DCU led project finds new potential treatment for breast cancer combining existing drugs
As recently covered by the Irish Independent, research arising from the HER2 project led by Dr Neil Conlon shows that a combination of two existing drugs has been shown to overcome a treatment-resistant form of breast cancer. This form of breast cancer makes up around one in five forms of the disease.
The study, published in the journal Translational Oncology, explored how combining two approved anti-cancer drugs, neratinib and dasatinib, may overcome or prevent treatment resistance in this cancer. Currently neratinib is an approved HER2-targeted therapy, and dasatinib is a drug used to treat certain types of leukaemia.
The results showed that these drugs, when used together, were much more effective at fighting the cancer than when used alone. In addition, both of these drugs are taken orally, making it easier for patients to use them at home.
HER2 is a protein that helps cancer cells to develop and HER2-positive cancers make too much. There are already treatments for HER2-positive cancers, but more choices are needed, particularly for those who are no longer getting a benefit from existing therapies. The research could potentially lead to more treatment options for patients with HER2-positive breast cancer, which can grow more quickly.
Speaking to the Irish Independent, Dr Neil Conlon said:
“The findings have the potential to improve treatment options for people with HER2-positive breast cancer, especially for those whose cancer no longer responds to current treatments. There are several drugs used to treat this disease that target HER2. These HER2-targeted drugs have had a profound effect on the prognosis for people with HER2-positive breast cancer. However, unfortunately for some people, their cancer doesn’t respond to these HER2-targeted drugs or, after initially responding, their cancer becomes resistant to this treatment.
What’s even more exciting is that this combination also helped prevent the cancer from becoming resistant to treatment and worked particularly well against cells that were already resistant to HER2-targeted drugs.”