p53

Scientists found that combining the notoriously flimsy anticancer protein p53 with a domain from a spider silk protein resulted in a more stable hybrid that’s more potent and easier for cells to synthesize.

New experiments suggest the famous tumor-suppressing protein uses viral elements lingering in the genome to get cancerous cells to announce their presence to the immune system.

A trio of papers shows that specialized antibodies can direct T cells to destroy cells that display portions of mutant cancer-related proteins, as well as T cells that have become cancerous themselves.

DNA damage kick-starts what was once a defunct duplicated gene, which kills off injured cells.

Two studies find the genome-editing technique works best when cells have a faulty DNA-damage response that’s frequently present in cancers.  

A screen of human embryonic stem cell lines finds several that accumulated changes in the gene TP53, including aberrations commonly seen in cancer.

Two studies reveal that the giant mammals have dozens of extra copies of a cancer-preventing gene.

The tale of p53, a widely studied tumor suppressor gene, illustrates the inventiveness of researchers who turn mishaps into discoveries.

In Chapter 12, "Of Mice and Men," author Sue Armstrong recounts the point at which researchers moved from working with p53 in tissue culture to studying the gene in animal models.

Why obese individual are more likely to get cancer could be partly explained by a gene that activates both pathways.

A group of microRNAs can inhibit the formation of induced pluripotent stem cells, and may provide a target for more efficient reprogramming of somatic cells.

Editor's choice in developmental biology

A snapshot of the most highly ranked articles in molecular biology, from Faculty of 1000.

p53 has emerged as one of the top targets in the war against cancer.