Tumor Environment Reprograms Immune Cells to Fuel Cancer Growth

Researchers at the University of Geneva have uncovered a significant mechanism through which tumors manipulate the immune system to promote cancer growth. Their study reveals that neutrophils, typically the body’s defense cells against infections, can be reprogrammed within tumor environments to enhance cancer progression. This discovery, published on February 10, 2026 in the journal Cancer Cell, highlights the complexity of interactions between cancer cells and the immune system, shedding light on why some cancers advance more aggressively than others.

Understanding cancer growth is a substantial challenge for researchers. The study conducted in collaboration with the Ludwig Institute for Cancer Research demonstrates how neutrophils, rather than fighting tumors, can become unwitting allies of cancer. When these immune cells enter a tumor, they begin to produce a molecule called CCL3, which actively encourages tumor growth instead of inhibiting it. The implications of this finding are profound, as it suggests that CCL3 may serve as a potential marker for tracking cancer progression across various types of tumors.

Deciphering Tumor Interactions

Cancer does not develop in isolation; it exists within a complex environment where multiple cell types interact. Identifying which elements contribute to tumor growth poses a significant challenge. “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,” stated Mikaël Pittet, a full professor at the UNIGE Faculty of Medicine and member of the Lausanne Branch of the Ludwig Institute for Cancer Research.

Pittet’s team previously demonstrated in 2023 that specific gene expressions in macrophages correlate strongly with disease progression. The current study introduces a second variable—neutrophils—which appear to play a similar role in promoting tumor growth.

Neutrophils: From Defenders to Tumor Promoters

Neutrophils typically act as an early defense against infections and injuries. However, their recruitment to tumors often correlates with poorer patient outcomes. The researchers found that tumors actively recruit neutrophils and reprogram them to produce CCL3 locally. “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,” Pittet explained.

This transformation shifts the neutrophils’ role from protective defenders to facilitators of cancer proliferation.

Overcoming the technical challenges associated with studying neutrophils was essential for this research. “Neutrophils are particularly difficult to study and to manipulate genetically,” noted Evangelia Bolli, co-lead author of the study. The research team utilized various experimental strategies to control the expression of the CCL3 gene specifically in neutrophils without impacting other cell types.

The results were telling: when CCL3 was eliminated, neutrophils maintained their normal functions in the bloodstream but ceased to promote tumor growth.

Innovative Data Analysis Reveals Patterns

The research team further validated their findings by reanalyzing data from numerous independent studies. This process necessitated new analytical methods since neutrophils often exhibit low genetic activity, making them difficult to detect with standard tools. Pratyaksha Wirapati, co-first author and bioinformatics specialist, explained, “We had to innovate to detect neutrophils more accurately. By developing a new method, we have been able to show that, in many cancers, these cells share a common trajectory: they produce large amounts of CCL3, which is associated with pro-tumor activity.”

This identification of CCL3 as a critical factor in neutrophil-driven tumor growth presents a promising avenue for cancer research. Pittet emphasized the importance of understanding the “identity card” of tumors, stating, “We are deciphering the key variables that determine the evolution of the disease. Once they are properly identified, they could help better tailor the management of each patient and, ultimately, offer more effective and personalized care.”

The findings from the University of Geneva mark a significant step forward in the ongoing quest to understand the complexities of cancer biology and develop more effective treatment strategies.