Overexpression of BAG2—a novel mutant p53 binding protein—in tumors inhibits MDM2-mediated mutant p53 degradation, which leads to the accumulation of mutant p53 protein and promotes tumorigenesis.

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.

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

Clinical analysis corroborated with experimental data demonstrate that Δ133p53β, a naturally occurring isoform of p53 protein, induces a pro-metastatic program and is a clinical indicator of metastasis, independently of TP53 mutation status.

Drosophila p53 protein isoforms function during oogenesis to ensure the integrity of the transmitted genome, a function that is conserved to humans.

Single-cell tracking and cell-fate simulation suggest that low levels of p53 suppress aneuploid cell formation in unstressed cells and also reveal the dual fate of cells lacking p53 in the presence of p53-proficient cells.

Overlaying single cell readouts of cell cycle and apoptosis onto a multidimensional analysis of pulsed cisplatin signalling dynamics reveals targetable mechanisms of platinum resistance in lung adenocarcinoma.

Anti-tumor properties of sub-class of xanthine analogs involve restoration of p53 pathway transcriptome, independent of p53/p73, dependent on ATF3/ATF4 and Noxa in mutated-p53 tumors and the compounds trigger an S-phase checkpoint.

A resource of p63-regulated genes, genomic loci bound by p63, p63 DNA recognition motifs, and potential co-factors is generated through a meta-analysis of high-throughput datasets.

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.