If this were a Hollywood movie, the plot would go like this: the villains secretly reprogram some of the heroes fighting them and, without the heroes’ knowledge, use them to expand their empire. Scientists have found that tumour cells do something strikingly similar to neutrophils, the 'first responders' of our immune system.
Neutrophils make up the largest proportion of white blood cells (about 50 to 70 per cent ) and are essentially the infantry of the body’s biological defence: fast-acting, short-lived, and incredibly aggressive. Recent studies have shown that neutrophils do not just act as lone warriors. They function as a collective system with memory, coordinating their movements like an ant colony to repair tissue and manage long-term inflammation.
Now, scientists at the University of Geneva (UNIGE), working with the Ludwig Institute for Cancer Research, have found that it is because these warriors are reprogrammed that some cancers progress more aggressively.
The study found that, when exposed to a tumour ecosystem, these cells begin producing a molecule known as the chemokine CCL3. CCL3, in turn, encourages tumours to grow rather than helping the body fight disease.
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Today, cancer is seen not just as a mass of malignant cells but as a complex, dynamic biological system. The tumour actively recruits and “-'enslaves' surrounding healthy tissue to create its ecosystem.
Since it is made up of many different cell types, all influencing one another, it is highly complex, and scientists have not yet figured out which of these interactions truly drives tumour growth.
Like a small principality, it has its own physical fortress made up of stromal cells, specifically cancer-associated fibroblasts, that protect the tumour. The tumour also sends out signals to grow its own blood vessels. These are often 'leaky,' creating a high-pressure environment that blocks drug delivery.
It is within this ecosystem that the reprogramming of immune cells happens, and once they become turncoats because of CCL3 production, these cells act as 'guards' that hide the tumour from the rest of the body.
The research team used multiple experimental strategies to precisely control the CCL3 gene in neutrophils without affecting other cells. When they removed CCL3, neutrophils no longer supported tumour growth. They continued to function normally in the bloodstream and were still able to accumulate inside tumours, but the harmful reprogramming no longer occurred.
