Prior John O, Montemurro Michael, Orcurto Maria-Victoria, Michielin Olivier, Luthi François, Benhattar Jean, Guillou Louis, Elsig Valérie, Stupp Roger, Delaloye Angelika Bischof, Leyvraz Serge
Nuclear Medicine Department,Centre Hospitalier Universitaire Vaudois, University of Lausanne, Lausanne, Switzerland
J Clin Oncol. 2009 Jan 20;27(3):439-45. doi: 10.1200/JCO.2008.17.2742. Epub 2008 Dec 8.
Positron emission tomography with (18)F-fluorodeoxyglucose (FDG-PET) was used to evaluate treatment response in patients with gastrointestinal stromal tumors (GIST) after administration of sunitinib, a multitargeted tyrosine kinase inhibitor, after imatinib failure.
Tumor metabolism was assessed with FDG-PET before and after the first 4 weeks of sunitinib therapy in 23 patients who received one to 12 cycles of sunitinib therapy (4 weeks of 50 mg/d, 2 weeks off). Treatment response was expressed as the percent change in maximal standardized uptake values (SUV). The primary end point of time to tumor progression was compared with early PET results on the basis of traditional Response Evaluation Criteria in Solid Tumors (RECIST) criteria.
Progression-free survival (PFS) was correlated with early FDG-PET metabolic response (P < .0001). Using -25% and +25% thresholds for SUV variations from baseline, early FDG-PET response was stratified in metabolic partial response, metabolically stable disease, or metabolically progressive disease; median PFS rates were 29, 16, and 4 weeks, respectively. Similarly, when a single FDG-PET positive/negative was considered after 4 weeks of sunitinib, the median PFS was 29 weeks for SUVs less than 8 g/mL versus 4 weeks for SUVs of 8 g/mL or greater (P < .0001). None of the patients with metabolically progressive disease subsequently responded according to RECIST criteria. Multivariate analysis showed shorter PFS in patients who had higher residual SUVs (P < .0001), primary resistance to imatinib (P = .024), or nongastric GIST (P = .002), regardless of the mutational status of the KIT and PDGFRA genes.
Week 4 FDG-PET is useful for early assessment of treatment response and for the prediction of clinical outcome. Thus, it offers opportunities to individualize and optimize patient therapy.
采用（18）F - 氟脱氧葡萄糖正电子发射断层扫描（FDG - PET）来评估胃肠道间质瘤（GIST）患者在伊马替尼治疗失败后使用多靶点酪氨酸激酶抑制剂舒尼替尼治疗后的反应。
对23例接受1至12个周期舒尼替尼治疗（50mg/d，持续4周，停药2周）的患者，在舒尼替尼治疗的前4周前后进行FDG - PET评估肿瘤代谢。治疗反应以最大标准化摄取值（SUV）的变化百分比表示。根据实体瘤疗效评价标准（RECIST），将肿瘤进展时间的主要终点与早期PET结果进行比较。
无进展生存期（PFS）与早期FDG - PET代谢反应相关（P <.0001）。以SUV相对于基线变化的-25%和+25%为阈值，早期FDG - PET反应分为代谢部分缓解、代谢稳定疾病或代谢进展性疾病；中位PFS率分别为29周、16周和4周。同样，在舒尼替尼治疗4周后若仅考虑FDG - PET阳性/阴性，SUV小于8g/mL的患者中位PFS为29周，而SUV为8g/mL或更高的患者中位PFS为4周（P <.0001）。根据RECIST标准，代谢进展性疾病的患者随后均无反应。多因素分析显示，无论KIT和PDGFRA基因的突变状态如何，SUV残留较高（P <.0001）、对伊马替尼原发耐药（P =.024）或非胃GIST（P =.002）的患者PFS较短。
第4周的FDG - PET有助于早期评估治疗反应和预测临床结局。因此，它为个体化和优化患者治疗提供了机会。
