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. 2017 Oct 16;14(6):8213–8219. doi: 10.3892/ol.2017.7196

Table II.

Clinicopathological and experimental characteristics of GBMs with or without TERT promoter mutation.

TERT promoter mutation, n (%)

Variable + P-value
Age, years 56.5±8.3 47.2±14.6 0.050
Sex <0.001
  Male 12 (100) 0 (0)
  Female 4 (30.8) 9 (69.2)
Tumor size, cm 4.70±1.63 4.79±0.75 0.943
ATRX mutation 1.00
  + 7 (87.5) 1 (12.5)
  − 6 (75.0) 2 (25.0)
ATRX amplification 0.391
  + 0 (0) 1 (100)
  − 14 (63.6) 8 (36.4)
EGFR mutation 0.117
  + 11 (91.7) 1 (8.3)
  − 4 (57.1) 3 (42.9)
EGFR amplification 0.102
  + 10 (76.9) 3 (23.1)
  − 4 (40.0) 6 (60.0)
CDKN2A deletion 0.116
  + 12 (70.6) 5 (29.4)
  − 1 (20.0) 4 (80.0)
PTEN mutation 1.00
  + 3 (75.0) 1 (25.0)
  − 10 (83.3) 2 (16.7)
PTEN deletion 0.102
  + 10 (76.9) 3 (23.1)
  − 4 (40.0) 6 (60.0)
Subtype 0.176
  Classical 6 (100) 0 (0)
  Mesenchymal 2 (40.0) 3 (60.0)
  Proneural 3 (60.0) 2 (40.0)
  Not determined 5 (55.6) 4 (44.4)
In vivo tumor formation 0.004
  + 12 (80.0) 3 (20.0)
  − 0 (0) 5 (100)

Data are presented as the mean ± standard deviation. TERT, telomerase reverse transcriptase gene; GBM, glioblastoma multiforme; ATRX, α-thalassemia/mental retardation syndrome X-linked; EGFR, epidermal growth factor receptor; PTEN, phosphatase and tensin homolog; CDKN2A, cyclin dependent kinase inhibitor 2A.