Cancer Research UK scientists at Newcastle University are starting the first UK trial of a new drug which targets the 'Achilles' heel' in hereditary forms of both breast and ovarian cancer.
The trial is open to women who have already developed an advanced form of breast or ovarian cancer and have been diagnosed with faults in the known cancer susceptibility genes BRCA1 or BRCA2.
They will receive a new drug which works by knocking out a key DNA repair mechanism in cancer cells.
It does this by blocking the action of an important enzyme involved in DNA repair, known as PARP [poly (ADP-ribose) polymerase] and is part of a class of potent anti-cancer drugs known as PARP inhibitors.
Cancer Research UK's Dr Ruth Plummer is the chief investigator on the trial.
Dr Plummer, senior lecturer in medical oncology at Newcastle University, said: "People who inherit faults in the BRCA1 or BRCA2 genes have a 50-80 per cent chance of developing cancer."
She continued: "Currently women with hereditary forms of breast and ovarian cancer are treated in the same way as every other woman who develops the disease. We hope this trial will show that by using the PARP inhibitor we can offer them more targeted treatment."
Mutations in the BRCA1 or BRCA2 genes are responsible for around five per cent of the 44,000 cases of breast cancer diagnosed annually in the UK and for more than five percent of the 6,615 cases of ovarian cancer diagnosed each year.
The Newcastle team believe their research could offer hope for the future by paving the way for the drug to be used as a preventative treatment.
Dr Plummer continued: "In the future, we may be able to use the PARP inhibitor to offer protection to women who inherit these genetic faults. We may be able to use it to 'mop up' stray cancer cells before they actually develop into tumours, thereby sparing the need for preventative surgery."
Throughout our lifetime we accumulate small amounts of damage to our DNA.
This can occur naturally as cells work, divide or age.
Normal cells have two DNA strand-break repair mechanisms to patch up this damage or correct mistakes which may occur during replication.