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In this study the authors consider the structural variants (SVs) present within cancer cases of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium. They report hundreds of genes, including known cancer-associated genes for which the nearby presence of a SV breakpoint is associated with altered expression.

The role of germline variation in cancer remains underexplored. Here, the authors investigate the landscape of germline structural variants on tumour DNA methylation across pediatric brain and central nervous system tumour patients and suggest disease implications.

Somatic structural variants (SVs) in cancer can impact DNA methylation-mediated transcriptional regulation. Here, the authors analyse multi-omics data from over 2400 samples from the Children’s Brain Tumor Network and report SVs that are associated with altered gene expression or DNA methylation, including some with prognostic relevance.

Urological cancers have disparate tissues and cells of origin but share many molecular features. Here, the authors use multidimensional and comprehensive molecular characterization to classify urological cancers into nine major genomic subtypes, highlighting potential therapeutic targets.

The relevance of non-coding somatic mutations in cancer remains elusive. Here, the combination of mass spectrometry-based proteomics and whole genome sequencing data across multiple cancer types helps to assess the effects of somatic structural variant breakpoint patterns on protein expression of nearby genes.

Pan-cancer proteomics analysis enables the analysis of protein expression across multiple cancer types. Here, the authors compare proteomics from 14 cancer types and show 11 distinct subtypes across multiple cancer types. Proteome data could link higher pathway activity levels with somatic alteration of specific genes in the pathway.

The global impact of somatic structural variants (SSVs) on gene expression in childhood cancers is unclear. Here, the authors analyse cancer genome and RNA sequencing data of 854 pediatric brain tumours and report a landscape of genes deregulated by SSVs.

Ovarian cancer is common among women and is the leading cause of death from gynaecological malignancies. Here the authors identify two previously unknown genetic variants that increase the risk of epithelial ovarian cancer in Han Chinese women.

The synthesis of covalent organic frameworks with a multiple-dynamic-bonds strategy realizes selective extraction of uranyl tricarbonate anions from ultra-low concentrations and multiple interfering ions.

Hashimoto’s thyroiditis (HT) is the main cause of hypothyroidism. Here the authors develop a deep learning model for diagnosis of HT on a large multi-site dataset including image and video data.

Mass-spectrometry-based profiling can be used to stratify tumours into molecular subtypes. Here, by classifying over 500 tumours, the authors show that this approach reveals proteomic subgroups which cut across tumour types.

Next generation sequencing allows the identification of oncogenic driver genes in pancreatic cancer. Here, in an effort to identify additional causal genes, the authors develop a high throughput in vivoscreen and identify genes that whilst infrequently mutated in pancreatic cancer contribute to tumour formation.

Non-small cell lung cancer (NSCLC) is often associated with metastasis to the lungs. Here, the authors perform independent screens and identify NuRD as a co-repressor of ZEB1, and demonstrate TBC1D2b as a downstream target of ZEB1/NuRD complex regulating NSCLC metastasis.

Meta-analysis of 36,760 cases and 375,188 controls identifies 54 loci associated with susceptibility to cutaneous melanoma. Further analysis combining nevus count and hair color GWAS results provide insights into the genetic architecture of melanoma.

Glioblastoma tumours expressing oncogenic PIK3CA variants secrete the glycan GPC3, which promotes the formation of neural synapses, brain synaptic hyperexcitability and gliomagenesis.

KRAS-driven lung cancers represent an aggressive form of NSCLC. In this study the authors perform an in vivo functional screening and identify GATAD2B as a driver of tumor growth and metastasis in KRAS-driven lung cancer.

Building on the known role of BMP signalling in implantation, the authors define the role of uterine ACVR2A and ALK3 (via SMAD1/5) in vivo in regulating murine endometrial receptivity and embryo implantation.

Collagen is a dynamic component of both the tumor and metastatic niche. Here, the authors show that airway smooth muscle cells are a collagen III rich niche bladder cancer cells expressing CD167a, and Stat3 is a downstream target for abrogating  these collagen III/CD167a-driven metastatic foci.

Wounding induces changes in cell identity but the mechanisms regulating this are unclear. Here, the authors show that Sox11/Sox4 expression in the leading edge of wounds converts murine epidermal cells to an embryonic-like state and facilitates repair.

The nature of astrocyte diversity in the adult brain has remained poorly defined. The authors identify five astrocyte subpopulations in the brain that exhibit extensive molecular and functional diversity. They uncover correlative populations in malignant glioma, providing insight into how diverse astrocyte populations contribute to synaptogenesis, tumor pathophysiology and neurological disease.

Matthew Law, Mark Iles and colleagues report the results of a large-scale genome-wide meta-analysis of cutaneous malignant melanoma. They confirm previously reported association signals and identify five new susceptibility loci, with associated variants mapping within putative melanocyte regulatory elements.

Melanocytic nevus count is associated with melanoma risk. In this study, a meta-analysis of 11 nevus GWAS studies identifies novel SNPs in KITLG and 9q32, and bivariate analysis with melanoma GWAS meta-analysis reveals that most nevus genes affect melanoma risk, while melanoma risk loci do not alter the nevus count.

Using human bladder cancer xenograft models, a new mechanism involving an active proliferative response of cancer stem cells to chemotherapy-induced damage is shown, driven by prostaglandin E₂ (PGE₂) release in a manner similar to PGE₂-induced wound repair; pharmacological inhibition of the PGE₂/COX2 axis by celecoxib attenuates chemoresistance, suggesting a possible adjunctive therapy for bladder carcinomas.

Demonstration that SMAD2/3 regulate regeneration and differentiation of the endometrium in a manner important for suppression of endometrial carcinogenesis.