Glioblastoma multiforme classification

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sujit Routray, M.D. [2]

Overview

Glioblastoma may be classified into several subtypes based on its origin and molecular alterations.[1][2]

Classification

Glioblastoma may be classified according to its origin into two subtypes: Primary and secondary.[1]

Differential diagnosis Characteristic features of the differential diagnosis
Cerebral metastasis
  • May look identical
  • Both may appear multifocal
  • Metastases are centred on grey-white matter junction and spare the overlying cortex
Primary CNS lymphoma
  • In patients with AIDS
  • Central necrosis is more common
  • Homogeneously enhancing on MRI
Cerebral abscess
  • Central restricted diffusion is helpful
  • Hemorrhagic then assessment may be difficult
  • Presence of smooth and complete SWI low intensity rim
  • Presence of dual rim sign
Anaplastic astrocytoma
Tumefactive demyelination
  • Can appear similar
  • Open ring pattern of enhancement
  • Younger patients
Stroke
  • History is suggestive of diagnosis
  • No elevated choline
Cerebral toxoplasmosis
  • In patients with AIDS
Radiation necrosis
Encephalitis
Oligodendroglioma
Epilepsy
  • Multifactorial
  • Mass may or may not be observed on MRI depending on the cause


Primary glioblastoma

  • De novo origin
  • More aggressive
  • Occurs in older patients

Secondary glioblastoma

  • Arises from pre-existing lower grade gliomas
  • Less aggressive
  • Occurs in younger patients

Glioblastoma may be classified according to its molecular alterations into four subtypes:[2]

  • Classic
  • Proneural
  • Mesenchymal
  • Neural

References

  1. 1.0 1.1 Classification of glioblastoma multiforme. Dr Dylan Kurda and Dr Frank Gaillard et al. Radiopaedia 2015. http://radiopaedia.org/articles/glioblastoma
  2. 2.0 2.1 Verhaak RG, Hoadley KA, Purdom E, Wang V, Qi Y, Wilkerson MD; et al. (2010). "Integrated genomic analysis identifies clinically relevant subtypes of glioblastoma characterized by abnormalities in PDGFRA, IDH1, EGFR, and NF1". Cancer Cell. 17 (1): 98–110. doi:10.1016/j.ccr.2009.12.020. PMC 2818769. PMID 20129251.


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