Volume 7 Issue 6, June 2007

Three major tumour-suppressor proteins have recently been shown to undergo monoubiquitylation-mediated nuclear–cytoplasmic shuttling. Can our increasing knowledge of this mechanism be used to treat cancer?

This article reviews how the identification of Snail, ZEB and some basic helix–loop–helix (bHLH) factors as inducers of epithelial–mesenchymal transition (EMT) and potent repressors of E cadherin expression has opened new avenues for cancer research with potential clinical implications.

Metastatic capacity appears to be an inherent feature of breast tumours. In this context, the cofilin pathway has been identified as a major determinant of metastasis and, as discussed in this Review, studies indicate that the overall activity of the cofilin pathway determines the invasive and metastatic phenotype of tumour cells.

What leads to the incurable advanced phase of chronic myeloid leukaemia (CML)? This Review explores the mechanisms that underlie differentiation arrest, genomic instability and loss of tumour-suppressor function, which seem to drive the progression to blast crisis in CML and might help to identify new therapeutic targets. These findings can potentially be translated to other tumours that progress through similar mechanisms.

Nucleic acids and regulatory proteins are compartmentalized in microenvironments within the nucleus. These precise arrangements can be distrupted in cancer cells. How can we measure these changes and what might they tell us about cancer development and treatment?

We are all familiar with the concept of morphogens instructing tissue architecture during development, but how are tissue form and function maintained in the adult, and does this have a bearing on tumorigenesis?

Angiogenesis inhibitors are now being used in the treatment of patients with cancer. However, these agents can lead to toxicities. This Perspective discusses these toxicities and the possible molecular mechanisms behind them.