Breast cancer drug may stop women needing mastectomies

 
LONDON, ENGLAND - JUNE 02: Angelina Jolie attends the World Premiere of 'World War Z' at The Empire Cinema on June 2, 2013 in London, England.
Stuart C. Wilson/Getty Images for Paramount Pictures International
4 June 2013

Scientists in London today announced a possible breakthrough in the search for a drug to tackle the “faulty” gene that can cause breast cancer in women such as Angelina Jolie.

They have been testing the “most potent drug” of its kind to be studied in clinical trials and held out the “possibility” that it may eradicate the need for preventative mastectomies.

Initial tests on 70 patients by the Institute of Cancer Research saw “impressive responses” to the BMN 673 drug, a potential world-first in targeting BRCA — breast cancer — tumours.

Full-scale tests will now be carried out and if successful the treatment — discovered in conjunction with the Royal Marsden hospital following two years of research — could be available within three to five years.

Actress Jolie, 38, revealed last month that she had undergone a preventative double mastectomy after a blood test showed she had inherited the faulty gene BRCA1, which gave her an 87 per cent risk of developing breast cancer and a 50 per cent risk of ovarian cancer.

Jolie’s mother died of ovarian cancer aged 56 and her aunt died two weeks ago from breast cancer.

Today, scientists at the Institute of Cancer Research, who announced their results overnight at the world’s biggest cancer conference in Chicago, said patients with BRCA mutations had responded best to the new drug.

Study researcher Professor Johann de Bono, professor of experimental cancer medicine at the ICR and the Royal Marsden, said: “Patients with germline [able to be passed genetically] BRCA-associated tumours have no targeted treatment options, and there is a real need for these to be developed.

“Our promising study showed that BMN 673, a potent member of a family of potential drugs called PARP inhibitors, had excellent anti-tumour activity.

“It’s one of a range of new-style cancer therapies that target specific molecular defects in tumours and offer the potential of more personalised treatments to patients, including those with BRCA mutations.”

The drug works by attacking tumours that have a weakened DNA repair mechanism. The trials were on patients with breast, ovarian and peritoneal cancer, with the results showing “excellent anti-tumour activity”.

Some 11 of 25 ovarian cancer patients evaluated had a positive response to treatment, as did seven out of 18 breast cancer patients with BRCA mutations. Signs of some clinical benefit were also seen in several other patients.

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