The Catalyst Programme

Understanding how breast cancer becomes resistant to treatments

Research area: Better treatments

Professor Greg Hannon will investigate the difference between breast cancer cells that are resistant to certain drugs and those that are not. He hopes to find ways to improve treatments so that more people with breast cancer live, and live well.

In this section

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.

What's the challenge?

Breast tumours are made up of different kinds of cells, including cancer cells and healthy cells. And not all cancer cells in the tumour are the same. Researchers believe that the diversity of cancer cells in the tumour is the main reason why drugs stop working. While treatment can successfully destroy the majority of breast cancer cells, some cancer cells with different features may resist the treatment and survive.

Cancer’s resistance to treatment is the main reason someone’s breast cancer may return, spread around the body and become incurable. We need to understand how breast cancer becomes resistant to drugs and how we can stop this from happening.

Drug: Palbociclib

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

Drug: Talazoparib

Belongs to a class of drug called PARP inhibitors
Works by blocking the PARP protein so cancers with changes in BRCA genes can’t repair their DNA and die
A second generation, more potent PARP inhibitor

What is the science behind the project?

Professor Greg Hannon and his team at the University of Cambridge want to find a way to identify breast cancer cells that are sensitive to certain drugs and others that are resistant. The researchers want to understand the differences between these groups of cancer cells and hope this knowledge will improve breast cancer treatment.

Because cancer cells can sometimes only have subtle differences that can also change in response to treatment, the researchers will be tracking individual cancer cells. Each breast cancer cell type is given a unique barcode that the researchers can use to identify it. They will follow each cancer cell type over the course of treatment in mice. This will allow them to find the differences between breast cancer cells that survive and breast cancer cells that die.

What difference will this project make?

We hope that this project will help pave the way towards a future where people with breast cancer can receive a combination of specially selected drugs that will each target different types of cancer cells within their tumours. This could help make treatments more effective so that more people diagnosed with breast cancer can live and live well.

*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.