Post-GWAS in prostate cancer: from genetic association to biological contribution
Post-GWAS in prostate cancer: from genetic association to biological contribution, Published online: 11 December 2018; doi:10.1038/s41568-018-0087-3This 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.
A year of ups and downs
A year of ups and downs, Published online: 10 December 2018; doi:10.1038/s41568-018-0093-5Cancer research and Nature Reviews Cancer have both experienced many highs and lows in 2018, and we look forward to what 2019 has in store.
The lung microenvironment: an important regulator of tumour growth and metastasis
The lung microenvironment: an important regulator of tumour growth and metastasis, Published online: 10 December 2018; doi:10.1038/s41568-018-0081-9In 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.
Regulatory networks in AML
Regulatory networks in AML, Published online: 06 December 2018; doi:10.1038/s41568-018-0092-6Assi 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.
Cytokinesis defects and cancer
Cytokinesis defects and cancer, Published online: 06 December 2018; doi:10.1038/s41568-018-0084-6This Review discusses the evidence that whole-genome duplication as a consequence of cytokinesis failure can contribute to tumorigenesis.
Immunosuppressive lymphatics, Published online: 06 December 2018; doi:10.1038/s41568-018-0091-7Lane 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.
A source of calcium
A source of calcium, Published online: 03 December 2018; doi:10.1038/s41568-018-0089-1Wang 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.
Cancer chromatin accessed
Cancer chromatin accessed, Published online: 28 November 2018; doi:10.1038/s41568-018-0088-2A 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.
Cooperation among cancer cells: applying game theory to cancer
Cooperation among cancer cells: applying game theory to cancer, Published online: 23 November 2018; doi:10.1038/s41568-018-0083-7This 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.
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.