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Ubiquitin ligases (E3s) participate in many cellular processes, including cell cycle progression and cell death. This Review by Senftet al. discusses how deregulation of E3s can lead to tumorigenesis and highlights the opportunities for targeting E3s as an anticancer therapy.
Inactivating mutations in the tumour suppressor geneTP53are frequent in cancer. This Review provides a critical overview of reactivating p53 as a therapeutic strategy, describing preclinical and clinical compounds that re-establish the functions of wild-type p53 in tumours.
Field cancerization underlies the development of many types of cancer. This Review examines the biological mechanisms that drive the evolution of cancerized fields and discusses how measuring field evolution could improve cancer risk prediction in patients with pre-malignant disease.
Small-cell lung cancer is an aggressive form of lung cancer and has been difficult to treat due to therapy resistance. This Review discusses challenges and recent advances in uncovering molecular changes that allow potentially efficient therapies.
This Review by Dewhirst and Secomb describes the current understanding of drug transport to tumour cells and the progress that has been made in developing methods to enhance drug delivery.
The adenosinergic pathway is a major immunosuppressive mechanism in the tumour microenvironment. In this Review, Vijayanet al. discuss how targeting components involved in the generation and downstream signalling of extracellular adenosine represents an attractive novel cancer therapy.
Non-coding RNAs (ncRNAs) are functional molecules that regulate physiological programmes in developmental and disease contexts. This Review article discusses the complex networks of interactions that ncRNAs engage in and how these confer oncogenic or tumour-suppressive effects in cancer.
Sphingolipids, specifically ceramide and sphingosine-1-phosphate, have opposing roles in regulating cancer cell death and survival, respectively. This Review discusses the mechanistic and clinical studies of sphingolipid signalling and metabolism in cancer, highlighting current and emerging therapeutic strategies to target these bioactive lipids.
Despite advances in targeting oncogenic driver mutations, advanced-stage non-small-cell lung cancer (NSCLC) remains largely incurable due to therapeutic resistance. This Review focuses on how understanding the mechanisms of resistance to targeted therapies in NSCLC can inform improved treatment strategies.
This Review by Mitchellet al. summarizes how engineering and the physical sciences have advanced oncology by highlighting four important areas: the physical microenvironment of the tumour, drug delivery, cellular and molecular imaging, and microfluidics and microfabrication.
Genome-wide association studies (GWAS) uncover the impact of genetic variation on the risk of many common cancers. This Review discusses current insights and how understanding the biological basis of these associations is required to maximise the clinical benefit of GWAS.
Several types of human tumour are dependent on mutations in BRAF. This led to the development of RAF inhibitors, which prolong patient survival but are limited by resistance. This Review discusses the recent advances in our understanding of BRAF oncogenic signalling, RAF inhibitor activity and the implementation of this knowledge for the development of next-generation inhibitors.
This Review by Corbet and Feron summarizes recent data showing that tumour acidosis influences cancer metabolism and contributes to cancer progression; it also highlights advances in therapeutic modalities aimed at either inhibiting or exploiting tumour acidification.
Metaplasia, the replacement of one differentiated somatic cell type with another in the same tissue, is a precursor to dysplasia and eventually carcinoma. There are shared principles across different types of tissue metaplasia that may be helpful in clinical considerations.
Understanding how high-risk multiple myeloma evolves from more therapeutically tractable stages is crucial for improving outcomes for patients. This Review discusses the evolution of high-risk disease, how it may be diagnosed and how this might improve treatment.
Therapy-related myeloid neoplasms occur as a late complication following chemotherapy and/or radiotherapy administered for a primary condition. In this Review, McNerneyet al. discuss recent studies that have improved our understanding of the aetiology of this disease.
Autophagy is a process that delivers cytoplasmic components to lysosomes for degradation. This Review discusses clinical interventions to target autophagy in cancer and explains how understanding the context-dependent role of autophagy in cancer should dictate future clinical trial design.
Our understanding of mesothelioma pathobiology has increased dramatically in the past 5 years, with an improvement in our knowledge of mesothelioma genetics, epigenetics, tumour microenvironment and immunobiology. This Review discusses these advances and how they might affect therapeutic strategies.
This Review discusses the extrinsic regulation of angiogenesis by the tumour microenvironment, highlighting potential vulnerabilities that could be targeted to improve the applicability and reach of anti-angiogenic cancer therapies.
This Review describes our current understanding of the relationship between genotype and phenotype in myelodysplastic syndromes/myeloproliferative neoplasms (MDS/MPN) and discusses how this knowledge could be used to inform strategies to develop more effective treatments and improve clinical success.
