William Kaelin Jr and researchers at the Dana Farber Cancer Institute and Harvard Medical School in Boston, Massachusetts examined the properties of "p73", a gene which is a close cousin to the tumour-suppressor gene p53, linked to more than 50 per cent of all cancer cases. When p53, the most important suppressor gene known, is mutated or not working, tumours can develop.
In a report in the scientific journal Nature, Mr Kaelin said that p73 can mimic the work of p53 - inducing cancer cells to die. "Our study shows that in principle there is actually another gene which is very similar to p53 and which could perform the functions normally performed by p53."
Mr Kaelin said that one of the reasons cancer cells don't die, and with a lot of genetic damage they should, is because they were smart enough to inactivate p53 which would ordinarily induce the damaged cells to commit suicide. "What our study shows is that when you activate this unknown53 homologue, p73, it will likewise induce cancer to undergo cell death."
The discovery of what p73 could lead to the development of new drugs that would activate the expression of the p73 gene, which so far does not appear to be frequently mutated in human cancer.
"You may have a copy of the p53-like gene that is in a somewhat dormant state that could then be activated by a drug." Mr Kaelin said. "Our study shows that if you did induce the expression of p73 in a cancer cell you could reasonably expect that the cell would undergo cell suicide."Reuse content