Articles in 2011

A new phenomenon in which tens to hundreds of genomic rearrangements are acquired in one step has been identified.

The RAC-GEF PREX1 integrates signals from tyrosine kinase receptors and GPCRs to activate RAC1.

Experimental evidence suggests that platelets contribute to metastasis through adhesive and haemostatic functions that promote cancer cell survival, immune evasion and interactions with vascular cells to assist organ colonization from the bloodstream.

DNA polymerases have various roles from DNA replication to tolerating DNA damage through a process known as translesion DNA synthesis. This Review discusses the function of the DNA polymerase family and their possible roles in cancer.

Fundamental differences in the regulation of central metabolic pathways exist between tumours and normal tissue. This Review discusses how the Warburg effect is still applicable to our view of cancer metabolism and new advances in understanding beyond this hypothesis, including regulating anapleurosis and the redox balance.

The successful systemic therapy of advanced visceral metastatic disease remains a daunting challenge, but this therapeutic circumstance has rarely been modelled or studied preclinically. Strategies to develop models of advanced spontaneous metastasis in mice are discussed, and some of the results are summarized.

This Science and Society article discusses the major issues regarding cancer-related direct-to-consumer advertising (DTCA) and offers data from the United States as an illustration of communication inequalities in this arena — highlighting the need for closer and continuing attention to the issue of DTCA in the age of internet-based information and genomic revolution.

Medulloblastomas with a mutation in the Wnt pathway arise from cells that are distinct from those affected by mutations in the SHH pathway.

The Hippo pathway couples cell polarity complexes to extrinsic signalling pathways.

A new study identifies a regulatory mechanism controlling carbon source uptake.

Genes mutated in Wilms' tumours include oncogenes, tumour suppressor genes andWT1, which sometimes behaves as an oncogene and sometimes behaves as a tumour suppressor gene. This Review analyses, among other things, what it would take for WT1to fall into one or the other category.