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Immune cells don't just fight cancer — sometimes they help it spread. Researchers at ULB found that neutrophils and macrophages form distinct "neighborhoods" around cancer cells, using chemical signals to drive metastasis. Blocking one of those signals, oncostatin M, reduced metastatic spread in mice — and the same mechanism was spotted in human breast, pancreatic, lung, and bladder cancers.
Most cancer deaths aren't caused by the original tumor — they're caused by metastases, cancer cells that break away and colonize distant organs. A new study published in Nature Cancer reveals that immune cells play a surprising and active role in enabling this process, opening the door to potential new therapies.
Researchers at the Université libre de Bruxelles (ULB) discovered that tumors are organized into distinct immune "neighborhoods." Neutrophils cluster around cancer cells in a dangerous intermediate state (called hybrid EMT), releasing a molecule called oncostatin M that locks cancer cells in their most metastasis-prone form. Meanwhile, macrophages surround more advanced cancer cells, releasing TGFB21 to push them further along the metastatic pathway.
When researchers blocked oncostatin M in mice, the number of hybrid cancer cells dropped — and so did lung metastases. Crucially, the same neutrophil-oncostatin M neighborhoods were found in human breast, pancreatic, lung, and bladder cancers.
Key Takeaways:
Why it matters: This research reframes metastasis as a conversation between cancer cells and the immune system — not just a cancer-cell-autonomous process. Targeting these immune signals could one day help prevent cancer spread and improve responses to existing therapies.
