Articles in 2016

Two studies have revealed two possible mechanisms that might explain why VEGF inhibition can be rendered ineffective

Two papers examine the influence of different stem cell characteristics on tumorigenesis in an organ-specific and age-associated manner, continuing the debate on the influence of intrinsic and extrinsic factors on cancer risk.

An analysis of pancreatic ductal adenocarcinoma genomes indicates that many of these tumours undergo polyploidization and chromothripsis, leading to rapid acquisition of genetic changes required for tumour progression.

A subset of cancer cells is dependent on a large, stable multi-protein complex called the epichaperome for survival under conditions of stress.

This Review summarizes progress in applying nanotechnology to cancer treatment and discusses the challenges of clinical translation and opportunities to develop more effective nanotherapeutics through our increasing understanding of tumour biology and nano–bio interactions.

This Review discusses the molecular processes and clonal evolution that lead to myelodysplastic syndrome (MDS) and secondary acute myeloid leukaemia, highlighting the ways in which these insights are shaping the clinical management of MDS.

Daillèreet al. have identified two bacterial species that mediate systemic and tumour-infiltrating T cell responses associated with the antitumour efficacy of the chemotherapy drug cyclophosphamide.

Boice, Salloum, Mourcinet al. show that HVEM is an important tumour suppressor in lymphomas and that direct delivery of a soluble HVEM peptide using engineered T cells might be therapeutically beneficial.

In this Timeline article, Aasenet al. look back over 50 years of research linking gap junctions and connexins to cancer, highlighting the conditional nature of their role in cancer progression, future challenges and therapeutic strategies.

Two studies have looked at the roles of fatty acid synthesis and oxidation, and their therapeutic potential, in cancer.

Cell differentiation blockade in the early stages of AML can be overcome by inhibiting dihydroorotate dehydrogenase

Brand and colleagues show that increased tumour lactate dehydrogenase A (LDHA)-mediated lactic acid production dampens activation and cytokine production of infiltrating T and natural killer (NK) cells allowing tumours to escape immune detection and promoting tumour growth.

Mayers, Torrenceet al. show that lung tumours driven by oncogenic KRAS and loss of p53 depend on branched-chain amino acid metabolism, whereas pancreatic tumours driven by the same genetic defects do not.