Scientists Find How Tumors Hijack Immune Cells

Scientists at the University of Geneva have uncovered why some cancers grow more aggressively than others, and the answer lies in a surprising betrayal happening inside our own bodies.

Neutrophils are immune cells that normally protect us from infection and disease. But researchers found that tumors can actually reprogram these cellular defenders to work against us instead.

Once neutrophils enter a tumor's environment, something remarkable and troubling happens. The cancer flips a biological switch that transforms these protective cells into cancer supporters.

The key to this transformation is a molecule called CCL3. When reprogrammed neutrophils start producing CCL3, they actively promote tumor growth instead of fighting it.

"We are deciphering the 'identity card' of tumors by identifying, one by one, the key variables that determine the evolution of the disease," explains Professor Mikaël Pittet, who led the research published in Cancer Cell.

The discovery was technically challenging because neutrophils are notoriously difficult to study and manipulate in laboratory settings. The team had to develop innovative approaches to control the CCL3 gene specifically in neutrophils without affecting other cells.

Their breakthrough came when they successfully removed CCL3 from neutrophils in their experiments. Without CCL3, the neutrophils continued functioning normally in the bloodstream but could no longer support tumor growth, even when they accumulated inside tumors.

The Bright Side

This discovery opens a promising new pathway for cancer treatment. Because CCL3 production appears across many different cancer types, it could serve as a universal marker to track how aggressively a tumor is progressing.

The researchers strengthened their findings by reanalyzing data from numerous independent studies, developing new analytical methods to detect neutrophil activity that standard tools often miss. The pattern held true across multiple cancer types, suggesting this mechanism is fundamental to how many tumors grow.

Pittet believes there may be only a limited number of these critical variables that truly determine cancer progression. Once doctors can identify them all, they could tailor treatment to each patient's specific tumor profile, moving closer to truly personalized cancer care.

This research builds on the team's 2023 discovery about macrophages, another type of immune cell. Together, these findings are creating a clearer picture of how tumors manipulate their environment to survive and grow—and more importantly, where medicine can intervene to stop them.