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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.
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.
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.
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.
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 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.
This Review discusses the 2018 Catalogue of Somatic Mutations in Cancer (COSMIC) Cancer Gene Census (CGC), an expert-curated description of human cancer genes, which has recently been expanded to include functional descriptions of how each gene contributes to cancer.
This Review discusses how cells with stem cell characteristics often serve as the tumour cell of origin, as they are preferentially primed for transformation. Furthermore, the activation of stem cell programmes can be crucial for promoting cancer progression and therapy resistance.
This Review discusses the reprogramming of the urea cycle, the main metabolic liver pathway for nitrogen disposal, in cancer cells. The authors provide insight into the metabolic advantages and therapeutic opportunities stemming from urea cycle enzyme perturbations in cancer.
This Review discusses new insights into molecular mechanisms that link the dysregulation of polyamine metabolism with carcinogenesis and strategies for targeting this pathway for cancer therapy.
Cancer is ubiquitous in wildlife and is an increasing concern for endangered species. This Review discusses the impact of cancer on animal species and highlights how studying these effects could reveal shared mechanisms of cancer predisposition between animals and humans.
This Review discusses nutrient scavenging, a process by which cancer cells use macromolecules from their environment to fuel cell metabolism and growth even when nutrients are limiting.
In this Review, Di Virgilio et al. describe how extracellular ATP and P2 purinergic signalling can shape the tumour microenvironment to both promote and restrain tumour progression and outline the opportunities to harness nucleotide receptor signalling as an anticancer strategy.
In this Review, Hamidi and Ivaska discuss the contribution of integrins to the different steps of cancer progression, highlighting some of the recently identified unconventional roles of integrins and novel opportunities to target integrin signalling.
This Opinion provides insight into the potential of targeting the replication stress response in cancer and discusses the strategy of inhibiting ataxia telangiectasia and Rad3-related protein (ATR) and the need for reliable biomarkers to enable patient stratification.