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在胰腺神经内分泌瘤中,CD93阻塞克服了sunitinib耐药性

Yi Sun¹, Yuki Fujiwara¹, Robert J Torphy¹

¹Division of Surgical Oncology, Department of Surgery, the University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.

Molecular therapy : the journal of the American Society of Gene Therapy

|July 31, 2025

概括

用抗体向CD93-IGFBP7轴可以克服胰腺神经内分泌瘤 (PanNETs) 对sunitinib治疗的耐药性. 这种方法使瘤血管正常化,提高治疗疗效,并延长晚期PanNETs的存活时间.

科学领域:

在瘤学瘤学.
癌症生物学癌症生物学
免疫治疗是一种免疫疗法.

背景情况:

胰腺神经内分泌瘤 (PanNETs) 很少见,但恶性瘤的数量正在增加.
苏尼提尼布是一种抗血管原抑制剂,在晚期的PanNET中显示出益处,但面临耐药性.
像CD93和IGFBP7这样的瘤微环境 (TME) 因素在PanNET进展中起作用.

研究的目的:

调查在PanNET中准CD93-IGFBP7轴的治疗潜力.
为了评估抗CD93单克隆抗体 (mAbs) 和苏尼提尼的组合.
了解CD93阻断影响瘤血管和抵抗的机制.

主要方法:

使用了PanNETs的RIP1-Tag2鼠标模型.
单独使用抗CD93mAbs和与苏尼提尼布联合使用.
评估瘤血管正常化,进展,转移,缺氧和侵入性.
监测的整体存活率.

主要成果:

破坏CD93/IGFBP7相互作用使瘤血管正常化,抑制了PanNET进展和转移.
组合疗法协同减缓了瘤生长,改善了生存率.
CD93阻断减轻了苏尼替尼诱导的缺氧和侵入性.
反CD93 mAb治疗延长了晚期,抗苏尼替尼抗性的PanNETs的存活时间.

结论:

针对CD93-IGFBP7轴是一个有前途的策略,以提高PanNETs中的sunitinib疗效.
CD93阻断使瘤血管正常化,克服了抵抗机制.
这种方法为先进的泛网提供了潜在的新治疗途径.

关键词:

在CD93封锁中.IGFBP7 IGFBP7 IGFBP7 IGFBP7 IGFBP7 IGFBP7 IGFBP7 IGFBP7 这是一种反angiogenic.胰腺的神经内分泌瘤苏尼提尼布 (sunitinib) 的使用方法瘤缺氧瘤缺氧血管正常化血管正常化

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