CNS tumor
Astrocytic tumors
Glioblastoma multiforme

Author: Eman Abdelzaher, M.D., Ph.D. (see Authors page)

Revised: 6 June 2017, last major update March 2012

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PubMed Search: Glioblastoma multiforme [title] CNS

Related topics: Giant cell, pediatric nonbrainstem

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Cite this page: Glioblastoma multiforme. PathologyOutlines.com website. http://www.pathologyoutlines.com/topic/cnstumorglioblastoma.html. Accessed December 12th, 2017.
Definition / general
  • Malignant primary brain tumor with predominant astrocytic differentiation
  • WHO grade IV
  • "Multiforme" due to variegated gross appearance (firm white areas, yellow necrotic areas, hemorrhagic areas and cystic areas) as well as diverse histological features
Sites
  • Usually supratentorial; uncommon in cerebellum, rare in spinal cord
  • Glioblastoma of brain stem is infrequent and often affects children
Clinical features
  • 12 - 15% of adult intracranial tumors, 50 - 60% of astrocytic neoplasms
  • Either primary (denovo, without recognizable precursor lesions, with p53 mutation) or secondary (develops slowly from grade II or III astrocytoma, often with partial #10 deletion)
  • May be under graded on small stereotactic biopsies due to regional heterogeneity
  • Median survival is 1 year; 5 year survival < 5%; survival may be overstated due to low grade tumors that dedifferentiate to glioblastoma (Cancer 2003;98:1745)
Radiology description
  • Contrast enhancing (ring pattern is characteristic), large, surrounded by peritumoral edema, mass effect
Radiology images

Images hosted on other servers:

MRI sagittal view

With ring enhancement

Case reports
Gross description
  • Fast growing tumors may have apparent pseudocapsule
  • Large tumors are poorly delineated
  • Usually solitary but may cross midline through corpus callosum, massa intermedia or anterior commissure to produce a "butterfly" lesion
  • Often peritumoral edema
  • Cut section is variegated (yellowish necrotic central area, grayish peripheral rim, recent and old hemorrhage, cysts due to liquefied necrotic tumor tissue)
  • Usually intraparenchymal
  • Infrequently superficial, may grossly / radiologically resemble metastatic carcinoma or meningioma
Gross images

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Variegated tumor

Microscopic (histologic) description
  • High grade astrocytoma (anaplastic, nuclear atypia, cellular pleomorphism, mitotic activity) with either coagulation necrosis or microvascular proliferation (formerly "endothelial proliferation") with thickened vascular walls due to endothelial cell hyperplasia (increase in nuclei in vessel wall) and hypertrophy; also formation of multiple lumina resembling glomerulus
  • Usually hypercellular with mitotic figures (some atypical), multinucleated tumor cells, bizarre nuclei, karyorrhectic cells
  • May have pseudopalisading necrosis (tumor cells around necrotic zones), secondary structures of Scherer
  • Other less common features: epithelial structures (glandular or ribbon-like), epithelioid cells with well delineated cytoplasmic membranes, granular cells, lipidized cells, macrophages (Arch Pathol Lab Med 2001;125:637)
  • Small cell glioblastoma:
    • Densely packed small cells, resembles anaplastic oligodendroglioama on low power, may be calcification, perivascular pseudorosettes
    • May have a better prognosis than standard glioblastoma
    • Note: examine carefully to determine if low grade tumor also present, suggesting dedifferentiation
    • Glioblastoma with oligodendroglioma component: according to WHO classification (2007), anaplastic oligoastrocytoma associated with necrosis should be classified as "glioblastoma with oligodendroglial component"
Microscopic (histologic) images

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Prominent anaplasia, vascular proliferation and palisading of tumor cells around necrosis

Pseudopalisading necrosis

Various vascular patterns


H&E and HAM56+ macrophages

Previous resection and radiation therapy

Various images

Positive stains
Negative stains
Molecular / cytogenetics description
  • Amplification of EGFR (particularly in small cell variant, Clin Neuropathol 2005;24:163), mutations of p16, p53 and PTEN; loss of heterozygosity at 10q
Differential diagnosis