Research from the Université de Genève has revealed a significant mechanism by which tumors can manipulate the immune system to foster their own growth. The study, published in the journal Cancer Cell on February 10, 2026, highlights how neutrophils, typically known as defenders against infections, can be reprogrammed within tumors to assist in cancer progression.
The investigation, conducted in collaboration with the Ludwig Institute for Cancer Research, shows that neutrophils alter their function when they enter the tumor environment. Instead of combating cancer cells, these immune cells start producing a molecule known as CCL3, which actively encourages tumor growth. This discovery could provide insights into why certain cancers exhibit more aggressive behavior, as the presence of CCL3 appears across various cancer types.
Understanding Tumor Interaction with Immune Cells
Cancer does not develop in isolation; it exists within a complex cellular environment where various cell types interact. Identifying which of these interactions drive tumor growth is crucial, as explained by Mikaël Pittet, a full professor at UNIGE and a leading figure in this research. “One of the difficulties lies in identifying the elements that influence the tumor’s ability to grow,” he stated.
This study builds on previous findings where Pittet’s team identified a link between specific gene expressions in macrophages and disease progression. The new research introduces neutrophils as another critical factor influencing tumor dynamics.
Neutrophils are the body’s most abundant type of immune cell, typically serving as an early defense mechanism against infections. However, their presence in tumors correlates with poorer outcomes for patients. The study reveals that tumors actively recruit neutrophils and induce a shift in their behavior that supports cancer growth. “We discovered that neutrophils recruited by the tumor undergo a reprogramming of their activity, producing CCL3 locally, which promotes tumor growth,” Pittet explained.
Overcoming Research Challenges in Neutrophil Studies
Researching neutrophils poses significant technical challenges, particularly regarding genetic manipulation. Evangelia Bolli, co-lead author of the study, emphasized the difficulties in studying these cells. “Neutrophils are particularly difficult to study and to manipulate genetically,” she noted.
To navigate these challenges, the research team employed various experimental strategies to control the expression of the CCL3 gene specifically in neutrophils without affecting surrounding cells. They discovered that when CCL3 was removed, neutrophils no longer supported tumor growth while retaining their normal functions in the bloodstream.
The researchers further strengthened their findings by analyzing data from multiple independent studies. This required innovative methods to accurately detect neutrophils, as their low genetic activity often renders them difficult to identify using standard analysis tools. Pratyaksha Wirapati, a bioinformatics specialist, explained, “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.”
The identification of CCL3 as a critical driver of tumor growth opens new avenues in cancer research. “We are deciphering the ‘identity card’ of tumors by identifying key variables that determine the evolution of the disease,” Pittet stated.
This research not only enhances understanding of tumor biology but may also lead to more personalized treatment strategies for cancer patients in the future. By identifying specific markers and mechanisms such as CCL3, healthcare providers could tailor interventions more effectively, ultimately improving patient outcomes.
