可溶性sPD-L1和血清淀粉样蛋白A1作为肺癌潜在生物标志物
背景:这项前瞻性研究的目的是评估可溶性程序性细胞死亡-1 /程序性细胞死亡配体1(PD-1 / PD-L1)和血清淀粉样蛋白A1(SAA1)是否可能肺癌的诊断,预测或预后生物标志物。 方法:肺癌(115例)为晚期转移性疾病,101例为非小细胞肺癌,NSCLC(77例EGFR野生型NSCLC化疗患者,15例EGFR突变阳性腺癌患者,检查了9例mPD-L1表达≥50%NSCLC的患者-对免疫疗法有反应)和14例小细胞肺癌(SCLC)患者。用ELISA法测定患者血浆中sPD-L1和SAA1的浓度。 结果:与健康对照组相比,肺癌患者的sPD-L1和SAA1血药浓度明显更高。在PD-L1 + NSCLC患者中,与任何其他肺癌亚组相比,注意到sPD-L1水平显着更高,并且与其他亚组相比,SAA1的平均平均值最高。 结论:似乎sPD-1 / PD-L1可能是潜在的生物标志物,具有预后和/或预测性,特别是在接受免疫治疗的患者中。血清淀粉样蛋白A1可以作为患者生存的良好预测指标,也是更晚期疾病的生物标志物,具有预测不同时间点疾病进程的良好能力。**
Soluble sPD-L1 and Serum Amyloid A1 as Potential Biomarkers for Lung Cancer
Background: The objective of this prospective study was to evaluate whether soluble programmed cell death-1/programmed cell death-ligand 1 (PD-1/PD-L1) and serum amyloid A1 (SAA1) are potential diagnostic, predictive or prognostic biomarkers in lung cancer. Methods: Lung cancer patients (n=115) with advanced metastatic disease, 101 with non-small cell lung cancer, NSCLC (77 EGFR wild-type NSCLC patients on chemotherapy, 15 EGFR mutation positive adenocarcinoma patients, 9 patients with mPD-L1 Expression ≥50% NSCLC - responders to immunotherapy), and 14 patients with small cell lung cancer (SCLC) were examined. ELISA method was used to determine sPD-L1 and SAA1 concentrations in patients' plasma. Results: Significantly higher blood concentrations of sPD-L1 and SAA1 were noted in lung cancer patients compared with a healthy control group. In PD-L1+ NSCLC patients, a significantly higher sPD-L1 level was noticed compared to any other lung cancer subgroup, as well as the highest average SAA1 value compared to other subgroups. Conclusions: It seems that sPD-1/PD-L1 might be a potential biomarker, prognostic and/ or predictive, particularly in patients treated with immunotherapy. Serum amyloid A1 has potential to act as a good predictor of patients' survival, as well as a biomarker of a more advanced disease, with possibly good capability to predict the course of disease measured at different time points.
pmid: 31156344 J Med Biochem 影响因子: 2.0 发表日期: 20190701 官网 免费下载
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