Difference between revisions of "Glioblastoma"

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→‎IHC: + some molecular
(→‎IHC: + some molecular)
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==IHC==
==IHC==
*GFAP +ve (cytoplasm).
*GFAP +ve (cytoplasm).
*IDH-1 -ve.
*[[MAP2]] +ve.
**+ve if developed from lower grade astrocytoma. (???)
*[[IDH-1]] -ve (95%).
**+ve if developed from lower grade astrocytoma (secondary GBM).
*[[WT-1]] +ve (cytoplasm).
*p53 +ve (70%).
*Neurofilament -ve.
*Synaptophysin -ve (residual Cortex may be +ve).
*panCK -ve (except for GBM with epithelial component).
*[[ATRX]]: +ve (no loss, nuclei)
**-ve if developed from lower grade astrocytoma (secondary GBM).
*EMA: Dot-like expression less common than in [[ependymoma]]s.
*MIB-1 usu. 15-30%, but varies greatly.
 
 
==Molecular==
*Seen in inherited tumor syndromes:
**Lynch-Syndrome
**[[Neurofibromatosis 1]]
**Li-Fraumeni-Syndrome
**Turcot-Syndrome
 
*Most common alterations (TCGA<ref>{{Cite journal  | last1 = Verhaak | first1 = RG. | last2 = Hoadley | first2 = KA. | last3 = Purdom | first3 = E. | last4 = Wang | first4 = V. | last5 = Qi | first5 = Y. | last6 = Wilkerson | first6 = MD. | last7 = Miller | first7 = CR. | last8 = Ding | first8 = L. | last9 = Golub | first9 = T. | title = Integrated genomic analysis identifies clinically relevant subtypes of glioblastoma characterized by abnormalities in PDGFRA, IDH1, EGFR, and NF1. | journal = Cancer Cell | volume = 17 | issue = 1 | pages = 98-110 | month = Jan | year = 2010 | doi = 10.1016/j.ccr.2009.12.020 | PMID = 20129251 }}</ref>)
**Tp53 (42% of the tumors mutated)
**PTEN (33%).
**NF1 (21%).
**EGFR (18%).
**RB1 (11%).
**PI3K-pathway genes (7-10%).
 
 
*Diagnostic/therapeutic relevant markers:
**MGMT promoter methylation status
**Absence of LOH 1p/19q (otherwise classify tumor as [[oligodendroglioma]]).


==See also==
==See also==
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