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Updated: Jan 20, 2026

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Published on: June 19, 2016
La mutación KRASG12/13 modula los resultados del CCRC al alterar la retroalimentación positiva entre macrófagos y
Xuehan Yan1, Juncheng Su1, Hongyuan Liu2
1Department of Gastrointestinal Surgery, Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200127, China.
Abstract:
Kirsten rat sarcoma viral oncogene (KRAS) mutation influences colorectal cancer (CRC) progression, but their specific impact on the tumor immune microenvironment remains poorly defined. This study establishes that KRASG12/13 mutation disrupts critical positive feedback between macrophages and CD4+ T cells. Mechanistically, KRASG12/13-mutant tumor cells secrete elevated interleukin-10 (IL-10), which suppresses macrophage production of chemokine ligand 9/10 (CXCL9/10) and major histocompatibility complex II (MHC-II). This impairs the infiltration and activation of CXCR3+CD4+ T cells, fostering an immunosuppressive niche. By integrating multi-omics data from clinical cohorts and validating findings in vivo, we show that combining KRAS inhibitors with CXCL9/10 restoration effectively overcomes this immune suppression and controls tumor growth. Our work delineates a targetable immune evasion mechanism and provides a cohesive prognostic and therapeutic framework for KRASG12/13-mutant CRC.
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