Matthew R. Grimmer

TL;DR: An extensive assessment of mutation burden through sequencing analysis of >81,000 tumors from pediatric and adult patients, including tumors with hypermutation caused by chemotherapy, carcinogens, or germline alterations, uncovered new driver mutations in the replication-repair-associated DNA polymerases and a distinct impact of microsatellite instability and replication repair deficiency on the scale of mutation load.

TL;DR: The results suggest that the strongest selective pressures occur during early glioma development and that current therapies shape this evolution in a largely stochastic manner.

TL;DR: Transduced wild-type or mutationally stabilized murine N-myc(T58A) into neural stem cells (NSCs) from perinatal murine cerebellum, brain stem, and forebrain demonstrated context-dependent transformation of NSCs in response to a common oncogenic signal.

TL;DR: Transient pharmacological down-regulation of MYCN led to both clearance and senescence of tumor cells, and improved survival, suggesting a central role for MYCN in pathogenesis.

TL;DR: Evidence suggests that stabilization of Myc through inhibition of phosphoinositide 3-kinase signaling exhibits promise not only in medulloblastoma and neuroblastoma, but in a wide range of MyC-driven tumors.