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. Author manuscript; available in PMC: 2020 Jun 10.
Published in final edited form as: Nat Rev Neurol. 2019 Jun 21;15(7):405–417. doi: 10.1038/s41582-019-0220-2

Table 1 –

Additional frequent tumor alterations in and information about the five WHO 2016 subtypes of adult diffuse glioma.

WHO 2016 classification Frequent molecular aberrationsa MGMT promoter methylation (%)b Median age at diagnosis (years)c Median overall survival (years)c Proportion of 2019 diagnoses (%)d
Glioblastoma, IDH-wild type
  • EGFR amplification

  • CDKN2A or CDKN2B deletion

  • PTEN mutation

  • PDGFRA1 mutation

  • TP53 mutation

  • NF1 mutation

  • Chromosome 7 gain

  • Chromosome 10 loss

  • MDM2 amplification

~40 59 1.2 71
Glioblastoma, IDH-mutant
  • TP53 mutation

  • Chromosome 10q loss

  • CDKN2A or CDKN2B deletion

~90 38 3.6 7
Astrocytoma, IDH-wild type
  • PTEN loss

  • EGFR amplification

  • NF1 mutation

  • TP53 mutation

  • PIK3CA mutation

55 52 1.9 5
Astrocytoma, IDH-mutant
  • TP53 mutation

  • CDKN2A or CDKN2B deletion

  • MYC amplification

  • RTK or RIS mutation

~85 36 9.3 12
Oligodendroglioma, IDH-mutant and 1p19q co-deletion
  • CIC mutation

  • FUBP1 mutation

  • NOTCH1 mutation

  • PI3K mutation

  • CDKN2A or CDKN2B deletion

~65–100 44 17.5 5
a

Data from REFs.6,8,20,45,46.

b

Data from REFs.45,6062.

c

Data fromREF.37 and in agreement with REFs.8,11,38,39.

d

Data from CBTRUS (2011–2015)21 and REFs27,40.