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0The research explores how mutant lung stem cells actively reconstruct their surroundings to facilitate the early stages of tumor formation. By utilizing single-cell and spatial analysis, the study identifies a specific epithelial-stromal-immune circuit driven by an amphiregulin–EGFR signaling axis. This process begins when oncogenic AT2 cells adopt a regenerative state, triggering adjacent fibroblasts to transform into a fibrotic niche that further recruits and alters immune cells. These reprogrammed macrophages and fibroblasts create a self-sustaining, tumor-permissive environment that supports malignant growth before it becomes clinically advanced. Crucially, the researchers demonstrate that disrupting this signaling pathway can halt niche formation and prevent tumor initiation. This discovery highlights a therapeutic window for early intervention, potentially stopping lung cancer before it develops resistance to treatment.
References:
Cardoso E C, Lee H, England F J, et al. Early fibrotic niches establish tumour-permissive microenvironments[J]. Nature, 2026: 1-11.
