Identifying 1,907 mitochondrial somatic mutations from 1,675 tumor tissues provides new insights into the causes and effects of the mitochondrial genome mutations found in human cancers.

Different types of epigenetic DNA modifications affect the likelihood of cytosine mutations in cancer.

A new statistical approach identifies non-coding regulatory regions of genes as driver candidates with recurrent mutations across cancer samples that associate with gene expression, patient survival or mutational phenotype.

Two common mutant versions of estrogen receptor alpha achieve constitutive activity and hormone-resistance by preferentially adopting a suite of conformations that expose the coregulator-binding surface.

The reanalysis of data from a recent study that claimed retrotransposon mutations are ubiquitous in the human brain outlines a general framework for the design and analysis of single-cell genomics studies.

A distinct class of kidney tumors is characterized not by patterns of somatic mutations, but by a distinct metabolism.

Cancer is a consequence of the release of basal cellular functions inherited from our unicellular ancestors from the control of regulatory networks that evolved during the emergence of multicellularity.

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

Bazedoxifene's SERD activities enable it to resist the impact of activating ESR1 mutations in breast cancer.