Research Highlights

Looking at the effects of proteins encoded by DNA tumour viruses on the host genome could aid the interpretation of high-throughput sequencing data from cancer samples.

A recurrent oncogenic fusion of fibroblast growth factor receptor (FGFR) and transforming acidic coiled-coil (TACC) proteins in a subset of glioblastomas can directly interfere with cell division and induce aneuploidy, and this can be inhibited by FGFR kinase inhibitors.

Tumour cell-derived miRNAs carried in microvesicles can communicate with endothelial cells to activate angiogenesis through Janus kinase (JAK)–signal transducer and activator of transcription (STAT) signalling.

A new study uncovers a tumour suppressor role for SHARP1.

Stimulation of the sympathetic nervous system through prolonged emotional stress might increase bone metastases in patients with breast cancer owing to effects on the bone marrow microenvironment.

Blocking vascular endothelial growth factor (VEGF) can promote the invasive growth of glioblastoma through a mechanism that involves MET and VEGF receptor 2.

A new study shows that a catalytic DNA molecule might be an effective and safe treatment for some forms of skin cancer.

Joan Massagué and colleagues have identified a paracrine signalling network between tumour and stromal cells in breast cancer that seems to drive both metastasis and resistance to chemotherapy.

Three papers show that hepatocyte growth factor (HGF)–MET signalling is an important determinant of therapeutic responses and can be induced through paracrine, autocrine and endocrine production of HGF.

A paper published inNature Physicshas experimentally and mathematically modelled epithelial cell migration and identified mechanically generated waves that are important for cellular motility.

Two papers show that KRAS-G12D-transformed pancreatic tumour cells produce GM-CSF, which recruits MDSCs to promote an immunosuppressive microenvironment.

Arul Chinnaiyan and colleagues have attempted to map the position of pseudogenes that are expressed throughout the genome.

Wigard Kloosterman, Edwin Cuppen and colleagues have evidence that chromothripsis might arise owing to clustered DNA double-strand breaks (DSBs) and nonhomologous repair mechanisms.

Knockout of the Notch effectorRbpjkin mesenchymal fibroblasts enhances the formation of squamous cell carcinomas of the skin in mice, and similar changes can be induced by exposure of human skin to ultraviolet A irradiation.

Anin vivoshort hairpin RNA screen identifies tumour suppressor genes in commonly deleted regions in lymphoma.

Recently published papers using massively parallel sequencing to look at mutations in breast cancer provide food for thought.

A new study shows that a clinically approved drug might selectively target cancer stem cells for differentiation.

This paper suggests that recurrent regions of somatic hemizygosity might exist in tumours because they enable a reduction in the expression levels of genes that restrict cell proliferation and survival, and minimize the loss of genes that are essential for cell survival.

Peinado and colleagues find that exosomes produced by tumour cells can mediate premetastatic niche formation.

Gordenin and colleagues analyse the clustering of mutations in cancer genomes and identify a subfamily of APOBECs as a possible cause of mutation clustering.