May 18, 2007
The p53 gene's job is to tell faulty cells to self destruct, and so experts assumed it helped in killing cancer cells that chemotherapy had injured.
But a trial at the Georgia Institute of Technology has found chemotherapy patients with normally functioning p53 fare worse than those with mutated p53.
This suggests p53 may help some cancers come back, PLoS ONE journal reports.
If this is the case, a new strategy for fighting cancer might be to develop drugs to disable the functioning of p53 in the tumours of patients undergoing chemotherapy.
Lead researcher John McDonald explained: "We propose that p53 may help repair some of the cancer cells damaged by chemotherapy leading to tumour recurrence and explaining the higher mortality rate of patients whose tumours had a functioning p53.
"If we are correct, inhibiting p53 in tumours being treated with chemotherapy may substantially improve patients' long-term survival."
His team studied tumour samples from patients with ovarian cancer. Some of the cancer patients had been treated with chemotherapy prior to surgery, and some had not.
Only 30% of the chemotherapy patients who had normally functioning p53 were alive five years later, compared to 70% of those with mutated, non-functioning p53.
They are now doing studies on mice in the lab to test the relative effectiveness of chemotherapeutic agents in cells with normal p53 compared with mutant p53.
Professor Karen Vousden of Cancer Research UK, who has also been studying p53, said: "Although this study is small and doesn't directly implicate p53 in the poor response of some ovarian cancer patients to chemotherapy, it certainly gives us food for thought.
"The results suggest that p53 actually continues to protect some cancer cells from the effects of chemotherapy. This will be a very important finding if it is confirmed in other experiments - and it might help in developing better ways to treat ovarian cancers."