CDK4 Amplification Associated with Longer Term Response to Bevacizumab in Glioblastoma


John Villano, Rachael Morgan, Shulin Zhang, Jill Kolesar, Joanne Xiu, Hilary Seifert, Theodore Nicolaides, Stephanie Rock, Santosh Kesari, Sonikpreet Aulakh, Eric Wong, Michael Glantz


  • Using a large clinical genomic database with GBM subjected to comprehensive molecular profiling, we demonstrated that amplification of CDK4 and EGFR were associated with long-term and short-term responses to bevacizumab, respectively
  • Investigation into the tumors not treated with bevacizumab suggests that CDK4 amplification may be a predictive marker for bevacizumab while EGFR amplification may be prognostic of poor survival
  • SETD2 mutations and PIK3R1 mutations are suggested to be predictive of bevacizumab benefit and prognostic of poor survival, respectively
  • This warrants further investigation in independent cohorts controlled for age and other prognostic factors. If confirmed, a genetic basis for treatment optimization may provide meaningful clinical outcomes
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