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Genetic mutations are known causes of cancer, but scientists now suggest inflammation plays a critical role in stopping abnormal cells from becoming tumors. Miriam Merad at Mount Sinai explains that while mutations give cells an advantage, the immune system often keeps them in check. A new approach called cancer interception aims to boost this surveillance before growths turn malignant. Early trials for lung and pancreatic cancers show promise, with some studies indicating that training the immune system can recognize mutated cells effectively.

Researchers discovered that tumors send signals to bone marrow cells, causing protective macrophages to become pro-cancer allies. This shift happens earlier than previously thought, creating an environment that blocks immune defense. By targeting a protein called NRF2, which acts as a switch for inflammation, scientists found they could reverse this process. Blocking NRF2 strengthened the immune attack against early lung cancer in mice, suggesting treatments should alter the tumor’s surroundings rather than just attacking the mass itself.

Clinical trials are now testing these ideas in humans using existing drugs like canakinumab, which was originally developed for heart disease but reduced lung cancer deaths by over 67 percent in earlier studies. The Can-Prevent-Lung trial will test this drug on people with high-risk lung growths identified by CT scans. Other teams are exploring similar strategies for pancreatic cancer, including using AI to spot tiny abnormalities and evaluating blood tests to monitor inflammation levels before treatment is needed.