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

Breast luminal epithelial cells are the hotspots of aging-associated changes, which prime aged epithelia for oncogenic gene activation and may explain individual differences in breast cancer susceptibility due to the aging-associated increase in gene expression variances in luminal epithelia.

FOXM1 is co-expressed with its bidirectional gene partner RHNO1, and the two genes promote DNA repair, cell growth and survival, and chemotherapy resistance in ovarian cancer.

In contrast with earlier conclusions, negative selection has a major role in cancer evolution.

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.

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.

A novel Mendelian randomisation framework unravels one gene expression component, correlated with proliferation and genome stability-related features, associated with telomere length in lung adenocarcinoma tumours, which provides insights into how telomere length influences the genetic basis of lung cancer aetiology.

Transcription beyond annotated gene boundaries expands the diversity of the cancer transcriptome with overexpressed oncogenes and RNA chimeras.

Coregulators mediate selective interactions between DNA-bound androgen receptor and other transcription factors, which control distinct prostate cancer biology, suggesting disruption of critical interactions in these complexes as a novel therapeutic strategy.