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Researchers discover a new way to help prevent secondary breast cancer in the lung

Our scientists have uncovered a way in which breast cancer cells ‘wake-up’ and form secondary tumours in the lungs.

Researchers funded by us, have found how breast cancer cells can be triggered to form secondary tumours in the lungs. They found that a protein called PDGF-C plays an important role in ‘waking up’ inactive breast cancer cells that have spread there.

In the future, the researchers hope they can target PDGF-C with an existing drug called imatinib, to prevent secondary tumours.

Preventing secondary breast cancer

For some who’ve had breast cancer, the disease can come back in another part of the body. This is known as secondary breast cancer. And although it can be treated, it can’t be cured.

For people with oestrogen receptor positive (ER+) breast cancer, the risk of cancer returning in another part of the body can continue for many years, or even decades, after their initial diagnosis. 

That’s because some breast cancer cells can stay inactive and hide in organs like the lungs before growing into secondary tumours.

Dr Frances Turell and Professor Clare Isacke, from the Breast Cancer Now Toby Robins Research Centre at the Institute of Cancer Research, London, found molecular changes in the lungs that help breast cancer cells form secondary tumours.

PDGF-C and its role in breast cancer

The researchers found that a protein called PDGF-C plays a major part in influencing whether inactive breast cancer cells stay asleep or wake up.

The PDGF-C protein lives in the lungs, a common place for breast cancer to spread to. And PDGF-C levels increase when we get older, or when the lungs become damaged or scarred.

The scientists discovered that these high levels of PDGF-C can cause inactive cancer cells to grow and develop into secondary breast cancer.

Dr Frances Turrell added: "Cancer cells can survive in distant organs for decades by hiding in a dormant state. We’ve discovered how aging lung tissue can trigger these cancer cells to ‘reawaken’ and develop into tumours, and uncovered a potential strategy to ‘defuse’ these ‘time bombs’. "

A new target for treatment

The team then explored whether blocking PDGF-C action could prevent the cancer cells ‘waking up’ and forming secondary tumours in the lungs.

They treated mice with ER+ tumours with imatinib, an existing drug that can target the effects of PDGF-C. Researchers treated the mice with the drug both before and after the tumours had developed. For both groups, the treatment significantly reduced breast cancer growth in the lung.

The team now want to better understand how breast cancer patients might benefit from imatinib. And in the future, they hope to create treatments targeting the ‘reawakening’ mechanism.

Dr Simon Vincent, our director of research, support and influencing said: “We know that for years after finishing breast cancer treatment, many women fear the disease returning. With an estimated 61,000 people living with secondary breast cancer in the UK, more research to understand and treat it is vital.

“This exciting discovery brings us a step closer to understanding how we can slow down or stop the development of ER+ secondary breast cancer in the lung. It has the potential to benefit thousands of women living with this ‘time bomb’ in the future, ensuring fewer patients receive the devastating news the disease has spread.”

This research was published in Nature Cancer and funded by Breast Cancer Now.

To learn more about our research, visit the research section of our website.

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