Swiss researchers reveal mechanism behind breast cancer metastases
A certain type of white blood cell promotes the formation of metastases in breast cancer, according to researchers at the University of Fribourg, which says this discovery could be important for the development of new treatments.
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Pesquisadores suíços descobrem causa de metástases do câncer de mama
Although early detection and modern treatments offer most patients with breast cancer a good chance of recovery, around one in four of those affected develops metastases, the University of Fribourg wrote in a press release on Monday.
Metastatic cancer stem cells have the ability to break away from the original tumour and spread to other parts of the body, which promotes the spread of the cancer and makes treatment more difficult.
The development of metastases is promoted by inflammation inside the tumour and in its surroundings. The research team led by Curzio Rüegg has now identified a new mechanism that links this inflammation and the development of metastases. So-called granulocytes, a type of white blood cell that plays an important defence role in acute inflammation, facilitate the formation of metastases, the researchers showed in a study published in The Journal of Clinical Investigation.
“In a way, the cancer cells induce the granulocytes at the tumour site to produce inflammatory mediators, interleukin 6 and oncostatin,” Rüegg explained in the press release. In a second step, these two mediators then transform the breast cancer cells into a particularly aggressive form known as highly metastatic cancer stem cells.
In the study, the researchers showed in the laboratory that the inhibition of these two mediators suppresses the formation of cancer stem cells and metastases.
This work opens up real opportunities for the development of new treatments for patients with a high risk of metastasis, the university wrote. Interleukin-6 inhibitors are already available and are used to treat patients with chronic inflammatory diseases.
Translated from German by DeepL/ts
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