Oncologists have access to a variety of treatments for breast cancer patients, including chemotherapies. Unfortunately, certain treatments are only effective in some patients and it is very difficult for clinicians to know which patients are going to benefit from which drugs. Being able to understand why patients respond differently should allow the most effective drugs for each individual to be chosen straight away and could guide the development of new drugs that are effective in the highest possible number of people.
To that end, Cancer Research Wales is funding research at Bangor University, supervised by Dr Chris Staples, that aims to explore the ways cancer cells respond to common treatments.
In order for a tumour to grow, cancer cells must duplicate their DNA and then divide into two new cells – a process which is repeated a great number of times. Many cancer therapies work by disrupting the copying of the DNA, without which the cancer cells cannot divide. In recent years, a class of drugs called PARP inhibitors have been developed – these drugs work by preventing the repair of DNA damage that can occur during the copying process. However, PARP inhibitors have tended to be effective only in some patients.
Previous work by Dr Staple’s team has shown that the presence or absence of a protein called MRNIP determines how effective PARP inhibitors are in several cancer types, including breast cancer. Interestingly, they also found that those cancers where PARP inhibitors worked were resistant to Gemcitabine, a commonly used chemotherapy drug.
The team are now conducting in depth investigations of the DNA repair processes in cancer cells that occur before and during treatments with different drugs. These processes are very complex and involve a large number of different proteins – understanding how the interactions lead to resistance to different drugs will provide valuable insight into why certain therapies only work for certain patients.
