PO.TB10.03 · 肿瘤生物学

ANXA2表达的动态改变作为新诊断胶质母细胞瘤对新辅助贝伐珠单抗应答的预测因子

Dynamic alteration of ANXA2 expression as a predictor of response to neoadjuvant bevacizumab in newly diagnosed glioblastoma

编号 3454 展板 26 时间 4/20 02:00–05:00 区域 Section 29 主讲 Taketo Ezaki, MS

分会场 Microenvironmental Determinants of Therapy Response and Resistance 1

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作者与单位 Authors & Affiliations

Taketo Ezaki¹, Ryota Tamura¹, Yohei Yamamoto², Jun Takei², Akihiko Teshigawara², Kyoichi Tomoto², Yasuharu Akasaki², Masahiro Toda¹, Yuichi Murayama², Hikaru Sasaki³, Keisuke Miyake⁴, Toshihide Tanaka²

¹Department of Neurosurgery, Keio University School of Medcine, Shinjuku-ku, Japan,²Department of Neurosurgery, The Jikei University School of Medicine, Minato-ku, Japan,³Department of Neurosurgery, Tokyo Dental College Ichikawa General Hospital, Ichikawa-shi, Japan,⁴Department of Neurosurgery, Kagawa University School of Medcine, Miki-cho, Japan

摘要 Abstract

中文摘要

背景：贝伐珠单抗（Bev）在胶质母细胞瘤（GBM）中仅提供适度且短暂的获益，而Bev耐药的分子机制仍未充分阐明。膜联蛋白A2（ANXA2）在血管生成、细胞外基质重塑和侵袭性肿瘤表型中发挥关键作用，并已成为Bev耐药生物学的潜在介导因子。本研究旨在通过分析Bev治疗前后配对的肿瘤样本，阐明ANXA2表达动态在新诊断GBM中的临床意义，重点关注其与治疗应答和生存结局的关联。方法：我们分析了来自33例GBM患者的65份样本，包括未接受Bev治疗的新诊断GBM（Naïve Bev；n=15）、接受新辅助Bev治疗（NeoBev；n=18），以及Bev治疗后复发的GBM（Refractory Bev），后者包含同一患者Bev治疗前后的配对样本。通过qPCR和免疫组化评估ANXA2表达。还根据ANXA2表达水平评估了无进展生存期（PFS）和总生存期（OS），并比较了MRI上的复发模式。结果：配对分析显示，无论既往是否接受Bev，Refractory Bev中的ANXA2表达往往高于初次手术标本。免疫组化显示Naïve Bev、NeoBev和Refractory Bev队列之间ANXA2表达相当。ANXA2表达在Naïve Bev中与预后无关；然而，较低的表达在NeoBev中与更佳的PFS相关（p=0.1062），并与显著更长的OS相关（p=0.0025）。接受≥10个Bev周期的患者ANXA2表达显著低于<10个周期者（p=0.0168），且NeoBev中较低的表达带来更长的OS。T1Gd应答者显示出更长PFS的趋势（p=0.1037），T2/FLAIR不良应答者也呈现类似趋势（p=0.0688）。ANXA2表达与MRI上的复发模式之间未发现显著关联。结论：ANXA2可能代表血管生成和侵袭的关键分子决定因素，并可作为新辅助Bev应答的预后和预测生物标志物。

查看英文原文 English abstract

Background: Bevacizumab (Bev) provides only modest and transient benefit in glioblastoma (GBM), and the molecular mechanisms underlying Bev resistance remain insufficiently characterized. Annexin A2 (ANXA2) plays a key role in angiogenesis, extracellular matrix remodeling, and invasive tumor phenotypes, and has emerged as a potential mediator of Bev resistance biology. This study aimed to elucidate the clinical significance of ANXA2 expression dynamics in newly diagnosed GBM by analyzing paired tumor samples obtained pre- and post-Bev therapy, with a focus on their association with treatment response and survival outcomes. Method: We analyzed 65 samples obtained from 33 patients with GBM, including newly diagnosed GBM without Bev treatment (Naïve Bev; n=15), neoadjuvant Bev treated (NeoBev; n=18), and recurrent GBM after Bev therapy (Refractory Bev) comprising paired pre- and post-Bev samples in same patients. ANXA2 expression was evaluated by qPCR and immunohistochemistry. Progression-free survival (PFS) and overall survival (OS) were also evaluated according to ANXA2 expression levels, and recurrence patterns on MRI were compared. Results: Paired analyses showed ANXA2 expression tended to be higher in Refractory Bev compared with initial surgery specimens, regardless of prior Bev exposure. Immunohistochemistry demonstrated comparable ANXA2 expression across Naïve Bev, NeoBev, and Refractory Bev cohorts. ANXA2 expression was not associated with prognosis in Naïlve Bev; however, lower expression correlated with favorable PFS in NeoBev (p=0.1062) and significantly longer OS (p=0.0025). Patients receiving ≥ 10 Bev cycles showed significantly lower ANXA2 expression than those with < 10 cycles (p=0.0168), and lower expression in NeoBev resulted in prolonged OS. T1Gd responders showed a trend toward longer PFS (p=0.1037), with a similar trend in T2/FLAIR poor responders (p=0.0688). No significant association was found between ANXA2 expression and recurrence patterns on MRI. Conclusion: ANXA2 may represent a key molecular determinant of angiogenesis and invasion and could serve as both a prognostic and predictive biomarker for neoadjuvant Bev response.

利益披露 Disclosure

T. Ezaki, None.. R. Tamura, None.. Y. Yamamoto, None.. J. Takei, None.. A. Teshigawara, None.. K. Tomoto, None.. Y. Akasaki, None.. M. Toda, None.. Y. Murayama, None.. H. Sasaki, None.. K. Miyake, None.. T. Tanaka, None.

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