953-肺癌早期的纤维化微环境构建

这份研究详细阐述了肺腺癌发病初期，突变上皮细胞如何通过构建特定的微环境来促进肿瘤生长。研究发现，携带KrasG12D突变的肺泡干细胞会分泌双调蛋白（AREG），进而激活相邻成纤维细胞中的EGFR信号通路。这种相互作用诱导成纤维细胞转化为纤维化状态，并随后触发肺泡巨噬细胞的重新编程与免疫抑制回路的形成。通过单细胞测序和类器官模型，研究人员证实了这种由上皮细胞驱动的多细胞信号轴是肿瘤启动的核心。实验表明，阻断AREG-EGFR通路可以有效瓦解这种支持肿瘤的“生态位”，为预防早期肺癌向耐药性疾病演变提供了潜在的治疗靶点。References:* Cardoso E C, Lee H, England F J, et al. Early fibrotic niches establish tumour-permissive microenvironments[J]. Nature, 2026:...去小宇宙查看完整单集简介前往小宇宙评论区与主播互动

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953-肺癌早期的纤维化微环境构建

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