The Breast Cancer Now Catalyst Programme
To achieve our aim that by 2050 everyone who develops breast cancer will live and be supported to live well, we need to speed up the translation of research in the lab into new and effective treatments for patients. We’re bringing together leading researchers and top pharmaceutical companies to pool ideas and resources and ultimately stop people dying from breast cancer.
As part of the Breast Cancer Now Catalyst Programme, we have collaborated with leading pharmaceutical company Pfizer to give researchers unprecedented access to a number of Pfizer’s licensed and investigative drugs as well as vital funding for researchers to test these drugs. This allows us to combine the expertise of our researchers with Pfizer’s compounds and deliver new treatments to patients more quickly.
Researcher: Professor Agnes Noel
Location: University of Liege, Belgium
Triple negative breast cancer tends to be more aggressive than other types of the disease, and does not always respond well to currently available treatments. There is an urgent need for new effective treatments to ensure more people with breast cancer survive. In contrast to other types of breast cancer, which make hormone receptors or a molecule called HER2 that can be targeted with treatments, triple negative breast cancer currently lacks targeted treatments. Surgery and chemotherapy remain the main treatment options for this type of breast cancer.
- This drug stops a group of closely-related molecules that can stimulate cell growth from working. Blocking all of them at once helps to ensure that breast cancer cells can’t use an alternative way to stimulate their growth.
- Dacomitinib is currently undergoing Phase III clinical trials for lung cancer.
- Blocks the activity of proteins called CDK4 and CDK6, which prevents cells from multiplying
- Currently in Phase III trials in combination with other drugs for high risk early breast cancer
- Already used to treat oestrogen receptor positive (ER+) HER2 negative breast cancer that has spread, in combination with hormone (endocrine) therapy
The science behind the project
By carefully studying triple negative breast cancer samples donated by patients, Professor Agnes Noel’s team discovered that over 70% of these had two molecules called MT4-MMP and EGFR. These molecules are known to stimulate breast cancer cell growth.
Previous clinical research tested drugs blocking the EGFR molecule in triple negative breast cancer. It found that blocking EGFR alone was insufficiently effective. However, when the EGFR-blocking drug erlotinib was used together with a drug palbociclib, both in cancer cells in the lab and in mice, the triple negative breast cancer cells were much more sensitive to this treatment.
Agnes and her team are now building on this work. They are testing the effectiveness of different doses of dacomitinib, a drug which can block multiple molecules stimulating cancer growth including EGFR, and palbociclib. To see how well these treatments work together, the team are first testing the drugs in triple negative breast cancer cells in the lab. Then, the drug treatment combinations will be tested in mice with triple negative breast tumours. This project will allow the researchers to assess what treatment regimen would be most effective at treating triple negative breast cancer, whilst also looking out for potential side effects.
What difference will this project make?
New and targeted treatments for triple negative breast cancer are urgently needed. If successful, this project could find new effective treatment combinations for this type of breast cancer. The next step would then be recommending this drug combination for clinical trials. This could lead to a new opportunity to improve current treatments and ultimately to stop people dying from triple negative breast cancer.
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* Pfizer has provided funding and Pfizer compounds for this research study as an Independent Medical Research grant as part of the Breast Cancer Now Catalyst Programme. Pfizer has no other involvement in this research study.