Faithful models of RMC require SMARCB1 loss for survival, and genetic and small-molecule screens identify inhibition of the ubiquitin-proteasome system (UPS) as a potential therapeutic approach for SMARCB1 deficient cancers.

Sequentially expressed temporal transcription factors in neural stem cells during early development determine which progeny can undergo malignant transformation upon dedifferentiation.

L-mimosine and dopamine protect against cisplatin-induced oto- and nephrotoxicity in zebrafish and human cell line models.

H3-G34R, V, and W oncohistonesin fission yeast cause differential K36 modification, DNA damage sensitivity and genome stability outcomes, highlighting the need for a thorough evaluation of distinct mutations.

Pre-clinical and patient data show that inhibition of autophagy with an approved, inexpensive, well-tolerated drug can overcome resistance to BRAF^V600E inhibition in multiple brain tumor subtypes with different resistance mechanisms.

The percentage of a tumor’s genome with alterations in copy number is correlated with increased mortality across a range of tumor types and can be measured using a clinically approved sequencing assay.

Mutation of Glycine 34 to Arginine within the N-terminal tail of histone H3 alters post-translational modifications on Lysine 36 and is associated with a delay in replication restart, defective homologous recombination and an increase in genomic instability.

About twenty temporal patterning genes are identified that drive an irreversible differentiation trajectory governing the heterogeneity and proliferative properties of cells in neural tumors with an early developmental origin.

The combination of ceritinib with CGM097 demonstrates remarkable antitumor activity in TP53 wild-type neuroblastoma models with ALK aberrations and is able to overcome the resistance acquired during ceritinib treatment.

Acute one-hour treatment of Pik3ca mutant mice with a novel anti-epilepsy drug suppresses seizures despite continued developmental brain dysmorphology, promising a new therapeutic strategy for patients with intractable pediatric epilepsy.