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

Autor:	Ma S; Department of Radiation Oncology, Washington University School of Medicine, St. Louis, Missouri, USA., Rudra S; Department of Radiation Oncology, Washington University School of Medicine, St. Louis, Missouri, USA., Campian JL; Department of Medicine, Oncology Division, Washington University School of Medicine, St. Louis, Missouri, USA., Dahiya S; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri, USA., Dunn GP; Department of Neurological Surgery, Washington University School of Medicine, St. Louis, Missouri, USA., Johanns T; Department of Medicine, Oncology Division, Washington University School of Medicine, St. Louis, Missouri, USA., Goldstein M; Department of Radiation Oncology, Washington University School of Medicine, St. Louis, Missouri, USA., Kim AH; Department of Neurological Surgery, Washington University School of Medicine, St. Louis, Missouri, USA., Huang J; Department of Radiation Oncology, Washington University School of Medicine, St. Louis, Missouri, USA.
Jazyk:	angličtina
Zdroj:	Neuro-oncology advances [Neurooncol Adv] 2020 Sep 18; Vol. 2 (1), pp. vdaa126. Date of Electronic Publication: 2020 Sep 18 (Print Publication: 2020).
DOI:	10.1093/noajnl/vdaa126
Abstrakt:	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. (© The Author(s) 2020. Published by Oxford University Press, the Society for Neuro-Oncology and the European Association of Neuro-Oncology.)
Databáze:	MEDLINE
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