Glioblastoma multiforme pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
===Genetics=== | |||
* Almost all cases of GBM are sporadic, without a familial predilection, although [[chromosome|chromosomal]] aberrations such as [[PTEN (gene)|PTEN]] mutation, and [[p53]] mutation are commonly seen in these tumors. | |||
* Growth factor aberrant signaling associated with [[Epidermal_growth_factor_receptor|EGFR]], and [[PDGF]] are also seen. | |||
===Gross Pathology=== | |||
===Microscopic Pathology=== | ===Microscopic Pathology=== | ||
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</gallery> | </gallery> | ||
</div> | </div> | ||
==References== | ==References== |
Revision as of 17:45, 12 September 2015
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
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.