The male-specific tumor-suppressive effects of minor p53 isoforms were correlated with higher Ackr4 expression levels, which have implications for sex-specific cancer prognosis in humans.

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 protein p53 negatively impacts the ability of a CRISPR screen to discriminate between essential and non-essential genes, hence, p53 status should be considered in these screens.

In a mouse model of the hotspot mutant TP53^Y220C, the mutant p53 exhibited oncogenic gain of function in males and teratogenic gain of function in females, both correlated with inflammation.

Elephants escaped enhanced cancer susceptibility by evolving more master tumor suppressor genes.

Zebrafish are an optimal model organism to study rare TP53 mutations whose functions are not readily understood.

Genetic and molecular analysis of TP53 exon-6 truncating mutations reveal that these mutations, contrary to current belief, promote tumorigenesis and point towards strategies for treating cancers driven by these prevalent mutations.

The loss of p53 in bone cells activates critical signaling pathways; these are also essential in bone cancer.

The nerve growth factor receptor (NGFR) protein regulates p53 via two negative feedback mechanisms, which are hijacked by cancer cells.

Syngeneic tp53-null zebrafish develop a wide range of tumors that engraft into recipient animals with loss of Tp53 leading to increased metastasis in embryonal rhabdomyosarcoma (ERMS), likely accounting for increased aggression in TP53-inactivated human ERMS.