Arthritis drug could offer hope to millions with the 'Angelina Jolie gene'

A rheumatoid arthritis drug can kill off ovarian cancer cells in women with the BRCA1 mutation, scientists revealed.

Auranofin reduces the survival rates of cancerous cells with deficiencies of the BRCA1 gene by 37 per cent, according to a new study. 

BRCA1 - dubbed the 'Angelina Jolie gene' - is a DNA repair gene, which is mutated in nearly 20 per cent of ovarian cancer cases.

It was previously thought that the best way to treat cancer cells with the mutation was through chemotherapy.

But, scientists from Plymouth University determined that BRCA1 genes have 'increased sensitivity' to auranofin.

The finding could lead to new therapies to treat ovarian cancer, they said.

Study author Dr Awadesh Jha said: 'Using drugs such as auranofin to treat cancer is highly promising since they are readily available and their pharmacological and toxicological properties are well documented.'

Previous studies found that BRCA1 mutations predispose women to an increased risk of developing ovarian and breast cancers.

Yet, those studies also found the genes are more sensitive to DNA damaging chemotherapeutics and as a result, can often indicate a good prognosis. 

The BRCA1 and BRCA2 mutations received widespread attention when Hollywood actress Angelina Jolie revealed she underwent a double mastectomy after discovering she was a carrier.

The mutation increased the mother-of-six's risk of breast cancer by around 87 per cent. Jolie more recently had her ovaries removed in a bid to prevent ovarian cancer. 

Scientists from Plymouth University tested the drug on two types of ovarian cancer cells - OVCAR5 and SKOV3.

Researchers depleted the BRCA1 expression levels in some of the genes, and compared them to a control set.

SKOV3 cells were found to be relatively sensitive to auranofin generally.

But, when BRCA1 was depleted, cell survival was significantly reduced with an auranofin concentration of one part per million.

Furthermore, BRCA1-depleted OVCAR5 cells also exhibited decreased survival.

Thus, the scientists determined that the cells had increased sensitivity to auranofin in a dose-dependent manner.

Dr Jha said: 'Studies carried out with cells grown under laboratory conditions showed faults in the BRCA1 gene render these cells more vulnerable to auranofin compared to ovarian cells with BRCA1 genes.

'It suggests that auranofin has the potential to be considered for future clinical studies to treat such ovarian cancers and this could serve as the springboard to use other available drugs which are not used as chemotherapeutic drugs.'

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