For decades, the end of breast cancer treatment has offered only conditional relief — a remission shadowed by the knowledge that dormant cells may yet stir. Researchers at the Institute of Cancer Research in London have now identified the biological mechanism behind this reawakening: an aging lung protein called PDGF-C that signals dormant ER+ cancer cells to grow into secondary tumors. The discovery, published in Nature Cancer, not only explains why recurrence strikes some patients and not others, but points toward an existing drug — imatinib — that may one day help prevent it. In the long hu
Scientists identify mechanism behind breast cancer recurrence, propose prevention strategy
Patients with ER+ breast cancer face years of uncertainty about recurrence; one patient experienced cancer spread to sternum and spine after initial treatment completion.
Cancer cells that lie dormant for years, sometimes decades, before suddenly awakening
Mark
Why does this particular protein, PDGF-C, matter so much? Couldn't there be dozens of other triggers?
Mimi
There probably are other factors at play, but PDGF-C appears to be a major one—and crucially, it's something we can actually target with drugs we already have. That's the difference between understanding a problem and being able to do something about it.
Mark
So the drug imatinib worked in mice. How confident are researchers that it will work in people?
Mimi
That's the honest question. Mouse studies are a necessary step, but human biology is messier. What they're saying now is that they want to test whether existing patients might benefit from it. That's the next phase—moving from the lab to actual clinical trials.
Mark
Rachel Davies said she worries about women who finish treatment and celebrate too early. Is that worry justified?
Mimi
Completely. For ER+ breast cancer, it is justified. The disease can return years later, sometimes a decade or more. That's not pessimism; that's the biology. What changes now is that patients and doctors might have tools to intervene before recurrence happens.
Mark
If PDGF-C increases with age, does that mean older patients are at higher risk of recurrence?
Mimi
That's a logical question, but the research doesn't quite answer it yet. Aging tissue produces more of the protein, yes, but how that translates to individual risk depends on many other factors—genetics, the specific characteristics of someone's cancer, their overall health. That's what they need to figure out next.
Mark
What does it mean that the drug worked both before and after tumours formed?
Mimi
It suggests two possible strategies: you could give it preventatively to high-risk patients to stop recurrence before it starts, or you could use it therapeutically if secondary cancer has already appeared. That flexibility is valuable because it gives doctors options depending on what they know about each patient.
O Pulso
- Up to 80% of UK breast cancer patients carry ER+ diagnoses, meaning tens of thousands live indefinitely with the silent threat of cancer cells that can reawaken years or even decades after treatment ends.
- Rachel Davies, 38, believed her treatment was behind her — until a scan three months later revealed the cancer had spread to her sternum and spine, a devastating reminder of how suddenly dormancy can break.
- Scientists have pinpointed PDGF-C, a protein produced by aging or damaged lung tissue, as the molecular trigger that wakes dormant cancer cells and sets secondary tumors in motion.
- In laboratory studies, the existing cancer drug imatinib successfully blocked PDGF-C activity and reduced tumor growth in mice — whether administered before or after secondary tumors had already formed.
- Researchers are now working to understand how and when age-related lung changes vary between individuals, with the goal of tailoring preventive treatments to those most at risk before recurrence can occur.
For decades, the end of breast cancer treatment has offered only conditional relief — a remission shadowed by the knowledge that dormant cells may yet stir. Researchers at the Institute of Cancer Research in London have now identified the biological mechanism behind this reawakening: an aging lung protein called PDGF-C that signals dormant ER+ cancer cells to grow into secondary tumors. The discovery, published in Nature Cancer, not only explains why recurrence strikes some patients and not others, but points toward an existing drug — imatinib — that may one day help prevent it. In the long human struggle to reclaim time from illness, this represents a rare and meaningful foothold.
Rachel Davies finished her breast cancer treatment in early 2022 believing the worst was over. Three months later, a scan revealed the cancer had spread to her sternum and spine. At 38, she became one of thousands living with what researchers now describe as a biological time bomb — dormant cancer cells that can lie silent for years before suddenly awakening in distant parts of the body.
Patients with oestrogen receptor positive breast cancer, which accounts for up to 80 percent of UK cases, face this prolonged and invisible threat long after initial treatment ends. Around 44,000 people in the UK are diagnosed with ER+ breast cancer each year, and many carry the risk of late recurrence indefinitely. Until now, the mechanism behind this reawakening has remained poorly understood.
