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Lim et al. show that there is an association between germline genetic variants and the immune features of a tumour, and that genetic background might affect responses to immunotherapy.
Genomic instability in cancer models presents a major challenge in the design and reproducibility of research and its clinical translation. This Opinion article discusses the causes and consequences of intra-tumour genomic heterogeneity and instability in commonly used models and implications thereof.
This Review discusses how excessive signal transducer and activator of transcription 3 (STAT3) activation within cancer cells and cells of the tumour microenvironment can be viewed as a neoplastic mimic of an inflammation-driven repair response that promotes tumour progression.
New findings published in Nature Medicine highlight a role for the anti-CTLA4 antibody ipilimumab when combined with radiotherapy in treating metastatic NSCLC.
Two studies published in Cell have characterized the inhibitory immune receptor NKG2A expressed on cytotoxic lymphocytes, such as natural killer cells and CD8+ T cells, as a novel checkpoint for cancer immunotherapy.
This Review discusses causal germline variants in prostate cancer identified through genome-wide association studies (GWAS) and post-GWAS analyses. The latter are vital to identify causal variants and molecular mechanisms by which these variants promote prostate tumorigenesis, with potential clinical applications.
In this Review, Altorki et al. discuss how the tumour-reprogrammed lung microenvironment can contribute to primary lung tumour progression as well as lung metastasis from extrapulmonary neoplasms by promoting inflammation, angiogenesis, immune modulation and therapeutic responses.
Lane et al. have shown that interferon-γ (IFNγ)-mediated activation of the lymphatic vasculature, as a non-haematopoietic component of the tumour stroma, serves to limit local CD8+ T cell accumulation in melanoma in mice as a mechanism of immune suppression.
Assi et al. have generated multi-omics data on leukaemic blasts from acute myeloid leukaemia (AML) patients with defined genetic alterations. These data provide a comprehensive overview of the specific transcriptional and signalling networks in certain AML subtypes.
Wang et al. demonstrate that increased flux of calcium derived from osteogenic cells into cancer cells promotes early-stage bone colonization. Calcium signalling in cancer cells can be targeted by arsenic trioxide, thereby reducing bone metastasis progression.
A study in Science reports the genome-wide chromatin accessibility profiles across 23 cancer types from The Cancer Genome Atlas and notably increases the number of known gene regulatory elements.
This Opinion argues that understanding the interactions between cells that occur in tumours requires concepts from evolutionary game theory. Game theory can provide insights into the stability of cooperation among cells in a tumour and how this might be used therapeutically.
Grohmann, 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.
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.
Xie 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.
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.
Martincorena, Fowler et al. have characterized the mutational landscape of normal oesophageal tissue during ageing, which has provided important insights into early cancer development.
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.
