Journal
MOLECULAR NEUROBIOLOGY
Volume 29, Issue 1, Pages 61-71Publisher
SPRINGER
DOI: 10.1385/MN:29:1:61
Keywords
glioma; glutamate; excitotoxicity; chloride; cell migration; invasion; metastasis; cell volume; ion channel
Categories
Funding
- NCI NIH HHS [P50 CA097247-010003, P50-CA97247, P50 CA097247] Funding Source: Medline
- NICHD NIH HHS [P01 HD038760-050005, P01-HD38760, P01 HD038760-040005, P01 HD038760-030005, P01 HD038760] Funding Source: Medline
- NINDS NIH HHS [R01 NS036692-06, R01 NS036692, R01 NS036692-08, R01 NS031234, R01 NS031234-10, R01 NS036692-07, R01 NS036692-05A1, R01 NS-36692, R01 NS031234-11, R01 NS-31234] Funding Source: Medline
Ask authors/readers for more resources
The malignant growth of glial support cells causes gliomas, highly invasive, primary brain tumors that are largely resistant to therapy. Individual tumor cells spread by active cell migration, invading diffusely into the normal brain. This process is facilitated by Cl- channels that endow glioma cells with an enhanced ability to quickly adjust their shape and cell volume to fit the narrow and tortuous extracellular brain spaces. Once satellite tumors enlarge, their growth is limited by the spatial constraints imposed by the bony cavity of the skull and spinal column. Glioma cells circumvent this limitation by active destruction of peritumoral neural tissue through the release of glutamate, inducing peritumoral seizures and ultimately excitotoxic neuronal cell death. Hence, primary brain tumors support their unusual biology by taking advantage of ion channels and transporters that are designed to support ion homeostatic functions in normal brain.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available