A breakthrough drug can drastically reduce the risk of women with the ‘Angelina Jolie gene’ dying from breast cancer.
Scientists studied nearly 2,000 women with early-stage cancer, all of whom carried BRCA1 and BRCA2 mutations.
Half received olaparib tablets to be taken twice daily for a year, while the others received a placebo.
The results showed that death rates were 32% lower in patients who received the drug four years later.
Charities today called the findings ‘hugely exciting’, saying the discovery could save the lives of thousands of women.
A team of UK and US researchers studied 2,000 women with early-stage BRCA1 and BRCA2 cancer and gave half of them olaparib tablets (pictured) twice a day for a year. The results showed that those taking the drug, which kills cancer cells, were 32% less likely to die from the disease four years later.
Angelina Jolie (left) drew attention to the BRCA1 gene in 2013 when she revealed she opted to have a double mastectomy and had her ovaries and fallopian tubes removed at the age of 37 years. Jolie’s mother Marcheline Bertrand (pictured right, with actress Jacqueline Bisset, right) died aged 56 after battling breast and ovarian cancer
Everyone has the BRCA1 and BRCA2 genes, which normally protect against breast and ovarian cancer by repairing cell damage.
But mutations in genes can cause cells to malfunction, increasing women’s risk of disease.
About 5% of all breast cancers are linked to the faulty gene pair made famous by the Hollywood actress.
Jolie underwent a preventative double mastectomy in 2013 after testing positive for the mutated BRCA1 gene.
Olaparib, sold under the brand name Lynparza, has already been shown to reduce the risk of spreading hereditary cancer.
But the new findings, by a team of UK and US researchers, are the first to show the drug also cuts the risk of death by a third.
NHS medicines watchdogs are assessing whether it should be widely available to patients in the UK. Only a selected group can currently access it.
WHAT ARE BRAC MUTATIONS, KNOWN AS THE “PRETTY GENE”?
BRCA1 and BRCA2 are examples of genes that increase your risk of cancer if they are altered.
We all carry certain genes that are normally protective against cancer. These genes correct any DNA damage that occurs naturally when cells divide.
Inheriting faulty versions or “variants” of these genes greatly increases your risk of developing cancer because the altered genes cannot repair damaged cells, which can accumulate and form a tumour.
Having a variant of the BRCA gene greatly increases a woman’s risk of developing breast cancer and ovarian cancer.
They also increase a man’s risk of developing male breast cancer and prostate cancer.
About one in 400 people has a defective BRCA gene.
For every 100 women who carry the BRAC gene, 65 to 79 will develop breast cancer and 36 to 53 will develop ovarian cancer.
Last week, the United States approved olaparib, made by AstraZeneca and Merck, for people with breast cancer who have an altered BRCA gene.
The experts recruited 1,836 women from 600 hospitals around the world who had breast cancer classified as HER2 negative, meaning it is less likely to develop.
All of the participants had a mutation in their BRCA1 and BRCA2 genes and had undergone standard cancer treatment, including surgery, chemotherapy and radiation therapy.
Half received 300 mg of olaparib twice a day for a year, while the others received a placebo drug.
Cancer cells whose BRCA genes have been altered depend on a protein called PARP to keep their DNA healthy.
Olaparib, which can cost around £2,500 for a two-week course, prevents PARP from repairing DNA damage in cancer cells, causing them to die.
The researchers, who have so far followed the participants for four years, found that those who took the drug were 32% less likely to die.
The study was conducted by a team from the Institute of Cancer Research London (ICR), the American research center NSABP Foundation, the Dana-Farber Cancer Institute in Boston and the University of Edinburgh.
Professor Andrew Tutt, chair of the study’s steering committee, said the results show that olaparib can “keep more women with hereditary breast cancer disease-free and alive after their initial treatment”.
He said the results show that olaparib can “directly target the weakness” of cancer in women with BRCA mutations and “improve their survival”.
The oncologist said, “I hope to see BRCA1 and BRCA2 testing used for more women diagnosed with early-stage breast cancer, so we can determine who can benefit from this personalized treatment approach.
“Olaparib provides a new individualized, targeted treatment option that is much needed to keep more women with hereditary breast cancer disease-free and alive and well after their initial treatment.”
Professor Tutt presented the results of the study today at the European Society for Medical Oncology Congress.
Professor Kristian Helin, chief executive of the ICR, said the results signaled “a major advance in the treatment of hereditary early-stage breast cancer”.
He added: “Olaparib has major benefits for this group of patients, increasing their chances of remaining cancer-free and potentially cured after initial treatment.
“We hope that olaparib will now be authorized in Europe and approved in the UK for NHS patients without delay.”
Dr Simon Vincent, director of research, support and influence at the charity Breast Cancer Now, said: “It is extremely exciting that this research shows that olaparib could save lives and prevent recurrence in some women and men with primary breast cancer with an inherited altered BRCA gene, often known as the “Jolie gene”.
He said the ‘groundbreaking’ results would hopefully lead to a ‘positive decision’ from NICE on the use of olaparib on the NHS, so that ‘thousands of people with altered BRCA genes who could be eligible for the benefit of the drug as soon as possible’.
NICE in January rejected the use of the drug on the NHS to treat prostate cancer after finding it was not good value for money.
A trial of the drug found that men treated with olaparib lived 7.4 months before their cancer progressed, compared with 3.6 months when given ‘one size fits all’ hormone treatments.