According to a study led by researchers at the University of Plymouth in the UK, a drug used to treat rheumatoid arthritis – called auranofin – could improve patient outcomes for women with ovarian cancer with a BRCA1 mutation. The research was conducted in association with the Plymouth Oncology Centre at Derriford Hospital, and was published in the journal, Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis.
The BRCA1 gene encodes a protein responsible for repairing damaged DNA. If the DNA sequence encoding the repair protein itself contains a mutation, it can lead to reduced or abnormal functionality of BRCA1. As mutations in other genes begin to accumulate, a person is at an increased risk of developing cancer.
Individuals with a mutation in BRCA1 have a particularly higher risk of developing ovarian and breast cancers, compared to those with normal copies of the gene. It’s estimated that approximately 15 to 20 percent of women with ovarian cancer carry a mutated copy of BRCA1.
According to previous research conducted on BRCA1-positive breast and ovarian cancers, these tumor types could be more susceptible to drugs that cause damage to DNA. While auranofin is currently used to treat rheumatoid arthritis, the drug is currently being used in a clinical trial to treat recurrent epithelial ovarian cancer. This type of ovarian cancer is the most dominant, and accounts for 90 percent of all ovarian cancers.
“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,” said Awadhesh Jha, Professor of Toxicology and Associate Head of Research in the School of Biological Sciences at the University of Plymouth. “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 cancer cells with normal BRCA1 genes.”
Jha and his colleagues tested the effects of auranofin on BRCA1-depleted cancer cells in the lab and found that the survival of the cancer cells was reduced by up to 37 percent, when compared to cells with a normal BRCA1 gene. Additionally, the damage induced by auranofin – including DNA double-strand breaks – was irreparable, causing death of the cells.
According to Jha, the result “suggests that auranofin has the potential to be considered for future clinical studies to treat such ovarian cancers and this could serve as the spring board to use other available drugs which are not used as chemotherapeutic drugs.” As auranofin is already a well-characterized pharmaceutical, companies could face fewer regulatory hurdles if it is proven effective at treating cancer in further clinical trials.
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