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影响转移性结直肠癌维持治疗持续时间的因素

Factors Influencing the Duration of Maintenance Therapy in Metastatic Colorectal Cancer.

作者信息

Fourrier Théo, Truntzer Caroline, Peroz Morgane, Derangère Valentin, Vincent Julie, Bengrine-Lefèvre Leila, Hennequin Audrey, Palmier Rémi, Orry David, Rabel Thomas, Ghiringhelli François

机构信息

Cancer Biology Transfer Platform, Georges François Leclerc Cancer Center, UNICANCER, 21000 Dijon, France.

Department of Medical Oncology, Georges François Leclerc Cancer Center, UNICANCER, 21000 Dijon, France.

出版信息

Cancers (Basel). 2024 Dec 30;17(1):88. doi: 10.3390/cancers17010088.

DOI:10.3390/cancers17010088
PMID:39796718
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11720154/
Abstract

BACKGROUND/OBJECTIVES: Metastatic colorectal cancer (mCRC) is mainly treated with 5-Fluoro-Uracil (5-FU), Oxaliplatin and Irinotecan chemotherapies and anti-Epidermal Growth Factor Receptor (EGFR) or anti-Vascular Endothelial Growth Factor (VEGF) targeted therapies. Due to chemotherapy-related toxicity, patients receive induction treatment to achieve tumour response followed by maintenance therapy with less cytotoxic molecules or a chemotherapy-free interval to reduce chemotherapy-related toxicity. In this study, the aim was to determine the patient, cancer and treatment factors that influence the duration of maintenance therapy (DMT).

METHODS

We collected retrospective data on a cohort of 133 patients treated at the Centre Georges François Leclerc (CGFL) cancer centre in Dijon between March 2014 and June 2022. Patients had unresectable or potentially resectable diseases. They received first-line induction treatment with chemotherapy and/or targeted therapy and maintenance treatment, defined as the interruption of at least one chemotherapy agent.

RESULTS

In the multivariate analysis, age (HR: 1.02, 95% CI 1.00-1.04, = 0.031), N2 nodal status (HR: 1.78, 95% CI 1.09-2.89, = 0.021) and the presence of peritoneal metastases (HR: 2.05, 95% CI 1.25-3.36, = 0.004), as well as baseline carcino-embryonic antigen (CEA) level (HR: 1.10, 95% CI 1.00-1.20, = 0.052), were significantly associated to poor DMT. Local treatment of liver metastases also significantly reduced the DMT (HR: 0.49, 95% CI 0.28-0.86, = 0.013). In our cohort, induction triplet chemotherapy significantly increased the CEA delta (70% vs. 44%, = 0.047) compared to doublet chemotherapy and led to a higher rate of liver surgery (40% vs. 21%, = 0.014) and a trend for a higher rate of local treatment of metastases (62% vs. 45%, = 0.059).

CONCLUSIONS

Duration of maintenance therapy is determined by the initial patient and colorectal cancer characteristics. However, it is significantly increased by local treatment of liver metastases. By reducing the tumour burden, a triplet induction chemotherapy regimen increases the rate of liver metastase resection.

摘要

背景/目的:转移性结直肠癌(mCRC)主要采用5-氟尿嘧啶(5-FU)、奥沙利铂和伊立替康化疗以及抗表皮生长因子受体(EGFR)或抗血管内皮生长因子(VEGF)靶向治疗。由于化疗相关毒性,患者接受诱导治疗以实现肿瘤缓解,随后使用细胞毒性较小的分子进行维持治疗或进行无化疗间期以降低化疗相关毒性。在本研究中,目的是确定影响维持治疗持续时间(DMT)的患者、癌症和治疗因素。

方法

我们收集了2014年3月至2022年6月期间在第戎的乔治·弗朗索瓦·勒克莱尔中心(CGFL)癌症中心接受治疗的133例患者的回顾性数据。患者患有不可切除或潜在可切除疾病。他们接受了一线诱导化疗和/或靶向治疗以及维持治疗,维持治疗定义为至少中断一种化疗药物。

结果

在多变量分析中,年龄(HR:1.02,95%CI 1.00 - 1.04,P = 0.031)、N2淋巴结状态(HR:1.78,95%CI 1.09 - 2.89,P = 0.021)和腹膜转移的存在(HR:2.05,95%CI 1.25 - 3.36,P = 0.004),以及基线癌胚抗原(CEA)水平(HR:1.10,95%CI 1.00 - 1.20,P = 0.052),均与不良DMT显著相关。肝转移的局部治疗也显著缩短了DMT(HR:0.49,95%CI 0.28 - 0.86,P = 0.013)。在我们的队列中,与双联化疗相比,诱导三联化疗显著增加了CEA下降幅度(70%对44%,P = 0.047),并导致更高的肝手术率(40%对21%,P = 0.014)以及更高的转移灶局部治疗率趋势(62%对45%,P = 0.059)。

结论

维持治疗的持续时间由初始患者和结直肠癌特征决定。然而,肝转移的局部治疗可显著延长其持续时间。通过减轻肿瘤负担,三联诱导化疗方案可提高肝转移灶切除率。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9824/11720154/359659706786/cancers-17-00088-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9824/11720154/57619d356bf8/cancers-17-00088-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9824/11720154/b8be823cb4ee/cancers-17-00088-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9824/11720154/04550028f1eb/cancers-17-00088-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9824/11720154/359659706786/cancers-17-00088-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9824/11720154/57619d356bf8/cancers-17-00088-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9824/11720154/b8be823cb4ee/cancers-17-00088-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9824/11720154/04550028f1eb/cancers-17-00088-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9824/11720154/359659706786/cancers-17-00088-g004.jpg

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