2019
ATIM-37. PHASE II, OPEN-LABEL, SINGLE ARM, MULTICENTER STUDY OF AVELUMAB WITH HYPOFRACTIONATED RADIATION (HFRT) FOR ADULT PATIENTS WITH SECONDARILY TRANSFORMED IDH-MUTANT GLIOBLASTOMA (GBM)
Kurz S, Silverman J, Hochman T, Nayak L, Arrillaga-Romany I, Lee E, Patel A, Delara M, Hsu F, Imtiaz T, Magnelli L, Taylor J, Cloughesy T, Sulman E, Golfinos J, Zagzag D, Snuderl M, Goldberg J, S A. ATIM-37. PHASE II, OPEN-LABEL, SINGLE ARM, MULTICENTER STUDY OF AVELUMAB WITH HYPOFRACTIONATED RADIATION (HFRT) FOR ADULT PATIENTS WITH SECONDARILY TRANSFORMED IDH-MUTANT GLIOBLASTOMA (GBM). Neuro-Oncology 2019, 21: vi9-vi10. PMCID: PMC6847193, DOI: 10.1093/neuonc/noz175.036.Peer-Reviewed Original ResearchIDH-mutant glioblastomasHypofractionated radiationFollow-upMedian follow-up timeCohort of adult patientsEfficacy of avelumabSafety lead-inAnti-PD-L1Dose-limiting toxicityTime of progressionIDH-mutant gliomasIncreased cerebral edemaMedian OSMedian PFSWorsened hemiparesisPhase IIOpen-labelSlow accrualTransaminase elevationAvelumabDiscontinued treatmentSingle-armMulticenter studyTreatment regimenAdult patients
2018
GENE-16. CLINICALLY AGGRESSIVE MENINGIOMAS ARE CHARACTERIZED BY MUTATIONAL SIGNATURES ASSOCIATED WITH DEFECTIVE DNA REPAIR AND MUTATIONS IN CHROMATIN REMODELING GENES
Kurz S, Liechty B, Kelly S, Vasudevaraja V, Bledea R, Wu P, Serrano J, Katz L, Silverman J, Pacione D, Golfinos J, Chi A, Snuderl M. GENE-16. CLINICALLY AGGRESSIVE MENINGIOMAS ARE CHARACTERIZED BY MUTATIONAL SIGNATURES ASSOCIATED WITH DEFECTIVE DNA REPAIR AND MUTATIONS IN CHROMATIN REMODELING GENES. Neuro-Oncology 2018, 20: vi106-vi106. PMCID: PMC6216611, DOI: 10.1093/neuonc/noy148.442.Peer-Reviewed Original ResearchSingle nucleotide variantsChromatin remodeling genesCancer-associated genesDefective DNA repairChromatin remodelingAggressive meningiomasMutational signaturesDNA repairIncreased copy number variationDNA methylation array analysisSomatic mutationsRemodeling genesClinically aggressive meningiomasUnfavorable clinical courseAssociated with more aggressive behaviorCopy number variationsPattern of somatic mutationsWhole-exome sequencingMethylation array analysisDNA methylation phenotypeMedian PFSNucleotide variantsAggressive tumorsClinical courseRecurrence rate