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'Tipping the balance' by Lara Crow, inspired by the Opinion on p747, which discusses poised epigenetic states as a mechanism of drug resistance in cancer.
This Comment article argues that we should more comprehensively study the biology of benign tumours, as this might provide crucial insights into our understanding of cancer biology and metastasis.
LeBleuet al. show that the metabolism of migratory and circulating tumour cells is different to that of primary tumour cells and this difference enables migration and metastasis.
Wanget al. show differential requirements for the glycolytic enzymes pyruvate kinase M2 and lactate dehydrogenase A in maintaining haematopoietic stem cells and progenitor cells. Although this difference does not seem to apply to leukaemias derived from these two different cell populations, leukaemia cells are more sensitive to glycolysis inhibition than normal cells.
Several tumour-promoting roles of cathepsin Z (CTSZ) in pancreatic neuroendocrine tumours (PanNETs) depend on its RGD motif, and CTSZ derived from tumour cells or tumour-associated macrophages has different functions.
Chenet al. have shown that growth of isocitrate dehydrogenase 1 (IDH1)-mutant gliomas is promoted by expression of glutamate dehydrogenase 2 (GLUD2) protein.
Reactive oxygen species (ROS) are generated through various mechanisms. Accumulating evidence indicates that these moieties have important roles in promoting tumorigenesis and tumour progression; modulating the redox balance could be a strategy in targeting cancer.
Survival for patients with metastatic or relapsed osteosarcoma has remained virtually unchanged during the past 30 years, and new therapeutic options are needed. This Review discusses normal bone biology relevant to osteosarcoma, including the immunobiology of bone, model systems for studying osteosarcoma, genetic and genomic studies on germline predisposition and tumour landscapes, and recent clinical trials.
The Janus kinases (JAKs) are major activators of signal transducer and activator of transcription (STAT) proteins, and this signalling axis is crucial for cancer development in both tumour cells and the tumour microenvironment. This Review discusses the new roles of JAK–STAT signalling in promoting cancer through inflammation, obesity, stem cells and the pre-metastatic niche, and the potential therapeutic strategies that these roles can offer.
Brownet al. argue that epigenetic heterogeneity leads to therapeutic resistance, such that bivalently marked gene promoters result in epigenetically poised gene expression that can become fixed by exposure to therapy. What are the opportunities to target this proposed mechanism of therapeutic resistance?
Cancer cachexia is a multifactorial syndrome that affects many cancer patients and that leads to substantial weight loss, primarily from loss of skeletal muscle and body fat. This Opinion article focuses on the molecular mechanisms underlying cancer cachexia, in hopes that a better understanding of these might lead to improved therapeutic approaches.
