Highly read on www.cell.com 10 June–10 July

The protein p53 is well known for its role as a tumour suppressor; however, p53 can also help breast tumour cells to dodge the effects of chemotherapy.

Normal p53 activates programmed cell death, or apoptosis, and the p53 gene is often mutated in cancer. Researchers expected that tumours with mutant p53 would be more difficult to treat than those with normal p53, but previous studies on breast cancer have not found this. Guillermina Lozano at the MD Anderson Cancer Center in Houston, Texas, and her team therefore tested the effects of a chemotherapy drug, doxorubicin, on mice bearing breast tumours with either normal or mutated p53.

Tumours in mice with normal p53 shrank little in response to treatment and relapsed more quickly than those with mutated p53. After treatment, many tumour cells with normal p53 entered a state of senescence in which they stopped dividing — however, the cells secreted signalling proteins that could trigger the proliferation of neighbouring cells, leading to relapse.

Cancer Cell 21, 793–806 (2012)