Even though a breast cancer has been cured, some of its cells that have spread to the lungs can “wake up« after years of sleep, forming secondary tumors, the vast majority of which are incurable. Now, a group of researchers have revealed why.
The research, which is published in “Nature Cancer», reveals the mechanism that triggers this ‘time bomb’ of breast cancer and also suggests a strategy to deactivate it.
“This exciting discovery brings us one step closer to understanding how we can slow or stop the development of ER+ secondary breast cancer in the lung. It has the potential to benefit thousands of women living with this ‘boba of watchmaking‘ in the future, ensuring that fewer patients receive the devastating news that the disease has spread,” said Simon Vincent, director of research at Breast Cancer Now.
Patients with estrogen receptor-positive (ER+) breast cancer, the vast majority of whom are women, the most common type, have an ongoing risk of their cancer recurring in another part of their body many years or even decades after its onset. original diagnosis and treatment.
When breast cancer cells spread from the primary breast cancer to other parts of the body, it is called metastatic or secondary breast cancer, and although it is treatable, it cannot be cured.
The new research reveals how molecular changes within the lung that occur during aging can encourage the growth of these secondary tumors.
The researchers of the London Cancer Research Institute (UK) has found that the PDGF-C protein, which is present in the lung, plays a key role in influencing whether quiescent breast cancer cells stay asleep or ‘wake up’.
They reveal how molecular changes in the lung that occur with aging promote the growth of secondary tumors
The study explains that if the level of PDGF-C increases, which is more likely in an aging lung or when its tissue becomes damaged or scarred, it can cause dormant cancer cells to grow and develop into secondary breast cancer.
But, in addition, the scientists explored whether blocking the activity of PDGF-C could help prevent the ‘awakening’ of these cells and the growth of secondary tumors.
Working with mice with ER+ tumors, the researchers blocked PDGF-C signaling with the drug imatinib, a drug currently used to treat patients with chronic myeloid leukemia.
The mice received the drug both before and after the tumors developed. For both groups, lung cancer growth was significantly reduced.
“Cancer cells can survive in distant organs for decades by hiding in a dormant state,” he explains. Clare Isacke, from the London Institute of Cancer Research.
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A new lump in the breast or armpit in the area under the arm.
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Sinking or pain in the nipple.
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Redness or scaling in the nipple or breast area.
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Irritation or sinking in the skin of the breast.
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Increased thickness or swelling of a part of the breast.
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Discharge from the nipple, other than milk, including blood.
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Any change in the shape or size of the breast.
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Pain in any part of the breast.
“We have seen how aging lung tissue can cause these cancer cells to ‘wake up’ and become tumors, and we have discovered a potential strategy to ‘defuse’ these ‘time bombs.'”
Scientists now plan to better unravel how patients might benefit from the drug imatinib and, in the long term, “creating more specific treatments targeting the ‘reactivation’ mechanism,” says Frances Turrell.
For Isacke this is an exciting advance in our understanding of advanced breast cancer, and how and why breast cancer cells form secondary tumors in the lungs. The next step, she says, is “pinpoint when these age-related changes occur and how they vary between people, so that we can create treatment strategies that prevent cancer cells from waking up.”
