Role of Cl− channels in primary brain tumour

Cell Calcium ◽  
2019 ◽  
Vol 81 ◽  
pp. 1-11 ◽  
Author(s):  
Tayyebeh Saberbaghi ◽  
Raymond Wong ◽  
James T. Rutka ◽  
Guan-Lei Wang ◽  
Zhong-Ping Feng ◽  
...  
Keyword(s):  
Brain Tumour ◽  
Primary Brain Tumour ◽  
Cl Channels

Brain tumor-initiating cells and cells of origin in glioblastoma

2011 ◽  
Vol 2 (4) ◽  
Author(s):  
Sameer Agnihotri ◽  
Diana Munoz ◽  
Gelareh Zadeh ◽  
Abhijit Guha
Keyword(s):  
Brain Tumour ◽  
Large Scale ◽  
Recent Literature ◽  
Cell Of Origin ◽  
Tumor Initiating Cells ◽  
Primary Brain Tumour ◽  
Cells Of Origin ◽  
Brain Tumor Initiating Cells ◽  
Candidate Regions

AbstractGlioblastoma Multiforme (GBM) is the most malignant and devastating primary brain tumour with a median survival of ∼12–16 months. Although recent large scale sequencing projects have shed considerable light into the complexity of the disease, there remains much to be elucidated in the hopes of generating effective therapeutic strategies. Although these studies investigate the mutations and expression of bulk tumour they have limits with respect to cell of origin and the concept of brain tumour initiating cells (BTIC). Current research has challenged the old paradigm of the stochastic model as recent evidence suggests that a subset of cancer cells within a tumor is responsible for tumor initiation, maintenance, and resistance to therapy. To gain a better understanding of the different compartment of cells that GBM comprise of require careful and elegant experiments. In addition to studying GBM, exploring the role of normal neural stem cells and progenitors cells is essential to partially explain whether these GBM BTIC behave similarly or differently then their non transformed counterparts. Here we discuss the recent literature between the two models, candidate regions of glioma genesis, candidate cells of origin for GBM, and possible therapeutic avenues to explore.

P17. Current role of 201Tl cerebral imaging in assessment of recurrent primary brain tumour

2003 ◽  
Vol 24 (4) ◽  
pp. 473
Author(s):  
J. D. Birchall ◽  
R. H. Ganatra ◽  
T. Jaspan ◽  
R. M. Smith ◽  
A. C. Perkins
Keyword(s):  
Brain Tumour ◽  
Cerebral Imaging ◽  
Current Role ◽  
Primary Brain Tumour

scholarly journals Inhibition of ATR prevents macropinocytosis driven retraction of neurites and opposes invasion in GBM

2021 ◽  
Author(s):  
Joanna Birch ◽  
karen Strathdee ◽  
Katrina Stevenson ◽  
Sarah Derby ◽  
Louise Dutton ◽  
...  
Keyword(s):  
Brain Tumour ◽  
Mouse Models ◽  
Ataxia Telangiectasia ◽  
Clinical Symptoms ◽  
Growth Patterns ◽  
Novel Treatments ◽  
Primary Brain Tumour ◽  
Associated Symptoms

Abstract Glioblastoma (GBM) is the most common and aggressive type of primary brain tumour and remains incurable despite decades of research. GBM are characterised by highly infiltrative growth patterns that contribute to the profound cognitive and neurological symptoms experienced by patients, and to inevitable recurrence following treatment. Novel treatments that reduce infiltration of the healthy brain have potential to ameliorate clinical symptoms and improve survival. Here, we report a novel role of the Ataxia telangiectasia and Rad 3 related kinase (ATR) in supporting the invasive properties of GBM cells through the regulation of macropinocytosis-driven internalisation of integrin adhesion receptors. We demonstrate that inhibition of ATR opposes GBM migration in vitro, and correspondingly reduces infiltrative behaviour in orthotopic mouse models. These results indicate that ATR inhibition, in addition to its use as a radiosensitiser, may be effective in reducing GBM infiltration and its associated symptoms.

