EPISODE · Jan 3, 2026 · 19 MIN
355-潘氏样分化驱动结直肠癌耐药
from 聊聊Sci
这项研究揭示了结直肠癌（CRC）在接受KRAS与EGFR联合靶向治疗时，会通过一种非遗传性的谱系可塑性机制产生耐药性。研究人员发现，存活的癌细胞会向类潘氏细胞（Paneth-like）状态转变，从而逃避药物杀伤，且这一现象在小鼠模型、类器官及临床患者样本中均得到了验证。通过CRISPR筛选和转录组分析，研究确认了SMAD1-FGFR3信号轴是驱动这种细胞状态转换及MAPK信号通路重新激活的关键因素。研究进一步证明，利用FGFR抑制剂（如futibatinib）阻断该轴线，可以有效抑制细胞向类潘氏状态转变并恢复药物敏感性。该成果为克服结直肠癌靶向治疗耐药提供了新的三联疗法策略。References: Zhang Y, Chen J, She Y, et al. Paneth-like transition drives resistance to dual targeting of KRAS and EGFR in colorectal cancer[J]. Cancer Cell, 2025.前往小宇宙评论区与主播互动
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355-潘氏样分化驱动结直肠癌耐药
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