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Medulloblastoma is the most common brain tumour in children; using exome sequencing of tumour samples the authors show that these cancers have low mutation rates and identify 12 significantly mutated genes, among them the gene encoding RNA helicase DDX3X.

Embryonal tumors with multilayered rosettes (ETMRs) are primitive neuroectodermal tumors arising in infants. A new study shows that these tumors are universally driven by fusion of the promoter of a gene with brain-specific expression, TTYH1, to C19MC, the largest human microRNA cluster, activating a fetal neural development program.

The demethylase KDM5C, mutations in which often lead to intellectual disability, is identified as a crucial player in regulating the precise timing of neurodevelopment together with the WNT signalling pathway.

The authors characterize a previously undescribed function of Snf5 that involves interaction with the transcription factor Gli1 and downregulation of its activity via chromatin remodeling. Snf5 is shown to restrict Hedgehog (Hh) signaling in normal development and cancer. Hh inhibition emerges as a potential therapeutic strategy for malignant rhabdoid tumors in which Snf5 is commonly lost.

Circular extrachromosomal DNA in high-risk medulloblastoma contributes to tumor heterogeneity and associates with relapse and survival. Enhancer rewiring events involving known oncogenes are frequent events, affecting transcription and proliferation.

Medulloblastoma is the most common malignant brain tumour in children; having assembled over 1,000 samples the authors report that somatic copy number aberrations are common in medulloblastoma, in particular a tandem duplication of SNCAIP, a gene associated with Parkinson’s disease, which is restricted to subgroup 4α, and translocations of PVT1, which are restricted to Group 3.

The role of developmental pathways in medulloblastoma tumours (MB) with sonic hedgehog (SHH) activation remains to be explored. Here, the authors perform multi-omic analysis and characterise the key transcriptomic and metabolic patterns of highly differentiated cells in SHH MBs.

Microvesicles containing RNA are released from tumour cells. Here, the authors show that microvesicles released from tumour cells in culture have amplified levels of thec-Myconcogene, which is also found in the cell of origin, suggesting that microvesicles could be used as biomarkers.

Characterization of medulloblastoma tissues using single-cell transcriptomics shows that the different molecular subtypes consist of distinct developmental phenotypes.

One way of discovering genes with key roles in cancer development is to identify genomic regions that are frequently altered in human cancers. Here, high-resolution analyses of somatic copy-number alterations (SCNAs) in numerous cancer specimens provide an overview of regions of focal SCNA that are altered at significant frequency across several cancer types. An oncogenic function is also found for the anti-apoptosis genes MCL1 and BCL2L1, which reside in amplified genome regions in many cancers.

Polyubiquitination of the tumor suppressor p53 (encoded by TP53) regulates its stability by targeting it for degradation. Wu et al. now report that UBE4B, an E3 and E4 ligase, is a key enzyme in this process and that overexpression of UBE4B in some brain tumors is associated with reduced p53 abundance, suggesting a previously unknown mechanism blocking p53 function in cancer.

Genomic analysis of 491 medulloblastoma samples, including methylation profiling of 1,256 cases, effectively assigns candidate drivers to most tumours across all molecular subgroups.

Deficiency in Gnas, encoding the Gs protein α subunit, is sufficient to induce medulloblastoma in mice due to derepression of the Sonic hedgehog pathway.

The measurement of the total cross-section of proton–proton collisions is of fundamental importance for particle physics. Here, the first measurement of the inelastic cross-section is presented for proton–proton collisions at an energy of 7 teraelectronvolts using the ATLAS detector at the Large Hadron Collider.

Medulloblastoma has been the subject of numerous genomics and transcriptomics studies that have led to this disease being subclassified into various clinically meaningful groups and to advances in understanding the biology of these subgroups, with implications for treatment.

Medulloblastoma is the most common brain tumour in children; using whole-genome sequencing of tumour samples the authors show that the clinically challenging Group 3 and 4 tumours can be tetraploid, and reveal the expression of the first medulloblastoma fusion genes identified.

Stefan Pfister and the ICGC PedBrain Tumor Project report whole-genome sequencing of 96 pilocytic astrocytomas. They identify recurrent activating mutations in FGFR1 and PTPN11 and novel NTRK2 fusion genes.

Charles Roberts, Peter Park, Bradley Bernstein and colleagues examine the consequences of SMARCB1 loss on enhancer landscapes in human rhabdoid tumors. They show that SMARCB1 is essential for the integrity and abundance of SWI/SNF complexes and facilitates their targeting to appropriate enhancers.

Super enhancers regulate oncogenes and other molecular targets in ependymomas, and identification of these genes provides potential therapeutic targets.

This Primer by Pfister and colleagues reviews the molecular genetics, diagnosis and management of medulloblastoma and touches upon the quality of life of patients and future outlooks.

Donor-based solid state quantum computing devices require atomically precise fabrication and atomic-scale control of the tunneling processes. The authors describe the reproducible fabrication of a series of single electron transistors with tunnel gaps that vary based on the surface lattice and demonstrate the exponential scaling of tunneling as a function of atomically precise changes as theoretically predicted.