- Cancer cells may reprogram neutrophils to produce CCL3, aiding tumour growth
- Neutrophils, usually infection defenders, can promote tumour progression when reprogrammed
- Identifying key tumour variables like CCL3 could improve personalized cancer treatment strategies
Cancer cells could be "reprogramming" immune cells to produce a molecule that promotes tumour growth, a new study has found, postulating that presence of the molecule may be an indicator of cancer progression.
Studies have shown that cancer cells can 'trick' the immune system into believing they are healthy and prevent themselves from getting destroyed.
Researchers, including those at the University of Geneva and the Ludwig Institute for Cancer Research in Switzerland, have discovered that a type of immune cells -- neutrophils -- undergo "reprogramming" upon encountering a tumour condition, contributing to cancer progression.
The study, published in the Cancer Cell journal, describes a mechanism which researchers said appears to be a major variable in tumour biology and could serve as an indicator of disease progression.
One of the difficulties is identifying the elements that truly influence the tumour's ability to grow, lead researcher Mikaël Pittet, a faculty in the department of pathology and immunology at the University of Geneva, said.
The research team had previously showed that expression of two genes in macrophages -- a type of immune cells -- is strongly linked to disease progression, constituting a simple but informative variable for understanding tumours and anticipating their trajectory, Pittet said.
"Our new study highlights a second variable, this time involving another population of immune cells, neutrophils," he said.
"These findings establish CCL3 as a conserved marker and functional driver of pro-tumour neutrophils in growing tumours, and provide a scalable framework for dissecting neutrophil biology across cancer types," the researchers wrote.
One of the most abundant of immune cells, neutrophils form the first line of defence against infections and injuries.
However, in the context of cancer, their presence is generally a bad omen, researchers held.
"We discovered that neutrophils recruited by the tumour undergo a reprogramming of their activity: they begin producing a molecule locally -- the chemokine CCL3 -- which promotes tumour growth," Pittet said.
He said the researchers controlled the behaviour of the CCL3 gene specifically in neutrophils -- considered particularly complex as immune cells are difficult to manipulate genetically.
Without CCL3, neutrophils lose their pro-tumour action. They retain their physiological functions in the blood and can even accumulate in tumours, but no longer adopt the deleterious reprogramming previously observed, the researchers said.
They also re-examined data from numerous independent studies. "We are deciphering the 'identity card' of tumours, by identifying, one by one, the key variables that determine the evolution of the disease," Pittet said.
"Our work suggests that there is a limited number of these variables. Once they are properly identified, they could help better tailor the management of each patient and, ultimately, offer more effective and personalised care," the researcher said.
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