Fig 3.

Genomic landscape of high-risk pediatric and young adult patients with brain tumors at diagnosis and recurrence. Activating DNA lesions (mutation, amplification, or fusion) were seen in 19 tumors (48%), most frequently in the mitogen-activated protein kinase signaling and mechanistic target of rapamycin/phosphoinositide 3-kinase pathways. Tumor suppressor mutations or deletions (germline and/or somatic) were seen in 32 tumors (80%), most frequently in DNA damage or apoptotic signaling pathways. AT/RT, atypical teratoid/rhabdoid tumor; DIPG, diffuse intrinsic pontine glioma; GBM, glioblastoma multiforme; SNV, somatic nucleotide variant.