underlying biology of gliomas and its correlation with imaging features.

    METHODS:: A literature search was done for articles published between 2002 and 2017 on Medline electronic databases. Of 249 titles identified, 38 fulfilled the inclusion criteria, with 14 articles related to quantifiable imaging parameters (heterogeneity, vascularity, diffusion, cell density, infiltrations, perfusion, and metabolite changes) and 24 articles relevant to molecular biomarkers linked to imaging.

    RESULTS:: Genes found to correlate with various imaging phenotypes were EGFR, MGMT, IDH1, VEGF, PDGF, TP53, and Ki-67. EGFR is the most studied gene related to imaging characteristics in the studies reviewed (41.7%), followed by MGMT (20.8%) and IDH1 (16.7%). A summary of the relationship amongst glioma morphology, gene expressions, imaging characteristics, prognosis and therapeutic response are presented.

    CONCLUSION:: The use of radiogenomics can provide insights to understanding tumour biology and the underlying molecular pathways. Certain MRI characteristics that show strong correlations with EGFR, MGMT and IDH1 could be used as imaging biomarkers. Knowing the pathways involved in tumour progression and their associated imaging patterns may assist in diagnosis, prognosis and treatment management, while facilitating personalised medicine.

    ADVANCES IN KNOWLEDGE:: Radiogenomics can offer clinicians better insight into diagnosis, prognosis, and prediction of therapeutic responses of glioma.

