Hypercellularity Components of Glioblastoma Identified by High b-Value Diffusion-Weighted Imaging.
Hypercellularity Components of Glioblastoma Identified by High b-Value Diffusion-Weighted Imaging.
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DOI：
10.1016/j.ijrobp.2015.02.058
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发表时间：
2015-07-15
期刊：
影响因子：
--
通讯作者：
Cao Y
中科院分区：
文献类型：
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作者：
Pramanik PP;Parmar HA;Mammoser AG;Junck LR;Kim MM;Tsien CI;Lawrence TS;Cao Y
使用常规MRI进行靶区定义时，胶质母细胞瘤可能未得到足够的辐射剂量覆盖非增强的多细胞亚体积。本研究旨在开发一种技术，通过使用高b值DWI来识别GB的高细胞成分，并研究其与规定的95%等剂量体积（PDV）和无进展生存期（PFS）的关系。21例胶质母细胞瘤患者在切除/活检后接受了放化疗。RT治疗计划基于常规MRI。在3个正交方向采集RT前DWI，b值为0、1000和3000 s/mm 2。通过阈值法在高b值（3000 s/mm 2）DWI上定义细胞过多体积（HCV）。“非增强”表示在T1加权图像上Gd增强的大体肿瘤体积（GTV-Gd）未覆盖的区域。PDV用于评估剂量计划对HCV的空间覆盖。使用单变量比例风险回归模型评估HCV与PFS或其他临床协变量之间的关联。HCV和非增强型HCV分别为0.58-67 cc（中位数：9.8cc）和0.15-60 cc（中位数：2.5cc）。14例患者的HCV剂量覆盖不完全，其中6例患者的95%-PDV（范围：1.01-25.4cc）遗漏了1+ cc HCV。在15名进展的患者中，5名在RT后6个月内进展较早，10名患者在RT后进展。复发性GTVs-Gd中的RT前HCV在5次最早进展中为78%（范围：65-89%），但在晚期进展中为53%（范围：0-85%）。HCV和非增强型HCV是PFS的显著阴性预后指标（分别为p < 0.002和p < 0.01）。未被95%-PDV覆盖的细胞过多亚体积是PFS的显著负预测因子（p < 0.05）。高b值DWI可识别GB的多细胞成分，并有助于RT靶体积定义。未来的研究将使我们能够研究高b值DWI在识别辐射增强体积和诊断进展中的作用。
Using conventional MRI for target definition, glioblastomas may receive inadequate radiation dose coverage of the nonenhanced hypercellular subvolume. This study aimed to develop a technique to identify the hypercellular components of GB by using high b-value DWI and to investigate its relationships with the prescribed 95%- isodose volume (PDV) and progression-free survival (PFS). Twenty-one patients with glioblastoma underwent chemoradiotherapy post-resection/biopsy. RT treatment planning was based upon conventional MRI. Pre-RT DWIs were acquired in 3 orthogonal directions with b-values of 0, 1000, and 3000 s/mm2. Hypercellularity volume (HCV) was defined on the high b-value (3000 s/mm2) DWI by a threshold method. “Nonenhanced” signifies regions not covered by the Gd-enhanced gross tumor volume (GTV-Gd) on T1-weighted images. The PDV was used to evaluate spatial coverage of the HCV by the dose plan. Association between HCV and PFS or other clinical covariates were assessed using univariate proportional hazards regression models. HCVs and nonenhanced HCVs varied 0.58-67 cc (median: 9.8cc) and 0.15-60 cc (median: 2.5cc), respectively. Fourteen patients had incomplete dose coverage of the HCV, of which 6 patients had 1+ cc HCV missed by the 95%-PDV (range: 1.01–25.4cc). Of the 15 patients who progressed, 5 progressed earlier, within 6 months post-RT, and 10 patients after. Pre-RT HCVs within recurrent GTVs-Gd were 78% (range: 65–89%) for the 5 earliest progressions but lower, 53% (range: 0–85%), for the later progressions. HCV and nonenhanced HCV were significant negative prognostic indicators for PFS (p < 0.002 and p < 0.01, respectively). The hypercellularity subvolume not covered by the 95%-PDV was a significant negative predictor for PFS (p < 0.05). High b-value DWI identifies the hypercellular components of GB and could aid in RT target volume definition. Future studies will allow us to investigate the role of high b-value DWI in identifying radiation boost volumes and diagnosing progression.