在吸烟者和从未吸烟者的高级非小细胞肺癌中,常见的驱动突变和编程死亡链接1表达在吸烟者和从未吸烟者中
Chong Kin Liam1,2, Chian Yih Yew3, Yong Kek Pang4,3
1Department of Medicine, Faculty of Medicine, University of Malaya, 50603, Kuala Lumpur, Malaysia. liamck@ummc.edu.my.
BMC cancer
|July 14, 2023
概括
沉重的吸烟和EGFR野生型瘤与非小细胞肺癌 (NSCLC) 中更高的编程死亡配体1 (PD-L1) 表达有关. 这一发现对理解NSCLC和开发向疗法具有重要意义.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 肺部病理学 肺部病理学
背景情况:
- 非小细胞肺癌 (NSCLC) 治疗可能会受到编程死亡配体1 (PD-L1) 表达,驱动突变和吸烟史的影响.
- 了解这些关系对于NSCLC个性化医学至关重要.
研究的目的:
- 调查驱动突变 (EGFR,ALK),PD-L1表达和晚期NSCLC中吸烟状态之间的关联.
- 为了确定吸烟强度是否影响NSCLC患者的PD-L1表达.
主要方法:
- 对191名晚期NSCLC患者的回顾性分析.
- 评估EGFR突变,ALK重组和PD-L1表达 (瘤比例得分).
- 根据吸烟史对患者进行分类 (从未吸烟,轻度,中度,重度吸烟者).
主要成果:
- 与吸烟者相比,从未吸烟者中EGFR突变的发生率更高.
- 吸烟者和重度吸烟者表现出更高比例的高PD-L1表达.
- 野生型EGFR瘤与高PD-L1表达显著相关,特别是在腺癌中.
- 沉重的吸烟和EGFR野生型状态是高PD-L1表达的独立预测因素.
结论:
- 沉重的吸烟和EGFR野生型状态与高PD-L1表达在NSCLC显著相关,包括腺癌.
- 这些因素可以指导治疗策略和患者选择NSCLC的免疫治疗.
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