    Matched MeSH terms: Brain Neoplasms/genetics
  10. Saunus JM, Quinn MC, Patch AM, Pearson JV, Bailey PJ, Nones K, et al.
    J Pathol, 2015 Nov;237(3):363-78.
    PMID: 26172396 DOI: 10.1002/path.4583
    Treatment options for patients with brain metastases (BMs) have limited efficacy and the mortality rate is virtually 100%. Targeted therapy is critically under-utilized, and our understanding of mechanisms underpinning metastatic outgrowth in the brain is limited. To address these deficiencies, we investigated the genomic and transcriptomic landscapes of 36 BMs from breast, lung, melanoma and oesophageal cancers, using DNA copy-number analysis and exome- and RNA-sequencing. The key findings were as follows. (a) Identification of novel candidates with possible roles in BM development, including the significantly mutated genes DSC2, ST7, PIK3R1 and SMC5, and the DNA repair, ERBB-HER signalling, axon guidance and protein kinase-A signalling pathways. (b) Mutational signature analysis was applied to successfully identify the primary cancer type for two BMs with unknown origins. (c) Actionable genomic alterations were identified in 31/36 BMs (86%); in one case we retrospectively identified ERBB2 amplification representing apparent HER2 status conversion, then confirmed progressive enrichment for HER2-positivity across four consecutive metastatic deposits by IHC and SISH, resulting in the deployment of HER2-targeted therapy for the patient. (d) In the ERBB/HER pathway, ERBB2 expression correlated with ERBB3 (r(2)  = 0.496; p < 0.0001) and HER3 and HER4 were frequently activated in an independent cohort of 167 archival BM from seven primary cancer types: 57.6% and 52.6% of cases were phospho-HER3(Y1222) or phospho-HER4(Y1162) membrane-positive, respectively. The HER3 ligands NRG1/2 were barely detectable by RNAseq, with NRG1 (8p12) genomic loss in 63.6% breast cancer-BMs, suggesting a microenvironmental source of ligand. In summary, this is the first study to characterize the genomic landscapes of BM. The data revealed novel candidates, potential clinical applications for genomic profiling of resectable BMs, and highlighted the possibility of therapeutically targeting HER3, which is broadly over-expressed and activated in BMs, independent of primary site and systemic therapy.
    Matched MeSH terms: Brain Neoplasms/drug therapy; Brain Neoplasms/enzymology; Brain Neoplasms/genetics*; Brain Neoplasms/secondary*
  11. Lim SW, Loh HS, Ting KN, Bradshaw TD, Zeenathul NA
    Biomed Pharmacother, 2014 Oct;68(8):1105-15.
    PMID: 25456851 DOI: 10.1016/j.biopha.2014.10.006
    The pure vitamin isomer, β-tocotrienol has the least abundance among the other vitamin E isomers that are present in numerous plants. Hence, it is very scarcely studied for its bioactivity. In this study, the antiproliferative effects and primary apoptotic mechanisms of β-tocotrienol on human lung adenocarcinoma A549 and glioblastoma U87MG cells were investigated. It was evidenced that β-tocotrienol had inhibited the growth of both A549 (GI50=1.38±0.334μM) and U87MG (GI50=2.53±0.604μM) cells at rather low concentrations. Cancer cells incubated with β-tocotrienol were also found to exhibit hallmarks of apoptotic morphologies including membrane blebbing, chromatin condensation and formation of apoptotic bodies. The apoptotic properties of β-tocotrienol in both A549 and U87MG cells were the results of its capability to induce significant (P<0.05) double-strand DNA breaks (DSBs) without involving single-strand DNA breaks (SSBs). β-Tocotrienol is said to induce activation of caspase-8 in both A549 and U87MG cells guided by no activation when caspase-8 inhibitor, z-IETD-fmk was added. Besides, disruption on the mitochondrial membrane permeability of the cells in a concentration- and time-dependent manner had occurred. The induction of apoptosis by β-tocotrienol in A549 and U87MG cells was confirmed to involve both the death-receptor mediated and mitochondria-dependent apoptotic pathways. These findings could potentiate the palm oil derived β-tocotrienol to serve as a new anticancer agent for treating human lung and brain cancers.
    Matched MeSH terms: Brain Neoplasms/drug therapy; Brain Neoplasms/enzymology*
  12. Abdul Rahman A, Jamal AR, Harun R, Mohd Mokhtar N, Wan Ngah WZ
    PMID: 24980711 DOI: 10.1186/1472-6882-14-213
    Gamma-tocotrienol (GTT), an isomer of vitamin E and hydroxy-chavicol (HC), a major bioactive compound in Piper betle, has been reported to possess anti-carcinogenic properties by modulating different cellular signaling events. One possible strategy to overcome multi-drug resistance and high toxic doses of treatment is by applying combinational therapy especially using natural bioactives in cancer treatment.
    Matched MeSH terms: Brain Neoplasms/drug therapy; Brain Neoplasms/pathology
  13. Sabir BI, Rahmat K, Bux SI, Rajagopal NS, Looi LM, Sia SF
    Clin Neurol Neurosurg, 2013 Oct;115(10):2192-6.
    PMID: 23791432 DOI: 10.1016/j.clineuro.2013.05.023
    Matched MeSH terms: Brain Neoplasms/pathology; Brain Neoplasms/secondary
  14. Muthusamy KA, Lian LH, Vairavan N, Chua KH, Waran V
    Genet. Mol. Res., 2012;11(3):2939-45.
    PMID: 22782629
    Studies of genetic mutations that have been used in predicting glioma prognosis have revealed a complex relationship between clinical and genetic factors. Epidermal growth factor (EGF) and the NAT2 gene play a central role in carcinogenesis. An adenine (A) to guanine (G) single nucleotide polymorphism at position 61 in the 5'-untranslated region (5'-UTR) of the EGF gene has been found to be associated with levels of EGF production, and the mutations in the NAT2 gene have been postulated as a risk factor for cancer. We investigated EGF and the NAT2 gene in 13 glioma tissue samples and 12 normal controls. In the EGF 5'-UTR 61G polymorphism, the heterozygote GA was the most common genotype in the glioma patients. In the NAT2 polymorphism at nucleotide position 857G/A, the G allele and the GG genotype were the most prevalent forms in both the glioma and normal samples. We did not find any homozygous AA genotypes in the glioma patients. Based on this preliminary evidence, the EGF 5'-UTR at position 61 and the NAT2 SNP at position 857 polymorphisms are associated with increased risk for glioma.
