Cancer epigenetics articles from across Nature Portfolio

Song et al. report that ATM maintains replication fork speed by counteracting chromatin-bound cGAS-induced fork slowing. They show that ATM and ATR phosphorylate MRE11 to release cGAS from chromatin in a process dependent on MRE11 nuclease activity.

Transcriptomic and proteomic data help clarify the functional effects of inherited structural variation in cancer. Here, the authors integrate germline structural variants with tumor proteomics across 1,637 patients spanning 11 tumor types and show that a subset of variants alters protein levels, contributing to molecular diversity across cancers.

The regulatory mechanisms that drive oncogene expression in gliomas remain poorly understood. A study now identifies a role for widespread rearrangements of the enhancer connectome. Such rearrangements are linked to known genetic risk variants, revealing how genetic predisposition contributes to malignancy.

Adipocytes can be isolated, genetically manipulated, and then reimplanted. In this study, these properties were leveraged to engineer adipocytes that can outcompete tumors for essential metabolic resources. In mouse cancer models, these adipocytes suppressed tumor growth, demonstrating a novel cancer therapy termed adipose manipulation transplantation (AMT).