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Background  We aimed to evaluate the clinical outcomes of molecular glioblastoma (mGBM) as compared to histological GBM (hGBM) and to determine the prognostic impact of  TERT  mutation,  EGFR  amplification, and  CDKN2A/B  deletion on isocitrate dehydrogenase (IDH)-wildtype GBM.    Methods  IDH-wildtype GBM patients treated with radiation therapy (RT) between 2012 and 2019 were retrospectively analyzed. mGBM was defined as grade II-III IDH-wildtype astrocytoma without histological features of GBM but with one of the following molecular alterations:  TERT  mutation,  EGFR  amplification, or combination of whole chromosome 7 gain and whole chromosome 10 loss. Overall survival (OS) and progression-free survival (PFS) were calculated from RT and analyzed using the Kaplan–Meier method. Multivariable analysis (MVA) was performed using Cox regression to identify independent predictors of OS and PFS.    Results  Of the 367 eligible patients, the median follow-up was 11.7 months. mGBM and hGBM did not have significantly different OS (median: 16.6 vs 13.5 months, respectively,  P  = .16), nor PFS (median: 11.7 vs 7.3 months, respectively,  P  = .08). However, mGBM was associated with better OS (hazard ratio [HR] 0.50, 95% CI 0.29–0.88) and PFS (HR 0.43, 95% CI 0.26–0.72) than hGBM after adjusting for known prognostic factors on MVA.  CDKN2A/B  deletion was associated with worse OS (HR 1.57, 95% CI 1.003–2.46) and PFS (HR 1.57, 95% CI 1.04–2.36) on MVA, but  TERT  mutation and  EGFR  amplification were not.    Conclusion  Criteria for mGBM may require further refinement and validation.  CDKN2A/B  deletion, but not  TERT  mutation or  EGFR  amplification, may be an independent prognostic biomarker for IDH-wildtype GBM patients.

Prognostic impact of CDKN2A/B deletion, TERT mutation, and EGFR amplification on histological and molecular IDH-wildtype glioblastoma