    Matched MeSH terms: Brain Neoplasms/enzymology; Brain Neoplasms/genetics*
  15. Rahman WF, Rahman KS, Nafi SN, Fauzi MH, Jaafar H
    Int J Clin Exp Pathol, 2015;8(6):6095-106.
    PMID: 26261487
    The relationship between DNA methyltransferase (DNMT) and O6-methylguanine-DNA methyltransferase (MGMT) in mediating tumorigenesis is still poorly understood. This study was carried out to investigate a correlation between DNMT1 and MGMT immunoexpression in astrocytic tumour samples.
    Matched MeSH terms: Brain Neoplasms/enzymology*; Brain Neoplasms/pathology
  16. Sivanesaratnam V, Sen DK
    J Reprod Med, 1988 Apr;33(4):402-3.
    PMID: 2452881
    Pregnancy after treatment of choriocarcinoma with cerebral metastases is uncommon. We treated a patient successfully with less-toxic chemotherapeutic agents than those advocated by others together with whole brain irradiation. She subsequently had two uneventful pregnancies.
    Matched MeSH terms: Brain Neoplasms/secondary*; Brain Neoplasms/therapy
  17. Ponnampalam SN, Kamaluddin NR, Zakaria Z, Matheneswaran V, Ganesan D, Haspani MS, et al.
    Oncol Rep, 2017 Jan;37(1):10-22.
    PMID: 28004117 DOI: 10.3892/or.2016.5285
    The aims of the present study were to undertake gene expression profiling of the blood of glioma patients to determine key genetic components of signaling pathways and to develop a panel of genes that could be used as a potential blood-based biomarker to differentiate between high and low grade gliomas, non-gliomas and control samples. In this study, blood samples were obtained from glioma patients, non-glioma and control subjects. Ten samples each were obtained from patients with high and low grade tumours, respectively, ten samples from non-glioma patients and twenty samples from control subjects. Total RNA was isolated from each sample after which first and second strand synthesis was performed. The resulting cRNA was then hybridized with the Agilent Whole Human Genome (4x44K) microarray chip according to the manufacturer's instructions. Universal Human Reference RNA and samples were labeled with Cy3 CTP and Cy5 CTP, respectively. Microarray data were analyzed by the Agilent Gene Spring 12.1V software using stringent criteria which included at least a 2-fold difference in gene expression between samples. Statistical analysis was performed using the unpaired Student's t-test with a p<0.01. Pathway enrichment was also performed, with key genes selected for validation using droplet digital polymerase chain reaction (ddPCR). The gene expression profiling indicated that were a substantial number of genes that were differentially expressed with more than a 2-fold change (p<0.01) between each of the four different conditions. We selected key genes within significant pathways that were analyzed through pathway enrichment. These key genes included regulators of cell proliferation, transcription factors, cytokines and tumour suppressor genes. In the present study, we showed that key genes involved in significant and well established pathways, could possibly be used as a potential blood-based biomarker to differentiate between high and low grade gliomas, non-gliomas and control samples.
    Matched MeSH terms: Brain Neoplasms/genetics*; Brain Neoplasms/pathology*
  18. 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: Brain Neoplasms/genetics*; Brain Neoplasms/pathology
  19. Megat Shiraz MA, Jong YH, Primuharsa Putra SH
    Singapore Med J, 2008 Nov;49(11):e310-1.
    PMID: 19037537
    Extramedullary plasmacytoma is a rare malignant plasma cell tumour. We report an extremely aggressive case of extramedullary plasmacytoma of the right maxillary sinus, which had metastasised to the brain and rib. A 56-year-old man presented with recurrent epistaxis and acute anaemia. Nasendoscopy revealed a medialised medial wall of the right maxilla and a mass occupying the whole nasopharynx. Magnetic resonance imaging revealed a right maxillary tumour with extension to the ipsilateral nasal cavity, nasopharynx, right sphenoid and ethmoidal sinuses. There was an extra-axial brain metastasis. There were metastases to the right parietal region and left eighth rib. Histopathology examination of the maxillary mass revealed abundant plasma cells with kappa-chain restriction. He was planned for four cycles of chemotherapy. Unfortunately, in view of the advanced stage of disease, he succumbed to his disease during the first cycle of chemotherapy.
    Matched MeSH terms: Brain Neoplasms/diagnosis*; Brain Neoplasms/pathology*
  20. Lim SY, Mason WP, Young NP, Chen R, Bower JH, McKeon A, et al.
    Arch. Neurol., 2009 Oct;66(10):1285-7.
    PMID: 19822786 DOI: 10.1001/archneurol.2009.203
    OBJECTIVE:
    To describe and provide audiovisual documentation of a syndrome of polymyoclonus, laryngospasm, and cerebellar ataxia associated with adenocarcinoma and multiple neural cation channel autoantibodies.

    DESIGN:
    Case report with video.

    SETTING:
    University hospitals. Patient A 69-year-old woman presented with subacute onset of whole-body tremulousness and laryngospasm attributed to gastroesophageal reflux.

    RESULTS:
    Further evaluation revealed polymyoclonus, cerebellar ataxia, and laryngospasm suspicious of an underlying malignant neoplasm. Surface electromyography of multiple limb muscles confirmed the presence of polymyoclonus. The patient was seropositive for P/Q-type voltage-gated calcium channel antibody; subsequently, whole-body fluorine 18 fluorodeoxyglucose positron emission tomography and cervical lymph node biopsy revealed widespread metastatic adenocarcinoma. Follow-up serologic evaluation revealed calcium channel antibodies (P/Q type and N type) and potassium channel antibody.

    CONCLUSIONS:
    We highlight the importance of recognizing polymyoclonus. To our knowledge, this is also the first description of a syndrome of polymyoclonus, laryngospasm, and ataxia associated with adenocarcinoma and these cation channel antibodies.
    Matched MeSH terms: Brain Neoplasms/complications*; Brain Neoplasms/pathology; Brain Neoplasms/radionuclide imaging
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