Researchers at the Barcelona Biomedicine Research Institute have identified that some cancer cells can “switch off” genes that trigger inflammation, allowing them to hide within the body. The finding, published in Cancer Research, points to an epigenetic process by which tumor cells suppress inflammatory signals and evade early immune detection. By quieting these alarms, cancer cells can pass unnoticed while they grow and spread, complicating efforts to eliminate them at initial stages. This hidden behavior helps explain why some cancers persist and recur after treatment, even when visible tumors seem to have diminished.
Experts describe a state called “persistence” in which cancer cells temporarily and reversibly downregulate their own activity and inflammatory signaling. After a course of therapy such as chemotherapy is completed, these dormant cells can awaken and resume growth, increasing the likelihood of relapse. This awakening provides a plausible mechanism for disease return and underscores why complete eradication remains challenging in some patients, even when initial responses appear favorable.
In laboratory experiments, scientists observed resident tumor cells using an epigenetic mechanism to block genes responsible for inflammation. Inflammation is a protective process that helps coordinate detection and elimination of threats. Suppressing this response can keep cancer cells from being recognized and destroyed by the immune system, effectively helping them hide in plain sight and persist despite immune pressure and treatment cycles.
Unlike senescent cells, which actively drive inflammation and use different strategies to escape immune attack, persistent cancer cells operate in a stealth mode. This quiet behavior makes them particularly dangerous because they can survive treatments and later give rise to renewed tumor growth, complicating patient prognosis and ongoing management of the disease.
Researchers believe that drugs targeting epigenetic control could reactivate inflammatory genes and undermine the viability of persistent cells. Yet translating this approach into safe, effective therapies will require more work to determine efficacy, safety, and how best to combine such drugs with standard care. Earlier studies described a factor linked to reduced survival in pediatric cancers, highlighting the urgency of understanding immune evasion across age groups and disease types.