Department of Nuclear Medicine, Centre Georges-François Leclerc, Dijon, France.
J Nucl Med. 2012 Apr;53(4):512-20. doi: 10.2967/jnumed.111.096834. Epub 2012 Feb 17.
The purpose of this study was to prospectively evaluate the relationship between tumor blood flow and glucose metabolism as evaluated by dynamic first-pass (18)F-FDG PET and by proliferation and endothelial pathologic markers in the setting of newly diagnosed breast cancer.
Forty patients were prospectively included. Biopsy samples of each tumor were used to assess the Ki67 index of proliferation and immunostaining for CD34 (a panendothelial cell marker) and CD105 (a proliferation-related endothelial cell marker). All patients underwent (18)F-FDG PET/CT at least 1 wk after sample biopsy and before any treatment. A dynamic 2-min acquisition was performed immediately after intravenous injection of a 5 MBq/kg dose of (18)F-FDG; tumor blood flow was then calculated using a single-compartment kinetic model. A static acquisition was performed 90 min after injection for quantification of delayed (18)F-FDG tumor uptake (standardized uptake value maximal index [SUV(max)]), reflecting tumor metabolism.
Pathologic and PET/CT data were available for all patients. The SUV(max) measured on delayed PET images correlated strongly and positively with the expression of Ki67 (r = +0.69; P < 0.0001). In contrast, there was no significant correlation between SUV(max) and endothelial markers (CD34 and CD105). Tumor blood flow correlated positively with the expression of CD34 and CD105 (P = 0.016 and P = 0.007, respectively) and with the expression of Ki67 (P = 0.028). By logistic regression analysis, only expression of Ki67 remained an independent predictor of high (supramedian) SUV(max); CD105 score and histopathologic grade 3 were independently associated with a high (supramedian) tumor blood flow level.
Tumor blood flow quantified by dynamic first-pass (18)F-FDG PET/CT is significantly associated with tumor angiogenesis as evaluated by immunohistochemistry in the setting of breast cancer, whereas tumor metabolism appears to be more associated with markers of proliferation. Thus, determination of tumor blood flow and metabolism with a single injection of (18)F-FDG could be an exciting alternative to more complex and less available techniques.
本研究旨在前瞻性评估新诊断乳腺癌患者中，动态首过（18）F-FDG PET 评估的肿瘤血流与葡萄糖代谢，与增殖和内皮病理标志物之间的关系。
40 例患者前瞻性纳入研究。对每个肿瘤的活检样本进行 Ki67 增殖指数评估，并用 CD34（泛内皮细胞标志物）和 CD105（增殖相关内皮细胞标志物）进行免疫组化染色。所有患者在样本活检后至少 1 周，在任何治疗前进行（18）F-FDG PET/CT。静脉注射 5MBq/kg 剂量（18）F-FDG 后立即进行 2 分钟动态采集，然后使用单室动力学模型计算肿瘤血流。注射后 90 分钟进行静态采集，用于量化延迟（18）F-FDG 肿瘤摄取（最大标准化摄取值指数[SUV(max)]），反映肿瘤代谢。
所有患者均有病理和 PET/CT 数据。延迟 PET 图像上测量的 SUV(max)与 Ki67 表达呈强正相关（r=+0.69；P<0.0001）。相反，SUV(max)与内皮标志物（CD34 和 CD105）之间无显著相关性。肿瘤血流与 CD34 和 CD105 的表达呈正相关（P=0.016 和 P=0.007），与 Ki67 的表达呈正相关（P=0.028）。通过逻辑回归分析，只有 Ki67 的表达仍然是 SUV(max)高（中位数以上）的独立预测因素；CD105 评分和组织学 3 级与肿瘤血流高（中位数以上）水平独立相关。
在乳腺癌中，动态首过（18）F-FDG PET/CT 定量的肿瘤血流与免疫组织化学评估的肿瘤血管生成显著相关，而肿瘤代谢似乎与增殖标志物更相关。因此，用单次注射（18）F-FDG 测定肿瘤血流和代谢可能是一种更令人兴奋的替代方法，而不是更复杂和更难获得的技术。
