Volume 18 Issue 12, December 2018

Albrengues et al. have characterized a mechanism by which sustained lung inflammation can cause a switch from cancer dormancy to metastasis through the induction of neutrophil extracellular traps.

Ye et al. show that leukaemia cells induce insulin resistance in the host to limit glucose consumption by healthy tissues, thereby augmenting the amount of available glucose for cancer growth.

Orlando et al. and Ruella, Xu, Barrett et al. identified distinct mechanisms of resistance to anti-CD19 chimeric antigen receptor (CAR) T cell therapy in relapsed leukaemia patients, based on loss of CD19 surface expression.

Song et al. show that in patients with ovarian cancer, intratumoural T cells and ascites-resident T cells experience endoplasmic reticulum stress triggered by activation of IRE1α–XBP1 signalling, leading to reduced antitumour activity.

Transcription elongation supported by the super elongation complex, and histone H3 lysine 9 methylation and gene repression by G9a mediate the oncogenic function of MYC.

Martincorena, Fowler et al. have characterized the mutational landscape of normal oesophageal tissue during ageing, which has provided important insights into early cancer development.

Therapy with live tumour-targeting bacteria represents a unique opportunity to address the limitations associated with molecularly targeted therapies and immunotherapies. In this Review, Zhou et al. discuss the benefits and challenges of this approach and outline advances in the engineering of bacteria, which have the potential to improve safety and efficacy.

This Review discusses the interdependencies of mTOR signalling and metabolism pathways in cancer and how metabolic reprogramming in response to changes in mTOR signalling and vice versa can sustain tumorigenicity. The authors highlight therapeutic opportunities when targeting metabolism and mTOR.

This Opinion describes cell-in-cell processes in cancer, providing insight into their functional purpose in tumour tissue. Entosis is a unique process in which cancer cells are actively invaded by other cells, conferring them a competitive advantage that may drive cancer evolution.

In this Opinion, Li et al. put forward the idea that there is a narrow window or ‘sweet spot’ in which oncogenic RAS signalling can promote tumour initiation in normal cells and present the evidence that RAS mutation patterns are the product of selection for optimal RAS mutations to achieve the ideal level of signalling.