Volume 12 Issue 7, July 2012

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

A new study identifies cancer-specific DNA-methylated genes the continued repression of which may be required for cell survival.

Liuet al. have identified MYC as a suppressor of metastasis, cell motility and invasion, and provide evidence that this newly uncovered role is dependent on the αv and β3 integrin extracellular matrix receptors.

Michael Yaffe and colleagues show that pretreatment with one targeted drug for a specific period of time can increase the sensitivity of triple-negative breast cancer cells to standard chemotherapy.

Two papers show that EPHA2 is a receptor for Kaposi's sarcoma-associated herpesvirus (KSHV) and is required for KSHV infection of endothelial cells.

Two papers have investigated the role of somatic mutations in prostate cancer and have looked more closely at the functional consequences of some of the most common alterations.

A screen for transcripts affected by the expression of the oncogeneBRAF^V600Ehas identified a long noncoding RNA as being crucial for melanoma cell migration.

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.

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

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

This Review discusses the links between the E3 ubiquitin ligase COP1 and cancer, as shown by mouse models and human tumour data. It describes the evidence for COP1 targeting both oncoproteins and tumour suppressor proteins for degradation, how these apparently contradictory data might be rectified and the therapeutic implications.

The bromodomain is a highly conserved motif found in proteins that interact with chromatin. Small molecules that inhibit bromodomain and extraterminal (BET) proteins have been described, and this Review examines these developments and discusses the implications for small molecule epigenetic targeting of chromatin networks in cancer.

This Opinion article discusses how alterations to epigenetic programmes during development (including in the uterus), which may arise from exposure to hormones, can increase the risk of developing metabolic diseases and cancer in adulthood.

All malignant cancers, whether inherited or sporadic, are fundamentally governed by Darwinian dynamics and consist of dynamically evolving clades of cells living in distinct microhabitats that almost certainly ensure the emergence of therapy-resistant populations. However, the principles of Darwinian dynamics also embody fundamental principles that can be used for the successful management of cancer.

Drug resistance is a common cause of treatment failure for HIV infection and cancer. Can HIV therapy provide a 'blueprint' for designing and validating patient-specific combination therapies in cancer?