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| ==Pathophysiology== | | ==Pathophysiology== |
| Glioblastomas multiforme are characterized by the presence of small areas of [[Necrosis|necrotizing]] [[tissue]] that is surrounded by highly-[[Tumor|anaplastic]] cells (pseudopalisading necrosis). This characteristic, as well as the presence of hyperplastic blood vessels, differentiates the tumor from Grade 3 [[astrocytomas]], which do not have these features. Although glioblastoma multiforme can be formed from lower-grade [[astrocytomas]], post-mortem autopsies have revealed that most glioblastomas multiforme are not caused by previous lesions in the brain
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| Unlike [[oligodendroglioma]]s, glioblastomas multiforme can form in either the [[gray matter]] or the [[white matter]] of the brain; but most GBM arises from the deep white matter and quickly infiltrate the brain, often becoming very large before producing symptoms. The tumor may extend to the meningeal or [[ventricular]] wall, leading to the high protein content of [[cerebrospinal fluid]] (CSF) (> 100 mg/dL), as well as an occasional [[pleocytosis]] of 10 to 100 cells, mostly [[lymphocyte]]s. [[Malignant]] cells carried in the CSF may spread to the [[spinal cord]] or cause meningeal gliomatosis. However, [[metastasis]] of [[GBM]] beyond the [[central nervous system]] is extremely rare. About 50% of GBM occupy more than one lobe of a hemisphere or are bilateral. Tumors of this type usually arise from the [[cerebrum]] and may exhibit the classic infiltrate across the [[corpus callosum]], producing a butterfly (bilateral) [[glioma]].
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| The tumor may take on a variety of appearances, depending on the amount of hemorrhage, [[necrosis]], or its age.
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| ===Microscopic Pathology=== | | ===Microscopic Pathology=== |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
Microscopic Pathology
Genetics
- Almost all cases of GBM are sporadic, without a familial predilection, although chromosomal aberrations such as PTEN mutation, and p53 mutation are commonly seen in these tumors.
- Growth factor aberrant signaling associated with EGFR, and PDGF are also seen.
References
Template:WikiDoc Sources