Study Shows Breast Cancer Drugs May Treat Prostate Cancer
25 June 2010 – Prostate cancers in men with mutations in their BRCA2 gene develop in the same way as breast cancers linked to the same genetic fault, a study published in PLoS Genetics has revealed.
Alterations in BRCA2 have previously been linked to an increased risk of breast, ovarian and prostate cancers. But this is the first time scientists have been able to show the role the mutated gene plays in tumour growth in the prostate.
Researchers at the ICR, led by Dr Amanda Swain, examined cells taken from the prostate glands of mice lacking the BRCA2 gene, which is involved in DNA repair. They found that these cells accumulated DNA damage faster than it could be repaired, leading to the build up of random DNA errors.
While not a direct cause of cancer, the researchers suspected that over time this could lead to key anti-tumour genes being damaged that would normally prevent cancer from developing. To test if this was the case the researchers knocked out an additional gene known as p53, which is known to be faulty or missing in more than half of all cancers.
They found that the second faulty gene tipped the cells over the edge, causing widespread DNA damage and greatly increasing the likelihood of cancer developing.
This discovery builds on research to show that a promising class of new drugs for BRCA2-linked breast cancers – known as PARP inhibitors – may also be effective in men who have developed prostate cancer due to a BRCA2 alteration.
“The discovery that BRCA2 alterations play the same role in the development of hereditary prostate cancer as they do in breast cancer is an important step,” Dr Swain said. “This sheds light on the relationship between the two conditions and could help highlight overlapping areas where similar treatments could be used to treat both.”
