For some breast cancer patients, the most frightening part of the disease may not be the original tumor.
It may be what happens years later.
Cancer cells can sometimes escape from the primary tumor and travel through the bloodstream or lymphatic system to other parts of the body. Some of these cells may remain dormant—essentially entering a quiet, inactive state that allows them to survive without immediately forming a detectable tumor.
Then, under certain conditions, those silent cells can begin multiplying again.
This phenomenon is particularly concerning in triple-negative breast cancer (TNBC), an aggressive form of breast cancer that lacks three commonly targeted receptors: estrogen receptor, progesterone receptor, and HER2.
Now, researchers are investigating a potential molecular explanation for how some dormant cancer cells switch back into a growth state—and an existing drug may provide a way to interfere with that process.
🎗️ Why Triple-Negative Breast Cancer Is So Difficult to Treat
Triple-negative breast cancer accounts for a significant proportion of breast cancers and is generally considered more aggressive than many other breast cancer subtypes.
Unlike hormone-receptor-positive breast cancers, TNBC does not depend on estrogen or progesterone receptors for its growth.
It also lacks overexpression of HER2, meaning therapies designed specifically to target HER2 are not applicable to most TNBC tumors.
Doctors can still use combinations of surgery, chemotherapy, radiation, immunotherapy, and other treatments depending on the individual patient’s disease.
But recurrence and metastasis remain major challenges.
And this is where dormant cancer cells become particularly important.
ADVERTISEMENT
