斯坦福大学医学院研究团队开发了一种名为TCIP3的双功能分子，能够将驱动B细胞淋巴瘤的BCL6蛋白重新编程，激活癌细胞的自我毁灭机制。1这一分子的设计巧妙地整合了两个功能单元，其中一侧与BCL6结合，另一侧与P300和CBP蛋白相互作用。1
在小鼠模型实验中，研究人员通过每天两次的治疗方案对侵袭性人类淋巴瘤进行了检验。1结果表明，接受TCIP3治疗的肿瘤在11天内完全消退，而对照组动物的肿瘤仍保持活跃。1此外，TCIP3在实验室环境中以极低浓度就能有效杀死淋巴瘤细胞。1治疗过程中，受试小鼠未出现明显毒性迹象，血液检测也未显示炎症标志物升高。1
研究团队还发现TCIP3能够消除生发中心，这为类风湿关节炎和重症肌无力等自身免疫病的治疗提供了潜在应用前景。1该研究成果已发表在《细胞》杂志2026年第189卷第18期。1
Researchers at Stanford University have developed a dual-function molecule called TCIP3 that reprograms BCL6, a protein driving B-cell lymphoma, to activate self-destruction mechanisms in cancer cells.1 The compound works by binding to BCL6 on one side while engaging P300 and CBP proteins on the other, effectively converting a cancer driver into a therapeutic agent.1
In mouse studies, TCIP3 demonstrated remarkable efficacy, completely eliminating aggressive human lymphoma tumors within eleven days when administered twice daily.1 Treated animals showed no significant signs of toxicity, and blood tests revealed no elevated inflammatory markers.1 The compound killed lymphoma cells at extremely low concentrations in laboratory settings.1
Beyond lymphoma treatment, TCIP3 eliminated germinal centers in the immune system, suggesting potential applications for autoimmune diseases including rheumatoid arthritis and myasthenia gravis.1 The findings were published in Cell in 2026, volume 189, issue 18, with DOI: 10.1016/j.cell.2026.06.037.1
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