Cancer doesn’t just grow in isolation; it actively corrupts the immune system to fuel its own expansion. A new study reveals how certain immune cells, specifically neutrophils, switch from fighting tumors to promoting their growth. This happens through a key molecule called CCL3, which tumors manipulate these cells into producing. The finding isn’t just another lab curiosity; it suggests a way to track disease progression and potentially tailor cancer treatments.
The Tumor Microenvironment: A Battlefield Turned Collaboration
The battlefield metaphor for cancer is incomplete. Tumors don’t simply invade; they exist within a complex ecosystem of cells that interact in ways we’re only starting to understand. Identifying which interactions drive tumor growth is a massive challenge. As Mikaël Pittet, lead researcher at the University of Geneva (UNIGE), explains, “One of the difficulties lies in identifying, in an environment we are only now beginning to understand, the elements that truly influence the tumor’s ability to grow.”
This research builds on previous work from 2023 showing links between other immune cells (macrophages) and disease progression. The new findings add another piece to the puzzle, focusing on neutrophils – a common type of immune cell usually associated with defense, not promotion.
Neutrophils: From First Responders to Accomplices
Neutrophils are among the most abundant immune cells in the body, typically rushing to fight infection and injury. But in cancer, their presence is often a bad sign. Researchers found that tumors actively recruit neutrophils, then reprogram them to produce CCL3. This chemokine doesn’t help the body; it actively encourages tumor growth.
“We discovered that neutrophils recruited by the tumor undergo a reprogramming of their activity: they begin producing a molecule locally — the chemokine CCL3 — which promotes tumor growth,” explains Pittet. This shift turns a protective response into something that helps cancer thrive.
Overcoming Technical Hurdles in the Lab
Studying neutrophils is difficult. They are notoriously hard to manipulate genetically without affecting other cells. Researchers overcame this by combining multiple experimental approaches to precisely control CCL3 gene expression only in neutrophils. When CCL3 was removed, neutrophils no longer supported tumor growth. They still accumulated inside tumors, but the harmful reprogramming didn’t occur.
Widespread Evidence from Large Datasets
The findings weren’t limited to a single lab. Researchers reanalyzed data from multiple independent studies, requiring new analytical methods to detect neutrophils accurately. Standard tools often miss them due to their low genetic activity. By developing a new approach, they confirmed that CCL3 production by neutrophils is a common pattern across many cancers.
CCL3: A Potential Biomarker for Tracking Cancer
Identifying CCL3 as a key driver of neutrophil-driven tumor growth provides a promising new variable for understanding how cancers evolve. Pittet describes it as “deciphering the ‘identity card’ of tumors,” identifying key variables that determine disease progression. Once identified, these variables could help tailor treatment and improve patient care.
This research suggests a limited number of key variables drive cancer evolution. Identifying these could lead to more personalized and effective treatments.
In essence, the study reveals how tumors don’t just invade; they co-opt the body’s own defenses, turning them into accomplices. This understanding could pave the way for new ways to track and treat cancer by targeting the mechanisms tumors use to manipulate the immune system.
