Wonder drug that stops breast cancer returning after treatment could save lives

Here’s some great news – a drug has been developed that cuts the likelihood of ­hereditary breast cancer caused by BRCA1 and BRCA2 genes coming back after treatment.

The results show how the drug reduces the risk of recurrence, second cancers and death by 42%.

The findings were so persuasive and clear that the trial was stopped early after two-and-a-half years instead of the planned 10 years.

They showed 85.9% of patients treated with Olaparib remained free of invasive breast cancer and second cancers, compared to 77.1% on a placebo.

Olaparib, which exploits a genetic weakness in cancer cells, could become a new treatment option to help women with inherited forms of high-risk early breast cancer – and lead to more patients being saved.

The trial was led by Professor Andrew Tutt, professor of oncology at King’s College London.

He said: “Our global academic and industry partnership has been able to help identify a possible new treatment for women with early stage breast cancer who have mutations in their BRCA1 or BRCA2 genes.

“Olaparib has the potential to be used as a follow-on to all the standard initial breast cancer treatments to reduce the rate of ­life-threatening recurrence and cancer spread for many patients identified through genetic testing to have ­mutations in these genes”.

“Up to now there has been no ­treatment that specifically targets these mutations to reduce the risk of recurrence beyond the standard ­treatments available for early breast cancer,” Professor Tutt says.

“This study, ­coordinated by the Breast International Group, shows that giving Olaparib for a year after chemotherapy to patients with BRCA mutations boosts the chances they will remain free of ­invasive or metastatic cancer.

“These results reinforce how ­collaborative research deepens our understanding of treating familial cancers and shows the value of testing for these mutations in patients with early breast cancer.”

Olaparib works by stopping cancer cells from being able to repair their DNA by inhibiting a molecule called PARP – causing cancer cells to die.

It works particularly well for patients with faulty versions of the BRCA1 or BRCA2 genes, which are normally involved in another system for repairing DNA.

Cancer cells are killed off if they don’t have functioning DNA repair factors involving either PARP, or BRCA1 or BRCA2.