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'Teamwork' by Lara Crow, inspired by the Reviews on p457 and p473, which discuss combinations of immunotherapies and subclonal cooperation in a heterogeneous tumour, respectively.
Most patient-derived tumours grown subcutaneously as xenografts do not metastasize, but metastasis can occur if intact tumour tissue is orthotopically implanted. This Comment argues that these orthotopic xenografts therefore better mimic patient tumours.
A paper inNatureidentifies glypican 1 as a marker of circulating exosomes derived from pancreatic ductal adenocarcinoma (and from some breast cancers) that could be an effective biomarker for early diagnosis and treatment monitoring.
Inducible short hairpin RNA (shRNA)-mediated silencing of adenomatous polyposis coli (Apc) in the intestines of mice has revealed that APC loss is crucial for tumour maintenance even in the presence of other oncogenic mutations, and that re-expression of APC can restore normal crypt homeostasis.
A paper published inMolecular Cell indicates that the production of ketones can promote the BRAFV600E–MEK–ERK oncogenic pathway and identifies a potential Achilles' heel.
Mohammedet al. have examined the functional interactions between oestrogen receptor-α (ERα) and progesterone receptor (PR) in mouse and human breast tumours. They found that activation of PR changes the pattern of ERα chromatin binding, resulting in the expression of antiproliferative genes.
Immunotherapy has undoubtedly become an effective treatment for many cancers, but how can we make the most of this approach? In this Review, Meleroet al. discuss how immune-targeted therapies can be synergistically combined to provide maximal benefit to patients.
Although most cancers exhibit some degree of intratumour heterogeneity, we are far from understanding the dynamics that operate among subclonal populations within tumours. This Review discusses the growing evidence that cooperative behaviour of tumour subclones can influence disease progression.
Obesity is associated with increased (and occasionally decreased) risk of developing several types of cancer. This Review discusses the epidemiological evidence available for, and the possible mechanisms that might lead to, this altered risk.
In this Opinion article, Brocket al. analyse how intrinsic variability in gene expression in proliferating cells, as well as microenvironmental signals, can drive cells to transform into a neoplastic state or revert to a normalized state.
