Stress management in T cells
Stress management in T cells, Published online: 19 November 2018; doi:10.1038/s41568-018-0082-8Song 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.
N6-mA marks the spot
<i>N</i><sup>6</sup>-mA marks the spot, Published online: 19 November 2018; doi:10.1038/s41568-018-0085-5Xie et al. have shown that a recently reported DNA modification in mammals, repressive N6-methyladenine, is enriched in human glioblastoma and targeting this modification can reduce cancer cell growth by restricting chromatin accessibility at oncogenic loci.
Dividing paths in fatty liver disease
Dividing paths in fatty liver disease, Published online: 19 November 2018; doi:10.1038/s41568-018-0086-4Grohmann, Wiede et al. report that obesity-associated nonalcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC) can be driven by independent pathways. In particular, HCC can be driven by STAT3 signalling, independently from STAT1-driven NASH.
mTOR signalling and cellular metabolism are mutual determinants in cancer
mTOR signalling and cellular metabolism are mutual determinants in cancer, Published online: 13 November 2018; doi:10.1038/s41568-018-0074-8This 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.
Cell-in-cell phenomena in cancer
Cell-in-cell phenomena in cancer, Published online: 12 November 2018; doi:10.1038/s41568-018-0073-9This 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.
A model for RAS mutation patterns in cancers: finding the sweet spot
A model for RAS mutation patterns in cancers: finding the sweet spot, Published online: 12 November 2018; doi:10.1038/s41568-018-0076-6In 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.
Colony takeover, Published online: 12 November 2018; doi:10.1038/s41568-018-0080-xMartincorena, Fowler et al. have characterized the mutational landscape of normal oesophageal tissue during ageing, which has provided important insights into early cancer development.
Tumour-targeting bacteria engineered to fight cancer
Tumour-targeting bacteria engineered to fight cancer, Published online: 07 November 2018; doi:10.1038/s41568-018-0070-zTherapy 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.
Ageing matrix promotes metastasis
Ageing matrix promotes metastasis, Published online: 02 November 2018; doi:10.1038/s41568-018-0079-3Two studies from Ashani Weeraratna’s group have examined how changes in the skin microenvironment associated with ageing promote melanoma metastasis and modify immune infiltration.
Sabotaging the host
Sabotaging the host, Published online: 01 November 2018; doi:10.1038/s41568-018-0078-4Ye 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.
MYC in elongation and repression
MYC in elongation and repression, Published online: 31 October 2018; doi:10.1038/s41568-018-0077-5Transcription elongation supported by the super elongation complex, and histone H3 lysine 9 methylation and gene repression by G9a mediate the oncogenic function of MYC.
Waking up in a trap
Waking up in a trap, Published online: 25 October 2018; doi:10.1038/s41568-018-0071-yAlbrengues 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.
CAR antigens beyond recognition
CAR antigens beyond recognition, Published online: 25 October 2018; doi:10.1038/s41568-018-0075-7Orlando 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.
Publisher Correction: Engineering and physical sciences in oncology: challenges and opportunities
Publisher Correction: Engineering and physical sciences in oncology: challenges and opportunities, Published online: 18 October 2018; doi:10.1038/s41568-018-0072-xPublisher Correction: Engineering and physical sciences in oncology: challenges and opportunities
Fasting and cancer: molecular mechanisms and clinical application
Fasting and cancer: molecular mechanisms and clinical application, Published online: 16 October 2018; doi:10.1038/s41568-018-0061-0This Opinion discusses the potential of fasting and fasting-mimicking diets to help overcome toxicities induced by anticancer therapy. The differential response of normal and cancer cells undergoing starvation is argued to make normal cells less sensitive to therapy-induced toxicity, while cancer cells become more sensitive to therapy-induced cell death.
Back to the beginning to understand metastasis
Back to the beginning to understand metastasis, Published online: 15 October 2018; doi:10.1038/s41568-018-0069-5Yang et al. have used genetically engineered mouse models of small cell lung cancer to show that the same genomic alterations in different cells of origin lead to the formation of tumours that follow distinct evolutionary paths to metastasis.
SPOP mutations disrupt phase separation
SPOP mutations disrupt phase separation, Published online: 11 October 2018; doi:10.1038/s41568-018-0066-8SPOP mutations disrupt phase separation
New targets for cancer immunotherapy
New targets for cancer immunotherapy, Published online: 11 October 2018; doi:10.1038/s41568-018-0067-7New targets for cancer immunotherapy
Oncogenic mRNA modification explained
Oncogenic mRNA modification explained, Published online: 11 October 2018; doi:10.1038/s41568-018-0068-6Oncogenic mRNA modification explained
BETting on YAP–TAZ
BETting on YAP–TAZ, Published online: 09 October 2018; doi:10.1038/s41568-018-0065-9Two papers recently published in Nature Medicine and Science Signaling highlight the various interdependent or independent ways by which YAP and TAZ can affect tumour growth.