Genome sequencing analysis dissects the origins and evolution of cancer transmission between clam species in the Seas of Southern Europe.

SPOP mutations underlie a novel, genomically unstable subclass of prostate cancer by altering DNA repair.

Copy number alteration heterogeneity exists in many shapes and forms in breast cancer genomes and single-cell genomics is a powerful tool to further our understanding of its nature and significance.

Partial copy loss of spliceosome genes are common non-driver gene dependencies in cancer.

Non-coding mutations in microsatellite-instable (MSI) colorectal tumors are prevalent and activate cancer-specific enhancers, thereby disrupting gene expression control.

A novel method predicts cancer and immune cell types from bulk tumor gene expression data with the ability to consider uncharacterized and possibly highly variable cell types, which is validated in human genome.

RNA-level regulation of gene expression is negatively associated with protein-level regulation across cellular pathways in normal tissues and cancer.

Deficiencies of several DNA damage response genes can be predicted by their association with genome-wide mutation patterns.

The absence of negative selection observed in most cancer genomes can be explained by the intrinsic genome-wide linkage in somatic evolution and creates a substantial proteotoxic load.

A comprehensive package for pedigree-based risk modeling, with a highly optimized computational back-end, extends existing models beyond syndrome-specific approaches and incorporates data from panel studies by allowing for an arbitrary number of gene and syndrome associations.