AI Insight
In EBV-positive gastric cancers, the microRNA miR-155 suppresses expression of ICOSL and SOCS1, two molecules critical for activating and sustaining cytotoxic T lymphocyte (CTL) responses. Although these tumors are infiltrated by abundant CTLs, the loss of ICOSL and SOCS1 renders these immune cells functionally ineffective, allowing cancer cells to evade immune destruction. This mechanism identifies a specific molecular pathway through which EBV-associated gastric cancers exploit host immune regulation to promote tumor survival.
Why it matters
Understanding how miR-155 drives immune evasion in EBV-positive gastric cancer could inform the development of targeted therapies, such as restoring ICOSL or SOCS1 function, potentially improving outcomes for patients who do not adequately respond to existing immunotherapies. Given that EBV-positive gastric cancer represents a distinct molecular subtype, these findings may also help stratify patients for more personalized treatment approaches.
Proceedings of the National Academy of Sciences, Volume 123, Issue 19, May 2026. <br/>SignificanceCytotoxic T cells [cytotoxic T lymphocytes (CTLs)] play a critical role in antitumor immunity; however, cancer cells have evolved immune evasion strategies that impair CTL recognition and effector function. Epstein–Barr virus (EBV)-positive …