Researchers have discovered why breast cancer cells that have spread to the lungs may wake up following years of sleep and form incurable tumours.
Around 44,000 Brits and 210,000 Americans are diagnosed with the most common type of breast cancer — oestrogen receptor positive (ER+) — every year.
These patients remain at risk of their cancer recurring in another part of their body for decades after their initial diagnosis, even after successful treatment.
Now, experts have discovered the mechanism that triggers this cancer ‘time bomb’ in the lungs — one of the most common places the cancer can spread to.
And an existing cancer drug can slow the growth of these secondary tumours, their study on mice suggests.
ER+ breast cancer patients remain at risk of cancer cells surviving in a dormant state in their organs for years after they have completed treatment.
In a bid to understand the cues that trigger these cells to spur into action and form tumours, researchers at The Institute of Cancer Research (ICR) in London studied mice with ER+ breast cancer who underwent scans.
The findings, published in the journal Nature Cancer, suggest molecular changes within the lung encourage secondary tumours to grow.
The PDGF-C protein — which is vital for tissue growth and survival — plays a key role in determining whether inactive breast cancer cells stay asleep or ‘wake up’.
As levels of the protein increase, which happens due to ageing or when the lung tissue becomes damaged or scarred, it can cause the dormant cancer cells to grow and develop into secondary breast cancer in the lung.
The researchers then explored whether blocking PDGF-C activity could help prevent the ‘reawakening’ of these cells.
They gave mice an existing cancer growth blocker called imatinib, which is currently used to treat patients with chronic myeloid leukaemia.
The mice were treated with the drug either before or after the tumours had developed.
Among both groups, the cancer growth in the lung was significantly reduced, according to the study which was funded by Breast Cancer Now.
Study author Dr Frances Turrell, postdoctoral training fellow in the Division of Breast Cancer Research at the ICR, said: ‘We’ve discovered how ageing lung tissue can trigger these cancer cells to “reawaken” and develop into tumours and uncovered a potential strategy to “defuse” these “time bombs”.
‘We now plan to better unpick how patients might benefit from the existing drug imatinib and, in the long term, aim to create more specific treatments targeted at the “reawakening” mechanism.’
Rachel Davies, 38, who lives in Swansea, was diagnosed with ER+ breast cancer in 2021 and underwent a mastectomy, lymph node removal, chemotherapy and radiotherapy.
Following a scan in May 2022, three months after finishing treatment, she was told the cancer had spread to her sternum and later her spine. She is now receiving a targeted cancer drug called ribociclib and hormone therapy.
Mrs Davies said: ‘I’ve seen some women finish treatment and ring that bell and celebrate it being over, and this always worries me as you can never be complacent that it won’t return.
‘Finding out the cancer had spread when I thought it was all in the past was heartbreaking.
‘That’s why it’s so important that research into secondary breast cancer happens so we can find new ways to stop women going through what I’m experiencing.’
She added: ‘Research like this gives me hope for women being treated for breast cancer in the future. I don’t want to waste my precious time being bitter or angry.’
Professor Clare Isacke, a professor of molecular cell biology at the ICR and study co-author, said: ‘This is an exciting stride forward in our understanding of advanced breast cancer – and how and why breast cancer cells form secondary tumours in the lungs.
‘Next, we need to pinpoint when these age-related changes happen and how they vary between people, so that we can create treatment strategies that prevent cancer cells “reawakening”.’
Dr Simon Vincent, director of research, support and influencing at Breast Cancer Now, said: ‘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.’
And this will be the last it is ever heard of again.
Big Pharma cant make money on cured people, PERIOD.
They will bury this.