Articles in 2017

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.

Vitamin C supplementation has shown limited benefits in patients with solid tumours. Two studies report that vitamin C supplementation can reduceTet-dependent leukaemia progression in mice, supporting the concept of high-dose vitamin C supplementation in certain patients with haematological malignancies.

Although speckle-type POZ protein (SPOP) is the most frequently mutated gene in primary prostate cancer, its therapeutic implications are incompletely understood. Now, three studies describe mechanisms of resistance to bromodomain and extraterminal (BET) protein inhibitors in SPOP-mutated prostate cancer.

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.

Both obesity and systemic inflammation promote cancer progression, although how obesity-associated inflammation affects cancer metastasis is poorly understood. Quailet al. now show that obesity induces cytokines that stimulate lung neutrophilia in mice, thereby promoting breast cancer metastasis.

Reporting inNature, the team led by Haining has identified that deletion of Ptpn2, among other genes, in tumour cells makes them more susceptible to PD1 inhibitors.

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.

In this Opinion article, Baslan and Hicks discuss how single-cell sequencing could be used to advance our understanding of tumour biology and genetics, in addition to translational applications in the clinic.

Since mesenchymal-like properties in cancer cells are often associated with therapy resistance, Viswanathanet al. explored vulnerabilities of these cells. They identified an enzyme of the lipid peroxidase pathway, inhibition of which caused ferroptosis in a range of cancer types.

A new study has looked at the evolutionary origins of lymphatic and distant metastases in human colorectal cancer and found that, in most cases, cancer spread to lymph nodes is not a precursor for seeding of cancer cells to other organs.

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.

Shafferet al. analysed resistance in melanoma at the single-cell level and found that non-genetic, transcriptional variability in rare cells can predict the eventual emergence of drug resistance.

Van Groningenet al. unravel the epigenetic nature of intratumoural heterogeneity in neuroblastoma, which comprises both lineage-committed adrenergic cells and undifferentiated mesenchymal cells that are defined by unique super-enhancer transcriptional networks and gene expression signatures.

Neutrophils carrying liposomes that contain the antimitotic drug paclitaxel can penetrate the brain and suppress the recurrence of glioma in mice, thereby significantly improving survival.