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Preview: Nature Reviews Cancer - Issue - science feeds

Nature Reviews Cancer - Issue - science feeds


Angiogenesis: Going with the flow


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

Tumorigenesis: Networking: a survival guide


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

Cancer risk: Generating tumours: it's all in the balance


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.

Tumour metabolism: RED(D1) or dead


Mathias Wenes and colleagues have studied metabolic changes in tumour associated macrophages (TAMs) and found that specific alterations of mTOR regulation through regulated in development and DNA damage response 1 (REDD1) results in defective blood vessel formation and increased metastasis.

Anticancer drugs: Breaking up a pro-survival interaction


A paper in Nature describes a highly specific and potent small molecule inhibitor of MCL1 that has single-agent activity and good tolerability in several cancer models.

Pancreatic cancer: Fast or slow?


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.

Lymphoma: Customized therapeutic delivery


Boice, Salloum, Mourcin et 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.

Tumour microenvironment: That gut feeling


Daillère et 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.

Metastasis: Caught in a trap


Neutrophils can capture and kill pathogens by releasing DNA and associated proteolytic enzymes into the extracellular space, forming structures known as neutrophil extracellular traps (NETs). Park et al. have shown that in the absence of infection, metastatic breast cancer cells can stimulate neutrophils to

Tumour metabolism: When metabolic and epigenetic states converge


Metabolic and epigenetic states in cells can be linked when intermediary metabolism generates substrates for chromatin regulation. Kottakis et al. have found that synergistic liver kinase B1 (LKB1) loss and KRAS activation can promote mTOR-mediated serine biosynthesis pathway dependency during pancreatic tumorigenesis. The subsequent

Tumour immunology: The consequences of concomitant challenges


Kohlhapp et al. found that acute influenza infection accelerates cancer-specific death of immunocompetent mice injected with B16 melanoma cells. Infection caused CD8+ T cells to move from the tumour to the site of infection, thus allowing increased tumour growth; this could be

Immunotherapy: Powerful combinations


Immunotherapies are not effective in all cancer patients, likely due in part to immunosuppressive networks in advanced tumours. Moynihan et al. found that combination immunotherapy consisting of four components (a tumour antigen-targeting antibody, extended half-life recombinant interleukin-2, a programmed cell death protein 1 (PD1)

Mouse models in oncoimmunology


Fundamental cancer research and the development of efficacious antineoplastic treatments both rely on experimental systems in which the relationship between malignant cells and immune cells can be studied. Mouse models of transplantable, carcinogen-induced or genetically engineered malignancies — each with their specific advantages and difficulties

Obesity promotes prostate cancer invasion


Nature Reviews Cancer16, 7010.1038/nrc.2016.129(2016)In the original version of this article the DOI number was incorrect. This error has been corrected in the HTML version of the article.

From Krebs to clinic: glutamine metabolism to cancer therapy


Nature Reviews Cancer16, 619–634 (2016)Reference 32 was incorrectly cited on page 626 and references 128, 129, 134 and 135 were incorrectly cited in Table 1. These have now been replaced with the correct references.

Gap junctions and cancer: communicating for 50 years


Fifty years ago, tumour cells were found to lack electrical coupling, leading to the hypothesis that loss of direct intercellular communication is commonly associated with cancer onset and progression. Subsequent studies linked this phenomenon to gap junctions composed of connexin proteins. Although many studies support

Epstein–Barr virus: more than 50 years old and still providing surprises


It is more than 50 years since the Epstein–Barr virus (EBV), the first human tumour virus, was discovered. EBV has subsequently been found to be associated with a diverse range of tumours of both lymphoid and epithelial origin. Progress in the molecular analysis of EBV

Maintaining cell identity: PRC2-mediated regulation of transcription and cancer


Enhancer of zeste homologue 2 (EZH2), the catalytic subunit of Polycomb repressive complex 2 (PRC2), has attracted broad research attention in the past few years because of its involvement in the development and maintenance of many types of cancer and the use of specific EZH2