在患有转移性神经内分泌瘤的患者中,PRRT加-166-SIRT (HEPAR PLuS) 与仅PRRT:一种倾向性得分匹配分析
W B Veldhuis1, T Walter2, D M V de Vries-Huizing3
1Department of Radiology and Nuclear Medicine, University Medical Center Utrecht, Utrecht, The Netherlands.
Journal of neuroendocrinology
|April 30, 2025
概括
在受体放射性核酸治疗 (PRRT) 后添加荷-166 (166Ho) - 微球选择性内部放射治疗 (SIRT) 在神经内分泌肝转移 (NELM) 患者中改善了肝脏无进展生存率. 然而,这种组合并没有显著提高整体存活率.
科学领域:
- 核医学是一种核医学.
- 在瘤学瘤学.
- 辐射疗法 辐射疗法
背景情况:
- 大量的神经内分泌肝转移 (NELM) 对接受受体放射性核素治疗 (PRRT) 的患者的存活率产生负面影响.
- 在PRRT后使用holmium-166 (166Ho) 微球的选择性内部放射治疗 (SIRT) 在NELM患者中显示出安全性和有效性.
研究的目的:
- 评估在NELM患者中与单独的PRRT相比,将PRRT与166Ho-SIRT结合使用的疗效和生存益处.
- 评估无进展生存期 (PFS),肝脏PFS (hPFS),客观反应率 (ORR) 和整体生存期 (OS).
主要方法:
- 一个倾向性得分匹配的历史队列研究,比较PRRT + 166Ho-SIRT与PRRT-only.
- 来自多个中心的回顾性数据收集,将患者与潜在的HEPAR PLuS研究队列匹配.
- 对人口统计,临床,实验室和成像数据的分析,以2年PFS和hPFS作为主要终点.
主要成果:
- 在PRRT+166Ho-SIRT组中,患有两年PFS和hPFS的患者比例较高 (68%和82%),相比只有PRRT组 (55%和50%).
- 平均PFS可比 (31个月与30个月),但PRRT + 166Ho-SIRT显示肝脏进展或死亡的初始延迟 (27个月与22个月).
- 最好的ORR显著高于PRRT+166Ho-SIRT (71%) 与仅使用PRRT (25%),特别是在肠道瘤中.
结论:
- 166PRRT后的Ho-SIRT对NELM患者的肝病进展产生了积极的影响,改善了2年的hPFS和瘤反应.
- 组合疗法延缓肝脏进展或死亡,但不会转化为改善整体PFS或整体存活率.
- 在NELM中,PRRT + 166Ho-SIRT为肝脏导向治疗提供了潜在的好处,因此需要进一步调查其对生存的影响.
更多相关视频
09:49A Whole Body Dosimetry Protocol for Peptide-Receptor Radionuclide Therapy PRRT: 2D Planar Image and Hybrid 2D+3D SPECT/CT Image Methods
Published on: April 24, 2020
9.6K
09:11Y-90 Radioembolization and PD-1 Inhibitor as Neoadjuvant Treatment in Hepatocellular Carcinoma
Published on: May 24, 2024
348
相关概念视频
Treatment Resistant Cancers
Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
Treatment Resistent Cancers
Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
