Turning on a key gene inside cancer cells dramatically slows their spread, researchers have found.
The discovery could lead to a new "class" of cancer drugs for the future, they say.
The team, from Hoffmann-La
Roche in New Jersey, US, have nicknamed their drug molecules after the town of Nutley, where their labs are based
They found that their "Nutlins" held back tumour growth by 90% when given to mice in which human tumours were growing.
There is hope that further improvements might lead to a drug which could shrink tumours.
The molecules appear to work by turning a gene,
which is inactivated in most human cancers, back on.
Mutations in the "p53" gene which stop it working properly have already been implicated in several different cancer types.
The discovery, published in the journal Science, is part of work to find cancer drugs by directly targeting gene defects known to be involved in cancer.
The p53 gene is a so-called "tumour suppressor" gene, because it is part of the body's defences against the type of cell growth typical of cancer.
Its role is to trigger a self-destruct mechanism in cells which have suffered genetic damage, perhaps through exposure to toxins or radiation.
This genetic damage increases the chance that a cell will begin to divide in an uncontrolled way, or fail to die off when it should - which starts the process of tumour growth.
Scientists already know that p53 is inactivated in most solid cancers.
The Hoffmann-La Roche team, lead by Lyubomir Vassilev, identified the molecules which can turn the
p53 back on.
The end result was that their molecule appeared to halt cell division within tumours, and even induce some degree of self-destruction.
The drugs did not appear to produce harmful side effects in the mice when they
were given to them.
However, further research would need to take place before any drugs would be ready for
The research was published in the journal Science.