In the absence of ROCK1 activation by caspases, apoptotic cells don’t undergo typical morphological changes, leading to sterile inflammation in the liver that increases tissue damage and suppresses tumor formation.

Studies of organoid morphogenesis, combined with proteomics and molecular profiling, identify the THBS1-YAP axis as a signalling mechanism that mediates paracrine communication between tumour cells and their wildtype epithelial neighbours.

What level of Ras genes activity leads to the development of cancer?

Monogamous rodents of the genus Peromyscus, upon disruption of pair bonds, acquire increased oncogenic activity.

P2ry12-mediated microglial interactions stimulate the proliferation of brain tumour initiating cells.

A novel Mendelian randomisation framework unravels one gene expression component, correlated with proliferation and genome stability-related features, associated with telomere length in lung adenocarcinoma tumours, which provides insights into how telomere length influences the genetic basis of lung cancer aetiology.

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.

Mutational inactivation of the JNK signaling pathway causes genomic instability and breast cancer development.

A mouse model of atopic dermatitis provides mechanistic evidence for an association between allergic disease and skin cancer.

Modeling glioblastoma using expression of relevant human oncogenes in syngeneic zebrafish offers a powerful platform for current and future biological discovery, diagnostics, and therapeutic testing in an intact tumor microenvironment.