Inactivation of a multifunctional RNA-binding protein can lead to the acquisition of pro-metastatic phenotypes, possibly by stabilizing large-scale transcriptomic changes that provide a selective advantage during cancer progression.

Genetic mouse models and human cell lines show that Musashi proteins promote an epithelial/luminal state and inhibit epithelial–mesenchymal transition (EMT), and genome-wide maps of translational regulatory targets connect Musashi proteins to an epithelial alternative splicing program and to the regulation of EMT.

In isogenically matched colorectal cancer (CRC) cell lines, mutant KRAS alters the composition of secreted miRNAs in extracellular vesicles that can then transfer repressive activity to wild type cells.

Arginine methylation regulates mRNA translation of key protooncogenes via an RGG/RG motif-containing protein called Aven.

The chemokine CXCL13 is critical to the development of air pollution- and tobacco smoke-induced lung cancers.

The functional relevance of stem cell niche perturbation in sarcomagenesis is defined and the mouse model presented provides a rationale for the use of combination therapy for the treatment of genetically heterogeneous sarcomas.

Proper gut health depends on the balance between two naturally occurring variants of a transcription factor in the colon.

EphrinB2 promotes glioblastoma stem-like cell malignancy through the interplay of cell-autonomous and non-cell-autonomous mechanisms and its targeting suppresses tumourigenesis in preclinical models of human glioblastoma.

GDC-0810 is a novel, orally bioavailable SERD that exhibits robust pre-clinical activity in models of ER+ breast cancer, including models of tamoxifen resistance, and those that express the ERα mutations, ER.Y537S and ER.D538G.