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

Evolution of tumor suppressor genes can involve a trade-off because the acquisition of certain anti-cancer characteristics diminishes the ability to regenerate damaged tissue.

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.

The SCF-family of ubiquitin ligases regulates the key cancer proliferation node by controlling the degradation of RB-like tumor suppressor RBL2/p130.

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

During tumorigenesis loss of p53 not only abrogates cell cycle arrest and apoptosis, but also suppresses the induction of replication-stress-induced DNA double-stranded breaks.

Nearly half of bladder cancers of solid organ transplant recipients harbor papillomaviruses or polyomaviruses, with many tumors showing evidence of clonal viral integration and viral oncogene effects on tumor gene expression patterns.

Lineage transformation in lung cancer is dictated by ERK activity and requires permissive chromatin alterations in the context of targeted therapy resistance.

3D culture of breast cancer in biologically relevant ECM potentiates the growth-inhibitory effects of unacylated ghrelin and AZP-531, and clinical response may be predictable based on a MAPK gene signature.

A novel master regulatory mechanism of cell proliferation and senscence employs the lncRNA UCA1 and a CAPERα/TBX3 corepressor.