CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:Tumor Growth Rate in Spinal Giant Cell Tumors of Bone and Association With the Immune Microenvironment and Denosumab Treatment Responsiveness: A Multicenter Study.
Tumor Growth Rate in Spinal Giant Cell Tumors of Bone and Association With the Immune Microenvironment and Denosumab Treatment Responsiveness: A Multicenter Study.
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这些数据支持将 TGR 作为脊柱 GCTB 临床相关结局和地舒单抗治疗反应的可靠预测工具,这可能有助于指导患者的预后风险分层和治疗优化。
目前,关于肿瘤生长速率(TGR)在脊柱骨巨细胞瘤(GCTB)中的预后价值知之甚少。
探讨TGR与脊柱GCTB的临床病理特征、免疫微环境、预后及地舒单抗治疗反应的相关性。
纳入2011年至2021年在5个中心接受治疗的128例脊柱GCTB患者。由2名独立的神经放射科医师使用至少2次术前薄层磁共振成像扫描评估TGR,最短间隔为2个月。采用免疫组织化学评估TIL(肿瘤浸润淋巴细胞)亚型,包括CD3、CD4、CD8、CD20、PD-1、PD-L1和Foxp3。随后分析这些参数与患者结局(无进展生存期和总生存期)、临床病理特征及地舒单抗治疗反应性的关联。
高 TGR 预示了较差的无进展生存期和总生存期(均 P < .001)。此外,TGR 与术后神经功能障碍(P < .001)、Enneking 分期(P = .016)、denosumab 治疗反应性(P = .035)以及 CD3 +(P < .001)、PD-1 +(P = .009)、PD-L1 +(P < .001)和 FoxP3 + TIL(肿瘤浸润淋巴细胞)(P = .02)的数量相关。重要的是,在预测脊柱 GCTB 的临床结局方面,TGR 优于传统的 Enneking、Campanacci 和美国癌症联合委员会分期系统。
Currently, little is known about the prognostic value of tumor growth rate (TGR) in spinal giant cell tumors of bone (GCTB).
To investigate the correlation of TGR with clinicopathological features, immune microenvironment, prognosis, and response to denosumab treatment of spinal GCTB.
A total of 128 patients with spinal GCTB treated at 5 centers from 2011 to 2021 were included. TGR was assessed by 2 independent neuroradiologists using at least 2 preoperative thin-section magnetic resonance imaging scans at a minimum interval of 2 months. Immunohistochemistry was used to assess tumor-infiltrating lymphocyte subtypes for CD3, CD4, CD8, CD20, PD-1, PD-L1, and Foxp3. Then, these parameters were analyzed for their associations with patient outcomes (progression-free survival and overall survival), clinicopathological features, and denosumab treatment responsiveness.
High TGR predicted both poor progression-free survival and overall survival (both P < .001). In addition, TGR was associated with postoperative neurological dysfunction ( P < .001), Enneking staging ( P = .016), denosumab treatment responsiveness ( P = .035), and the number of CD3 + ( P < .001), PD-1 + ( P = .009), PD-L1 + ( P < .001), and FoxP3 + tumor-infiltrating lymphocyte ( P = .02). Importantly, TGR outperformed the traditional Enneking, Campanacci, and American Joint Committee on Cancer staging systems in predicting the clinical outcomes of spinal GCTB.
These data support the use of TGR as a reliable predictive tool for clinically relevant outcomes and response to denosumab therapy of spinal GCTB, which may be helpful in guiding prognostic risk stratification and therapeutic optimization of patients.
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