Departments of Biomedical Informatics and Internal Medicine, The Ohio State University Columbus, Ohio.
Cancer Med. 2013 Aug;2(4):545-52. doi: 10.1002/cam4.102. Epub 2013 Jul 10.
The mTOR (mammalian target of rapamycin) inhibitor, everolimus, affects tumor growth by targeting cellular metabolic proliferation pathways and delays renal cell carcinoma (RCC) progression. Preclinical evidence suggests that baseline elevated tumor glucose metabolism as quantified by FDG-PET ([(18)F] fluorodeoxy-glucose positron emission tomography) may predict antitumor activity. Metastatic RCC (mRCC) patients refractory to vascular endothelial growth factor (VEGF) pathway inhibition were treated with standard dose everolimus. FDG-PET scans were obtained at baseline and 2 weeks; serial computed tomography (CT) scans were obtained at baseline and every 8 weeks. Maximum standardized uptake value (SUVmax) of the most FDG avid lesion, average SUVmax of all measured lesions and their corresponding 2-week relative changes were examined for association with 8-week change in tumor size. A total of 63 patients were enrolled; 50 were evaluable for the primary endpoint of which 48 had both PET scans. Patient characteristics included the following: 36 (72%) clear cell histology and median age 59 (range: 37-80). Median pre- and 2-week treatment average SUVmax were 6.6 (1-17.9) and 4.2 (1-13.9), respectively. Response evaluation criteria in solid tumors (RECIST)-based measurements demonstrated an average change in tumor burden of 0.2% (-32.7% to 35.9%) at 8 weeks. Relative change in average SUVmax was the best predictor of change in tumor burden (all evaluable P = 0.01; clear cell subtype P = 0.02), with modest correlation. Baseline average SUVmax was correlated with overall survival and progression-free survival (PFS) (P = 0.023; 0.020), but not with change in tumor burden. Everolimus therapy decreased SUVs on follow-up PET scans in mRCC patients, but changes were only modestly correlated with changes in tumor size. Thus, clinical use of FDG-PET-based biomarkers is challenged by high variability.
mTOR(哺乳动物雷帕霉素靶蛋白)抑制剂依维莫司通过靶向细胞代谢增殖途径影响肿瘤生长,并延缓肾细胞癌(RCC)的进展。临床前证据表明,基线时肿瘤葡萄糖代谢的升高(通过 FDG-PET[(18)F]氟脱氧葡萄糖正电子发射断层扫描)可以预测抗肿瘤活性。对血管内皮生长因子(VEGF)通路抑制耐药的转移性 RCC(mRCC)患者接受标准剂量依维莫司治疗。在基线和 2 周时获取 FDG-PET 扫描;在基线和每 8 周时获取连续 CT 扫描。对最 FDG 摄取的病变的最大标准化摄取值(SUVmax)、所有测量病变的平均 SUVmax 及其相应的 2 周相对变化进行检查,以与肿瘤大小在 8 周时的变化相关。共纳入 63 例患者;50 例患者可评估主要终点,其中 48 例患者同时进行了 PET 扫描。患者特征包括以下内容:36 例(72%)为透明细胞组织学,中位年龄为 59 岁(范围:37-80 岁)。中位基线和 2 周治疗平均 SUVmax 分别为 6.6(1-17.9)和 4.2(1-13.9)。实体瘤反应评估标准(RECIST)测量显示,8 周时肿瘤负担的平均变化为 0.2%(-32.7%至 35.9%)。平均 SUVmax 的相对变化是肿瘤负担变化的最佳预测指标(所有可评估的 P=0.01;透明细胞亚型 P=0.02),相关性适中。基线平均 SUVmax 与总生存和无进展生存(PFS)相关(P=0.023;0.020),但与肿瘤负担的变化无关。依维莫司治疗后,mRCC 患者的 FDG-PET 扫描 SUV 降低,但变化与肿瘤大小的变化仅中度相关。因此,基于 FDG-PET 的生物标志物的临床应用受到高变异性的挑战。