Volume 20 Issue 9, September 2020

Using a rapid mass-spectrometry based approach to analyse aerosol released during surgical cauterization of tumour tissue, Koundouros et al. derived metabolic signatures associated with the tumour genotype. Based on these signatures, they identified a new mechanism by which oncogenic PI3K signalling promotes tumour growth.

Aitken et al. have used mutagen-induced liver tumours to trace individual strands of the DNA double helix to which damage occurred and correlate this with mutational patterns to inform upon tumour evolution.

This Review discusses the emerging dual role played by neutrophils in the tumour microenvironment as part of tumour-promoting inflammation, while also mediating antitumour immune responses, and suggests that neutrophil function could be manipulated in myeloid cell-based therapeutic approaches to improve patient outcomes.

This Review discusses recent advances in cohesin biology in cancer, providing insights into the role of cohesin inactivation in cancer pathogenesis and opportunities for exploiting these findings for the clinical benefit of patients with cohesin-mutant cancers.

This Review discusses our current understanding of adaptive and innate immune cell metabolism in the context of the tumour microenvironment, providing insight into the interaction of cancer cell metabolism and immune metabolism, as well as the potential for leveraging metabolic vulnerabilities to enhance the antitumour immune response.

This Perspective advocates the study of tumour predisposition syndromes as an opportunity to better identify gene–environment interactions that influence cancer risk. Understanding syndrome-associated molecular mechanisms may provide new and more effective ways to prevent exposure-associated cancers in the general population.