323 The Subcellular Expression Patterns of Bcl-Xl in Primary Brain Tumour Samples

2021 ◽  
Vol 108 (Supplement_2) ◽  
Author(s):  
A Vassiliou ◽  
K Alavian ◽  
M Tsujishita ◽  
H Bae
Keyword(s):  
Brain Tumour ◽  
Tumour Progression ◽  
Expression Patterns ◽  
B Cell Lymphoma ◽  
Nuclear Antigen ◽  
Future Research ◽  
Metabolic Efficiency ◽  
Cell Detection ◽  
Primary Brain Tumour ◽  
Cancerous Cells

Abstract Introduction Primary brain tumours originate from cells within the brain. The commonest malignant types are gliomas which are graded from I-IV. Emerging evidence has elucidated the function of the mitochondrially localised B-cell lymphoma-extra-large (Bcl-xL) protein, and its promotion of tumour progression-associated properties. Our lab has previously established that Bcl-xL-overexpressing neurons increase metabolic efficiency by producing more adenosine triphosphate and consuming less oxygen, which we assumed, fuels cancer cells to proliferate. Method We quantified the subcellular expression patterns of Bcl-xL in primary brain tumour samples through immunohistochemistry on a brain tissue microarray containing 16 glioma cases from Grades II-IV. We used antibodies against Bcl-xL, heat shock protein 60 for mitochondrial detection and proliferating cell nuclear antigen for cancerous cell detection. Results Bcl-xL is overexpressed in cancerous cells of Grade IV gliomas and is significantly greater than cancerous cells of Grade III and Grade II gliomas. Cancerous cells express higher levels of Bcl-xL than non-cancerous cells in all grades of glioma. Conclusions Bcl-xL-overexpressing neurons exhibit enhanced metabolic efficiency, contributing to increased proliferation rates. Future research should focus on the characterisation of ATP levels and oxygen consumption in glioma cells. Conclusively, pharmacological inhibition of Bcl-xL will suppress the proliferation rate in gliomas and cease cancer cell growth.

Responding to primary brain tumour

Nursing ◽  
2007 ◽  
Vol 37 (1) ◽  
pp. 36-42 ◽  
Author(s):  
RACHEL L. PALMIERI
Keyword(s):  
Brain Tumour ◽  
Primary Brain Tumour

Role of diffusion- and perfusion-weighted MR imaging for brain tumour characterisation

2009 ◽  
Vol 114 (4) ◽  
pp. 645-659 ◽  
Author(s):  
L. Rizzo ◽  
S. Greco Crasto ◽  
P. Garcia Moruno ◽  
P. Cassoni ◽  
R. Rudà ◽  
...  
Keyword(s):  
Mr Imaging ◽  
Brain Tumour

scholarly journals Increased TMEM16A-encoded calcium-activated chloride channel activity is associated with pulmonary hypertension

2012 ◽  
Vol 303 (12) ◽  
pp. C1229-C1243 ◽  
Author(s):  
Abigail S. Forrest ◽  
Talia C. Joyce ◽  
Marissa L. Huebner ◽  
Ramon J. Ayon ◽  
Michael Wiwchar ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Electromechanical Coupling ◽  
Pulmonary Arteries ◽  
Doppler Imaging ◽  
Heart Weight ◽  
Channel Activity ◽  
Cl Channels ◽  
Pulmonary Arterial ◽  
Pulmonary Artery Smooth Muscle

Pulmonary artery smooth muscle cells (PASMCs) are more depolarized and display higher Ca2+ levels in pulmonary hypertension (PH). Whether the functional properties and expression of Ca2+-activated Cl− channels (ClCa), an important excitatory mechanism in PASMCs, are altered in PH is unknown. The potential role of ClCa channels in PH was investigated using the monocrotaline (MCT)-induced PH model in the rat. Three weeks postinjection with a single dose of MCT (50 mg/kg ip), the animals developed right ventricular hypertrophy (heart weight measurements) and changes in pulmonary arterial flow (pulse-waved Doppler imaging) that were consistent with increased pulmonary arterial pressure and PH. Whole cell patch experiments revealed an increase in niflumic acid (NFA)-sensitive Ca2+-activated Cl− current [ ICl(Ca)] density in PASMCs from large conduit and small intralobar pulmonary arteries of MCT-treated rats vs. aged-matched saline-injected controls. Quantitative RT-PCR and Western blot analysis revealed that the alterations in ICl(Ca) were accompanied by parallel changes in the expression of TMEM16A, a gene recently shown to encode for ClCa channels. The contraction to serotonin of conduit and intralobar pulmonary arteries from MCT-treated rats exhibited greater sensitivity to nifedipine (1 μM), an l-type Ca2+ channel blocker, and NFA (30 or 100 μM, with or without 10 μM indomethacin to inhibit cyclooxygenases) or T16AInh-A01 (10 μM), TMEM16A/ClCa channel inhibitors, than that of control animals. In conclusion, augmented ClCa/TMEM16A channel activity is a major contributor to the changes in electromechanical coupling of PA in this model of PH. TMEM16A-encoded channels may therefore represent a novel therapeutic target in this disease.

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