Researchers at the Institute of Cancer Research in London, funded by Breast Cancer Now, have identified the trigger: not the cancer cells themselves, but the tissue surrounding them. As lungs age or sustain damage, they produce increasing amounts of a protein called PDGF-C, which acts as a wake-up signal to dormant cancer cells, prompting them to grow into secondary tumors. The findings, published in Nature Cancer, offer the first clear explanation for why recurrence strikes some patients and spares others.
Critically, the team also identified a potential intervention. Imatinib, a drug already used to treat other cancers, can block PDGF-C activity. In mouse studies, it significantly reduced cancer growth in the lungs both before and after secondary tumors had formed — suggesting it could serve as either a preventive measure or a treatment for those already facing spread.
Davies described the emotional devastation of believing herself free of cancer, only to learn otherwise. Yet she has turned that pain toward advocacy. 'I don't want to waste my precious time being bitter or angry,' she said. Her experience gives weight to what the researchers acknowledge: secondary breast cancer cannot be cured, making prevention or delay the only realistic ambition.
Professor Clare Isacke framed the discovery as a beginning. The next steps involve mapping how age-related lung changes vary between individuals, enabling treatments tailored to personal risk. For Davies and thousands like her, the promise is not a cure but something quietly profound — the possibility that science might restore some measure of control over time itself.
A woman in Swansea finished her breast cancer treatment in early 2022 feeling, as many do, that the hardest part was behind her. Three months later, a routine scan delivered news that shattered that relief: the cancer had returned, this time in her sternum and spine. Rachel Davies, 38, is now one of thousands of patients living with what researchers have begun calling a biological time bomb—cancer cells that lie dormant for years, sometimes decades, before suddenly awakening in distant parts of the body.
This phenomenon has long puzzled oncologists. Patients with oestrogen receptor positive breast cancer, the most common form, accounting for up to 80 percent of all cases in the UK, face a peculiar and prolonged threat. Even after successful initial treatment, their cancer cells can spread to the lungs, bones, or other organs and remain inactive for years. Then, without warning, they stir to life. Around 44,000 people in the UK are diagnosed with ER+ breast cancer annually, and many carry this invisible risk forward indefinitely.
Now researchers at the Institute of Cancer Research in London, working with colleagues and funded by Breast Cancer Now, have identified the mechanism that triggers this reawakening. The culprit is not the cancer cells themselves but the tissue around them. As lungs age, or when they become scarred or damaged, they produce increasing amounts of a protein called PDGF-C. This protein acts like a wake-up call to dormant cancer cells, signalling them to grow and develop into secondary tumours. The discovery, published in Nature Cancer, offers the first clear explanation for why time passes so differently for different patients—and why some face recurrence while others do not.
Dr. Frances Turrell, a postdoctoral researcher at the Institute of Cancer Research, explained the implications: the team has identified not just the problem but a potential solution. An existing drug called imatinib, already used to treat other cancers, can block PDGF-C activity. In laboratory studies using mice with ER+ tumours, the drug significantly reduced cancer growth in the lungs, whether given before or after secondary tumours had already formed. This suggests a dual possibility: preventing recurrence in high-risk patients, or slowing progression in those where cancer has already spread.
The human stakes are substantial. Davies described the emotional whiplash of believing treatment had worked, only to learn her cancer had metastasized. "Finding out the cancer had spread when I thought it was all in the past was heartbreaking," she said. Yet she has channelled that experience into advocacy for research. "I don't want to waste my precious time being bitter or angry," she reflected. Her case underscores why this research matters: secondary breast cancer, while treatable, cannot be cured. Prevention or delay becomes the only realistic goal.
Professor Clare Isacke, a molecular cell biologist at the Institute of Cancer Research, framed the work as a beginning rather than an endpoint. The next phase involves understanding when age-related changes in lung tissue occur and how they vary from person to person. Only then can researchers design treatments tailored to individual risk profiles—interventions that might prevent cancer cells from waking at all, or at least postpone the moment they do. The team plans to investigate whether existing drugs like imatinib could benefit patients now, while developing more targeted therapies for the future.
Dr. Simon Vincent, director of research at Breast Cancer Now, called the discovery a step toward defusing what has long felt like an inevitable threat. "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." For Davies and others like her, the promise is not a cure but something more modest and, in its way, more precious: the possibility that science might finally give them back some measure of control over time itself.
Citações Notáveis
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'— Dr. Frances Turrell, Institute of Cancer Research, London
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.— Rachel Davies, patient
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