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IV 期对致癌基因成瘾的肺腺癌患者的基线和治疗期间的血清肿瘤标志物特征。

Baseline and On-Treatment Characteristics of Serum Tumor Markers in Stage IV Oncogene-Addicted Adenocarcinoma of the Lung.

机构信息

Division of Medical Oncology, Department of Medicine, University of Colorado School of Medicine, Aurora, Colorado.

Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado.

出版信息

J Thorac Oncol. 2018 Jan;13(1):134-138. doi: 10.1016/j.jtho.2017.08.005. Epub 2017 Aug 24.

DOI:10.1016/j.jtho.2017.08.005
PMID:28843358
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5810959/
Abstract

INTRODUCTION

The role of serum tumor markers in the modern management of advanced NSCLC remains poorly described.

METHODS

A single-center retrospective analysis of available carcinoembryonic antigen, CA125, CA19.9, and CA27.29 levels at baseline and during treatment of stage IV lung adenocarcinoma by oncogenic driver was conducted.

RESULTS

A total of 142 patients were analyzed (60 with anaplastic lymphoma kinase gene [ALK] rearrangement, 50 with EGFR mutation, four with ROS1 rearrangement, and 29 with KRAS mutation). Of these, 82% had at least one marker (95% if all four markers were measured), with CA27.29 being the most commonly increased and CA19.9 the rarest. Only CA27.29 differed significantly by oncogene (it was less common in KRAS) (p = 0.016). The median times to nadir during tyrosine kinase inhibitor (TKI) therapy in EGFR and ALK cases were 16.4 and 20 weeks, respectively. Of the 41 patients with EGFR mutation or ALK or ROS1 rearrangement, 24 (59%) demonstrated an initial increase within the first 4 weeks of TKI therapy, 58% of whom then had their levels fall below baseline. An increase in marker level of 10% or more from nadir occurred in 53% of systemic and 22% of central nervous system-only progression.

CONCLUSIONS

Serum tumor markers are frequently increased in lung adenocarcinoma regardless of driver oncogene. Changes within the first 4 weeks of therapy may be misleading. Progression is associated with marker increases, especially in sites other than the central nervous system.

摘要

简介

血清肿瘤标志物在晚期 NSCLC 现代治疗中的作用仍未得到充分描述。

方法

对 142 例经致癌驱动基因检测确诊的Ⅳ期肺腺癌患者进行回顾性分析,观察基线及治疗过程中癌胚抗原、CA125、CA19.9 和 CA27.29 水平。

结果

共分析了 142 例患者(60 例存在间变性淋巴瘤激酶基因[ALK]重排,50 例存在表皮生长因子受体突变,4 例存在 ROS1 重排,29 例存在 KRAS 突变)。其中,82%的患者至少有一种标志物(如果同时检测了所有四种标志物,则为 95%),CA27.29 升高最常见,CA19.9 升高最不常见。只有 CA27.29 在致癌基因上有显著差异(在 KRAS 中较少见)(p=0.016)。EGFR 和 ALK 病例中酪氨酸激酶抑制剂(TKI)治疗时达到最低点的中位时间分别为 16.4 和 20 周。在 41 例存在 EGFR 突变或 ALK 或 ROS1 重排的患者中,24 例(59%)在 TKI 治疗的前 4 周内首次出现标志物水平升高,其中 58%随后标志物水平下降至基线以下。在全身进展和中枢神经系统仅进展中,有 53%和 22%的患者标志物水平升高超过 10%。

结论

无论驱动基因是否存在,肺腺癌患者的血清肿瘤标志物通常都会升高。治疗的前 4 周内的变化可能会产生误导。标志物的增加与进展有关,尤其是在中枢神经系统以外的部位。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f55/5810959/03bc032dcbd2/nihms939498f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f55/5810959/deab384940ea/nihms939498f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f55/5810959/03bc032dcbd2/nihms939498f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f55/5810959/deab384940ea/nihms939498f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f55/5810959/03bc032dcbd2/nihms939498f2.jpg

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