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头颈部鳞状细胞癌患者肿瘤缺氧与代谢的影像学研究

Imaging of tumour hypoxia and metabolism in patients with head and neck squamous cell carcinoma.

作者信息

Zegers Catharina M L, van Elmpt Wouter, Hoebers Frank J P, Troost Esther G C, Öllers Michel C, Mottaghy Felix M, Lambin Philippe

机构信息

a Department of Radiation Oncology (MAASTRO) , GROW - School for Oncology and Developmental Biology, Maastricht University Medical Centre , Maastricht , The Netherlands.

b Helmholtz Zentrum Dresden-Rossendorf , Dresden , Germany.

出版信息

Acta Oncol. 2015;54(9):1378-84. doi: 10.3109/0284186X.2015.1062913. Epub 2015 Jul 27.

DOI:10.3109/0284186X.2015.1062913
PMID:26213313
Abstract

BACKGROUND

Tumour hypoxia and a high tumour metabolism increase radioresistance in patients with head and neck squamous cell carcinoma (HNSCC). The aim of this study was to evaluate the correlation between hypoxia ([(18)F]HX4 PET) and glucose metabolism ([(18)F]FDG PET) molecular imaging.

MATERIAL AND METHODS

[(18)F]HX4 and [(18)F]FDG PET/CT images of 20 HNSCC patients were acquired prior to (chemo)radiotherapy, in an immobilisation mask, with a median time interval of seven days (NCT01347281). Gross tumour volumes of the primary lesions (GTVprim) and pathological lymph nodes (GTVln) were included in the analysis. [(18)F]FDG PET/CT images were rigidly registered to the [(18)F]HX4 PET/CT images. The maximum and mean standardised uptake values (SUVmax, SUVmean) within both GTVs were determined. In addition, the overlap was compared between the [(18)F]HX4 high volume ([(18)F]HX4 HV) with a tumour-to-muscle ratio > 1.4 and the [(18)F]FDG high volume ([(18)F]FDG HV) with an SUV > 50% of the SUVmax. We report the mean ± standard deviation.

RESULTS

PET/CT scans including 20 GTVprim and 12 GTVln were analysed. There was a significant correlation between several [(18)F]FDG and [(18)F]HX4 parameters, the most pronounced being the correlation between [(18)F]FDG HV and [(18)F]HX4 HV (R = 0.93, p < 0.001). The fraction of the GTVprim with a high HX4 uptake (9 ± 10%) was on average smaller than the FDG high fraction (51 ± 26%; p < 0.001). In 65% (13/20) of the patients, the GTVprim was hypoxic. In four of these patients the [(18)F]HX4 HV was located within the [(18)F]FDG HV, whereas for the remaining nine GTVprim a partial mismatch was observed. In these nine tumours 25 ± 21% (range 5-64%) of the HX4 HV was located outside the FDG HV.

CONCLUSIONS

There is a correlation between [(18)F]HX4 and [(18)F]FDG uptake parameters on a global tumour level. In the majority of lesions a partial mismatch between the [(18)F]HX4 and [(18)F]FDG high uptake volumes was observed, therefore [(18)F]FDG PET imaging cannot be used as a surrogate for hypoxia. [(18)F]HX4 PET provides complementary information to [(18)F]FDG PET imaging.

摘要

背景

肿瘤缺氧和高肿瘤代谢会增加头颈部鳞状细胞癌(HNSCC)患者的放射抗性。本研究的目的是评估缺氧([(18)F]HX4 PET)与葡萄糖代谢([(18)F]FDG PET)分子成像之间的相关性。

材料与方法

在(化疗)放疗前,使用固定面罩对20例HNSCC患者进行[(18)F]HX4和[(18)F]FDG PET/CT成像,中位时间间隔为7天(NCT01347281)。分析原发灶(GTVprim)和病理淋巴结(GTVln)的大体肿瘤体积。将[(18)F]FDG PET/CT图像与[(18)F]HX4 PET/CT图像进行刚性配准。确定两个GTV内的最大和平均标准化摄取值(SUVmax、SUVmean)。此外,比较肿瘤与肌肉比值>1.4的[(18)F]HX4高体积([(18)F]HX4 HV)与SUV>SUVmax的50%的[(18)F]FDG高体积([(18)F]FDG HV)之间的重叠情况。我们报告平均值±标准差。

结果

分析了包括20个GTVprim和12个GTVln的PET/CT扫描。几个[(18)F]FDG和[(18)F]HX4参数之间存在显著相关性,最显著的是[(18)F]FDG HV与[(18)F]HX4 HV之间的相关性(R = 0.93,p < 0.001)。HX4摄取高的GTVprim部分平均(9±10%)小于FDG高摄取部分(51±26%;p < 0.001)。65%(13/20)的患者GTVprim存在缺氧。其中4例患者的[(18)F]HX4 HV位于[(18)F]FDG HV内,而其余9个GTVprim观察到部分不匹配。在这9个肿瘤中,25±21%(范围5 - 64%)的HX4 HV位于FDG HV之外。

结论

在整体肿瘤水平上,[(18)F]HX4与[(18)F]FDG摄取参数之间存在相关性。在大多数病变中,观察到[(18)F]HX4与[(18)F]FDG高摄取体积之间存在部分不匹配,因此[(18)F]FDG PET成像不能用作缺氧的替代指标。[(18)F]HX4 PET为[(18)F]FDG PET成像提供了补充信息。

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引用本文的文献

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Nucl Med Commun. 2019 Jan;40(1):73-78. doi: 10.1097/MNM.0000000000000933.
2
A phase 1 'window-of-opportunity' trial testing evofosfamide (TH-302), a tumour-selective hypoxia-activated cytotoxic prodrug, with preoperative chemoradiotherapy in oesophageal adenocarcinoma patients.一项1期“机会窗”试验,在食管腺癌患者中测试肿瘤选择性缺氧激活细胞毒性前药依沃福酰胺(TH-302)与术前放化疗联合应用的效果。
BMC Cancer. 2016 Aug 17;16:644. doi: 10.1186/s12885-016-2709-z.