18F-FDG - PET代谢反应在局部食管鳞状细胞癌诱导化疗或放化疗后的预后作用

IF 9.1
Yeong Hak Bang, Jong Hoon Kim, Yong-Hee Kim, Hyeong Ryul Kim, Jin-Sook Ryu, Yong-Il Kim, Joon Seon Song, Sung-Bae Kim, Sook Ryun Park
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引用次数: 0

摘要

食管鳞状细胞癌(ESCC)放化疗后18F-FDG PET代谢反应的预后意义尚不清楚,特别是诱导化疗后与放化疗后的代谢反应。本研究旨在评估和比较它们对预后的影响。方法:本回顾性研究分析了2006年至2018年峨山医疗中心604例局部ESCC患者,这些患者接受了诱导化疗和放化疗,伴或不伴手术。诱导化疗后(放化疗前)和放化疗后的代谢反应采用欧洲癌症研究和治疗组织的预后评估标准进行评估。结果:在接受终期放化疗(双峰治疗)的患者中,诱导化疗和放化疗后的代谢反应与无进展生存期(PFS)和总生存期(OS)显著相关。诱导化疗后完全代谢缓解与最长生存期(PFS, 58.9个月;OS, 90.8个月),而进行性代谢性疾病预测预后不良(PFS, 3.7个月;OS, 7.0 mo;P < 0.001)。在放化疗后的代谢反应中也观察到类似的模式。在接受手术(三段式治疗)的患者中,诱导化疗后的代谢反应对生存率没有显著影响。然而,在最初计划手术的患者中,它仍然是预后,表明其与术前设置的预后相关。放化疗后代谢反应在双峰治疗和三峰治疗中都是一个强大的独立预后因素。在完全代谢缓解组和部分代谢缓解组中,放化疗后弥漫性食管炎患者的生存结果中等,表明预后模式不同。结论:放化疗后代谢反应是局限性ESCC的一个强有力的预后指标,支持将其用于风险分层。诱导化疗后的早期代谢反应也可以为治疗决策提供信息,特别是在手术患者中。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Distinct Prognostic Roles of 18F-FDG PET Metabolic Response Assessed After Induction Chemotherapy or Chemoradiotherapy in Localized Esophageal Squamous Cell Carcinoma.

The prognostic significance of metabolic response by posttreatment 18F-FDG PET in esophageal squamous cell carcinoma (ESCC) treated with chemoradiotherapy remains unclear, particularly regarding metabolic response after induction chemotherapy versus after chemoradiotherapy. This study aimed to evaluate and compare their prognostic impact. Methods: This retrospective study analyzed 604 patients with localized ESCC who received induction chemotherapy followed by chemoradiotherapy, with or without surgery, at Asan Medical Center between 2006 and 2018. Metabolic responses after induction chemotherapy (before chemoradiotherapy) and after chemoradiotherapy were evaluated using European Organisation for Research and Treatment of Cancer-based criteria adapted for prognostic assessment. Results: In patients treated with definitive chemoradiotherapy (bimodality therapy), metabolic response after both induction chemotherapy and chemoradiotherapy was significantly associated with progression-free survival (PFS) and overall survival (OS). Complete metabolic response after induction chemotherapy correlated with the longest survival (PFS, 58.9 mo; OS, 90.8 mo), whereas progressive metabolic disease predicted poor prognosis (PFS, 3.7 mo; OS, 7.0 mo; P < 0.001). A similar pattern was observed for postchemoradiotherapy metabolic response. In patients who underwent surgery (trimodality therapy), metabolic response after induction chemotherapy did not significantly impact survival. However, in patients for whom surgery was initially planned, it remained prognostic, suggesting its prognostic relevance in the preoperative setting. Postchemoradiotherapy metabolic response was a strong independent prognostic factor in both bimodality therapy and trimodal therapy. Patients with diffuse esophagitis after chemoradiotherapy had intermediate survival outcomes, among complete metabolic response and partial metabolic response groups, indicating a distinct prognostic pattern. Conclusion: Postchemoradiotherapy metabolic response is a strong prognostic marker in localized ESCC, supporting its use for risk stratification. Early metabolic response after induction chemotherapy may also inform treatment decisions, particularly in surgery-intended patients.

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