Somatic mutations frequently disrupt cleavage and polyadenylation signals in tumour suppressor genes in human cancers, likely contributing to tumour progression.

Signalling that maintains rapid translation elongation in KRAS-mutant colorectal cancer models can be targeted by mutation of the ribosomal protein RPL24 to suppress tumour proliferation.

Major secondary tumor suppressors in kidney cancer are required to maintain the activity of a tumor suppressive transcription factor after the loss of the primary tumor suppressor VHL.

Loss-of-function screening identified transglutaminase 2 (TGM2) as a putative tumor suppressor in the TP53 pathway and revealed that TGM2-mediated autophagy and CDKN1A-mediated cell cycle arrest are two critical barriers that prevent oncogenic transformation.

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.

The oncogenic Ras^V12 keeps cells mutant for the tumor suppressor scribble in an undead-like condition, which is required for an amplification loop that promotes tumorigenesis.

IRE-1 manipulates tumor cell identity to restore apoptosis sensitivity and suppress an aggressive germline tumor in C. elegans.

Src, an oncogene, promotes both cell proliferation and cell death simultaneously, which can be regulated by dietary methionine.

An unrecognized regulation on MAGEA protein stability promotes pancreatic cancer progression via manipulating autophagy and may impact the clinical utility of MAGEA-targeted immunotherapy.