Myc expression is shown to cause sublethal activation of Caspase-3 and downstream endonuclease G, which causes DNA double strand breaks and oncogenic transformation in human cells.

HOXA9 is a transcriptional maintenance factor for anti-apoptotic genes that accelerate MYC-driven leukemia.

SPOP mutations underlie a novel, genomically unstable subclass of prostate cancer by altering DNA repair.

The retinoblastoma tumor suppressor regulates cell cycle progression when it's in 14 mono-phosphorylated isoforms.

Deletion and small-molecule inhibition of ubiquitin-specific protease 28 destabilizes the oncogenes c-MYC, c-JUN, and Δp63, and elicits regression of squamous cell lung carcinoma, a major cancer type with currently limited treatment options.

Genetic analyses and biochemical studies show that JMJD6 promotes MYC-mediated transformation and is required for neuroblastoma growth by complexing with pre-mRNA splicing factors.

Ploidy is stably maintained in Saccharomyces cerevisae by a tight coordination between histone levels and cell cycle events.

Tailoring Boolean models to 488 prostate cancer patients and 8 cell lines data allows for the experimentally validated personalisation of drug treatments.

A novel conditional mouse model to interrogate the requirements of structure-selective endonucleases in the development, functionality, and genome stability of B lymphocytes.

In contrast with earlier conclusions, negative selection has a major role in cancer evolution.