相关实验视频

Updated: Mar 6, 2026

Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure

Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure

Published on: August 11, 2017

对EGFR-TKIs耐药的晚期肺癌患者获得的融合突变的分析

Yuan Yang¹, Nana Zhang², Liang Shi¹

¹Department of Oncology, Beijing Chest Hospital, Capital Medical University, and Beijing Tuberculosis and Thoracic Tumour Research Institute, Beijing, China.

Journal of the College of Physicians and Surgeons--Pakistan : JCPSP

|March 4, 2026

概括

获得的融合基因如ALK,ROS1和RET可以在EGFR-TKI耐药性后出现非小细胞肺癌 (NSCLC). 包括ALK/RET/ROS1-TKIs在内的向疗法在这些NSCLC患者中显示出有效性.

科学领域:

在瘤学瘤学.
遗传学是一个遗传学.
分子生物学分子生物学

背景情况:

非小细胞肺癌 (NSCLC) 的治疗通常涉及表皮生长因子受体氨酸激酶抑制剂 (EGFR-TKI).
对EGFR-TKIs的获得性耐药性是NSCLC管理中的重大临床挑战.
基因融合的出现可能是获得耐药性的机制.

研究的目的:

为了表征非小细胞肺癌 (NSCLC) 患者,这些患者在对EGFR-TKI耐药后发展了融合基因.
描述这个患者队列中的临床特征,遗传情景和治疗结果.

主要方法:

追溯收集2800个具有EGFR敏感突变的NSCLC病例.
基于组织的下一代测序 (NGS) 用于识别获得的融合突变 (ALK,ROS1,RET等). ) 的情况.
对一系列病例 (n=9) 的临床数据,突变状态,治疗策略和随访的描述性分析.

主要成果:

确定了9名患有获得的融合突变的患者:6名ALK,2名RET,1名ROS1.
在大多数融合出现的患者中,EGFR丰度下降或变得无法检测.
用ALK/RET/ROS1-TKIs或组合疗法治疗显示出有效性,无进展生存期从5个月到39个月以上.
一名患者经历了ALK-TKI耐药性后的小细胞肺癌转变.

结论:

获得的基因融合是NSCLC中EGFR-TKI耐药性的机制.
针对这些融合的向治疗或组合策略是有效的治疗选择.
需要进一步的研究来了解融合驱动的NSCLC后EGFR-TKI耐药性的临床影响和管理.

更多相关视频

Establishment and Characterization of Three Afatinib-resistant Lung Adenocarcinoma PC-9 Cell Lines Developed with Increasing Doses of Afatinib

Establishment and Characterization of Three Afatinib-resistant Lung Adenocarcinoma PC-9 Cell Lines Developed with Increasing Doses of Afatinib

Published on: June 26, 2019

Author Spotlight: Advancements in Molecular Biomarker Testing for Non-Squamous Non-Small Cell Lung Cancer

Author Spotlight: Advancements in Molecular Biomarker Testing for Non-Squamous Non-Small Cell Lung Cancer

Published on: September 8, 2023

相关概念视频

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...