Daijiworld Media Network - Geneva

Geneva, Feb 7: Cancer cells may be capable of “reprogramming” immune cells to produce a molecule that actively promotes tumour growth, according to a new international study that suggests the presence of this molecule could indicate cancer progression.

Researchers from the University of Geneva and the Ludwig Institute for Cancer Research in Switzerland found that neutrophils — a key type of immune cell — undergo functional changes when exposed to tumour conditions, ultimately aiding cancer growth rather than fighting it.

The study, published in the journal Cancer Cell, explains that while immune cells are designed to defend the body, cancer cells can manipulate them into supporting tumour development. Neutrophils, which normally act as the body’s first line of defence against infections and injuries, were found to be reprogrammed by tumours to produce a chemokine called CCL3.

“Neutrophils recruited by the tumour undergo a reprogramming of their activity: they begin producing a molecule locally — the chemokine CCL3 — which promotes tumour growth,” said lead researcher Mikaël Pittet from the University of Geneva’s department of pathology and immunology.

The researchers described this mechanism as a major variable in tumour biology and a potential marker of disease progression. They noted that identifying such variables is crucial to understanding how tumours grow and spread.

In earlier work, the research team had shown that the expression of two genes in macrophages — another immune cell type — was strongly linked to cancer progression. The new findings highlight neutrophils as a second critical factor.

“These findings establish CCL3 as a conserved marker and functional driver of pro-tumour neutrophils in growing tumours,” the researchers said, adding that it offers a scalable way to study neutrophil behaviour across different cancers.

Importantly, when scientists suppressed the CCL3 gene specifically in neutrophils, the cells lost their tumour-promoting behaviour. While they continued to function normally in the bloodstream and could still accumulate in tumours, they no longer aided cancer growth.

By re-examining data from multiple independent studies, the team believes there may be only a limited number of such key variables that define how a tumour evolves.

“We are deciphering the ‘identity card’ of tumours, identifying the variables that determine disease evolution,” Pittet said. “Once properly identified, these could help better tailor patient management and offer more effective, personalised care.”