Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
'Obstructive environment' by Lara Crow, inspired by the Review on p409, which discusses how resistance to radiotherapy is mediated by the tumour stroma.
Coxet al. have shown that metastasis of certain breast cancers to bone can be driven by the enzyme lysyl oxidase (LOX), which induces bone lesions that provide a landing site for circulating tumour cells.
Zhuet al. find that the homing of multiple myeloma cells to the bone marrow is promoted by cyclophilin A–CD147 signalling between bone marrow endothelial cells and myeloma cells.
Two recent studies add to the evidence supporting an important role for extracellular vesicles in promoting metastasis and provide a new technique for analysing these vesiclesin vivo.
The CRISPR–Cas9 (clustered regularly interspaced short palindromic repeats–CRISPR-associated 9) system provides many avenues for improving how we generate models of cancer. This system has numerous uses, including providing a means to understand the importance of genetic alterations as a tumour evolves, and CRISPR–Cas9 may potentially constitute a therapeutic strategy in the future.
Three papers now present different aspects of a similar story: altered splicing can lead to myelodysplastic syndrome (MDS) and even to progression to acute myeloid leukaemia (AML).
'Cellular senescence' has been broadened to describe durable states of proliferative arrest induced by disparate stress factors. This Review discusses the limitations of senescence-associated biomarkers and provides suggestions for how to improve the phenotypic description of senescence.
In this Review, Barker and colleagues describe the mechanisms of radioresistance that are mediated by the tumour stroma and explore how these mechanisms can be targeted to improve radiotherapy responses.
This Review discusses what we have learned about the biology of rhabdomyosarcoma using various model systems, and how these models might be used to discover new targetable pathogenic mechanisms.
Inborn errors of metabolism are inherited monogenic disorders caused by mutations in genes encoding metabolic enzymes that can result in malignancy. This Opinion article discusses how studying these rare diseases might provide insight into how specific metabolic changes contribute to cancer initiation, development, diagnosis and treatment.
