Volume 12 Issue 2, February 2012

Whole-genome sequencing indicates few genetic changes in retinoblastoma and hints at epigenetic changes instead.

Regulation of a splicing factor kinase by the Wilms' tumour suppressor WT1 contributes to alternative splicing ofVEGFA.

Cancer cells target active SRC for autophagy when SRC signalling is deregulated through the loss of focal adhesion kinase.

Two papers indicate the importance of TAZ in cancer biology.

A recent study proposes a new drug combination strategy to target drug-resistant chronic myeloid leukaemia.

The primary role for small nucleolar RNAs (snoRNAs) has typically been considered to be the guiding of the post-transcriptional modifications of particular RNAs. This Progress article discusses the intriguing recent findings that various snoRNAs, and the host genes that encode them, could have previously unsuspected and varied roles in cancer.

Signalling through the receptor tyrosine kinase MET and its ligand hepatocyte growth factor/scatter factor (HGF/SF) has been associated with various types of cancer, which has led to numerous efforts to try and target these proteins. This Review discusses HGF/SF–MET signalling in cancer and current progress with targeting this pathway.

Alkylating agents can both induce tumorigenesis and be used to treat cancer patients. However, responses to alkylating chemotherapeutic drugs are variable. This Review discusses the molecular responses to alkylating agents and the causes for such variation.

Nuclear factor-κB (NF-κB) has many functions in cancer, hence the need for drugs that can modulate its activity. In order to achieve this, Neil D. Perkins argues that the complex roles of the individual NF-κB subunits must be considered.

There is increasing debate about what is meant by the term 'cancer stem cell' (CSC) and the degree to which the concept of CSCs can provide insights into cancer biology and therapy. This Timeline article traces the historical milestones in normal and cancer stem cell biology as a backdrop to a discussion of how these fields have informed each other.

Although mouse models have improved our understanding of cancer biology, their inbred nature does not accurately model the inherited variability in human populations that can influence cancer susceptibility and outcomes. This Opinion article discusses how inherited variability influences cancer phenotypes, how it can confound experiments and how it can be exploited to reveal new truths about cancer biology.