下一代基于抗体的癌症治疗:抗体-药物偶联物和双特异性抗体在血液系统恶性肿瘤和实体瘤中的应用
Next-generation antibody-based therapeutics in cancer: antibody-drug conjugates bispecific antibodies across hematologic malignancies and solid tumors
肿瘤学的治疗范式正在经历由抗体药物偶联物(ADC)和双特异性抗体(bsAb)驱动的深刻变革。
FRONTIER PAPERS
Next-generation antibody-based therapeutics in cancer: antibody-drug conjugates bispecific antibodies across hematologic malignancies and solid tumors
肿瘤学的治疗范式正在经历由抗体药物偶联物(ADC)和双特异性抗体(bsAb)驱动的深刻变革。
A novel triple-knockout allogeneic BCMA CAR T-cell therapy (CT0590) for multiple myeloma: preclinical and phase 1 study.
这些结果提示,CAR-NKG2A技术可能克服HVGR,尤其是在NK细胞上NKG2A表达升高的患者中。
Anti-BCMA/GPRC5D CAR T cells in patients with relapsed or refractory multiple myeloma who have extraosseous extramedullary disease.
这些发现支持抗 BCMA/GPRC5D 双特异性 CAR T 细胞在伴骨外 EMD 的复发/难治性多发性骨髓瘤(RRMM)患者中诱导了高缓解率,且安全性可控。
PD-L1(+) exosomes as biomarkers and therapeutic targets in multiple myeloma: implications for CAR-T efficacy and combination immunotherapy.
PD-L1+外泌体可能作为MM疾病侵袭性和CAR-T治疗结局的生物标志物。通过损害CD8+ T细胞功能并促进终末耗竭,它们可能促进免疫抵抗。联合外泌体释放通路阻断与PD-1阻断作为增强CAR-T疗效的策略值得进一步研究。
Frontline T cell-redirecting therapies in newly diagnosed multiple myeloma: key signals from the 2025 ASH Annual Meeting.
2025年ASH年会上公布的早期一线数据表明,T细胞重定向策略,包括嵌合抗原受体(CAR)-T细胞和双特异性抗体(BsAbs),可在新诊断多发性骨髓瘤(NDMM)中诱导快速、高比例的微小残留病(MRD)阴性缓解,包括不适合移植(TI)和高危人群。
Subsequent CAR-T and engineered antibody for relapsed/refractory multiple myeloma following BCMA-targeted treatment: a systematic review and meta-anal
GPRC5D CAR-T 在 BCMA 治疗后场景中显示出优于工程化抗体的疗效。
Programmable engineered bacteria manipulate metabolism and remodel the TME in situ for enhancing adoptive cell therapy.
我们的研究结果共同表明,工程化细菌是可编程的免疫代谢调节剂,能够在实体瘤中实现有效且安全的 ACT。
Dexamethasone activates anti-tumor immunity in multiple myeloma by dismantling the GR-PPP1CB complex to restore STING/IRF3 signaling.
本研究揭示了一条对糖皮质激素敏感的抑制轴,其中 GR-PPP1CB 在 MM 中持续抑制 STING-TBK1-IRF3 信号通路。
Iron-mediated ferroptosis impairs CAR-T cell function and antitumor efficacy.
这些发现共同确定,铁驱动的铁死亡是 CAR-T 细胞功能障碍的决定因素,也是阻碍 CAR-T 获得持久疗效的可靶向屏障。
NAT10-Mediated ac4C Modification of circANKRD12 Reprograms the Tumor Microenvironment.
开发同时靶向肿瘤增殖和免疫抑制微环境的抗癌策略仍然是一项重大挑战。
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