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KRAS-mutant tumours frequently accumulate regulatory T cells (Tregs), myeloid-derived suppressor cells (MDSCs) and tumour-associated macrophages, which collectively dampen cytotoxic T-cell activity through the secretion of inhibitory cytokines (eg, interleukin 10 (IL-10), transforming growth factor beta 1) and the expression of immune checkpoint ligands.86 In parallel, dense stromal fibrosis, driven by activated cancer-associated fibroblasts, creates a physical barrier to immune infiltration and drug delivery, while also releasing growth factors and extracellular matrix components that sustain tumour survival.87 Collectively, these intrinsic mutations and extrinsic microenvironmental factors blunt KRASi activity, underscoring the need for rational combination strategies to overcome primary resistance

Coord Chem Rev 63:127160