Research Highlights in 2012

Two papers providein vivoevidence for plasticity of epithelial and mesenchymal transitions, showing that EMT reversion is required for metastatic outgrowth.

Joan Massagué and colleagues have found that epigenetic changes contribute to metastasis in clear-cell renal-cell carcinomas in which the tumour suppressor gene von Hippel–Lindau (VHL) is inactivated.

Using theDrosophila melanogastermidgut as a model of intestinal hyperproliferation, Julia Cordero, Owen Sansom and colleagues have identified non-cell-autonomous crosstalk among WNT–MYC, EGFR and JAK–STAT signalling pathways downstream of APC loss; importantly, this pathway may also operate in human colorectal tumours.

A sensitive method to detect and monitor glioblastomas through the analysis of microvesicles in the blood is reported inNature Medicine.

A new study shows how angiogenesis may be controlled by epsin proteins, the targeting of which can result in a tumour-suppressive form of angiogenesis.

The loss of a component of the transcriptional mediator complex MED12 is implicated in resistance to a number of targeted and standard chemotherapeutic agents.

Phospholipase D1 signalling may promote both tumour angiogenesis and metastasis through integrin-dependent pathways.

The activation of YAP is linked to the PI3K–mTOR regulation of cell size (growth) through the regulation of PTEN by the miR-29 family of microRNAs.

Two new studies published inCancer Cellcharacterize a context-dependent tumour suppressive role for the interleukin-like inflammatory protein TSLP.

Jenkins and colleagues identify a non-inflammatory role of TLR2 in gastric tumorigenesis.

Tavazoie and colleagues show that three microRNAs target apolipoprotein E, which is a suppressor of melanoma metastasis.

Editing of a microRNA (miRNA) is impaired in gliomas, and the non-edited and edited miRNAs have different gene targets, which promote and suppress invasive activity, respectively.

Inder Verma and colleagues provide evidence that, at least in mice, mature neurons and astrocytes can be transformed and can dedifferentiate to form gliomas.

A recent publication inNature Cell Biology indicates that the transcription factor ELF5 suppresses epithelial to mesenchymal transition and metastasis through repression of SNAI2.

A new study finds that metabolism might converge with epigenetic gene regulation to explain the context-dependent effects of the metabolite butyrate on colon cell proliferation.

Two groups have reported the discovery of small-molecule inhibitors of EZH2 that have the ability to selectively kill lymphoma cells with EZH2-activating mutations.

Three groups have used human trisomy 21 fetal liver cells or human trisomy 21 induced pluripotent stem cells (iPSCs) to examine the effects of trisomy 21 on the early stages of haematopoiesis.

An analysis of the structual binding and potency of vascular endothelial growth factor receptor (VEGFR) inhibitors indicates that the inclusion of interactions with the juxtamemebrane domain better reflects the efficacy of these drugs in renal cell carcinoma.

Mitochondrial defects in cells expressing oncogenic RAS^V12can induce surrounding cells to proliferate owing to effects on the Hippo pathway.

A new mouse model of adoptive cell transfer for the treatment of melanoma indicates that dedifferentiation of melanoma cells, driven by an inflammatory response, might have a role in resistance.