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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.
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.
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 paper inNaturedescribes a highly specific and potent small molecule inhibitor of MCL1 that has single-agent activity and good tolerability in several cancer models.
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.
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.
In this Review, Zitvogelet al. describe the mouse models of transplantable, carcinogen-induced and genetically engineered tumours that have laid the foundations of oncoimmunology.
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.
This Timeline article describes the discovery of the Epstein–Barr virus and summarizes the key advances in the field that have led to our current understanding of the role this virus plays in a number of different lymphoid and epithelial malignancies.
In this Opinion article, the authors propose that the function of Polycomb repressive complex 2 (PRC2) in maintaining, rather than specifying, transcriptional repression can explain its seemingly contradictory roles in cancer.