通过向瘤微环境来克服EGFR-TKI耐药性
Jinsong Zhang1, Natalie Vokes2, Man Li1
1State Key Laboratory of Molecular Oncology, CAMS Key Laboratory of Translational Research on Lung Cancer, Department of Medical Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 17, Panjiayuannanli, Chaoyang District, Beijing 100021, China.
在非小细胞肺癌 (NSCLC) 中,对表皮生长因子受体 (EGFR) - 铁氨酸激酶抑制剂 (TKIs) 的耐药性是一个重大挑战. 本综述探讨了抵抗机制,重点关注瘤微环境和克服TKI抵抗的策略.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 癌症研究 癌症研究
背景情况:
- 向疗法,特别是表皮生长因子受体 (EGFR) - 铁氨酸激酶抑制剂 (TKIs),是对具有敏感EGFR突变的非小细胞肺癌 (NSCLC) 精准医学的基石.
- 尽管最初的疗效,药物耐药性的发展仍然是一个重要的临床障碍,限制了长期的患者益处.
- 抵抗机制是多因素的,涉及内在的癌细胞变化和复杂的瘤微环境 (TME).
研究的目的:
- 巩固目前关于NSCLC中EGFR-TKI耐药机制的知识.
- 具体阐明瘤微环境在介导EGFR-TKI耐药性的作用.
- 概述克服TKI抗性的潜在策略.
主要方法:
- 本综述综合了现有的科学文献和研究成果.
- 它的重点是分析研究研究EGFR-TKI在NSCLC的耐药性.
- 重点是研究详细说明瘤微环境对治疗结果的影响.
主要成果:
- EGFR-TKI耐药性是由各种机制驱动的,包括获得的突变和绕过信号通路.
- 瘤微环境,包括树皮细胞,免疫细胞和细胞外基质,显著影响药物反应和耐药性.
- 在TME内部的特定相互作用可以促进癌细胞的存活和增殖,尽管TKI治疗.
结论:
- 了解癌细胞和TME之间的复杂相互作用对于破译EGFR-TKI耐药性至关重要.
- 针对瘤微环境与EGFR-TKI结合,有望克服抗性.
- 对TME调节策略的进一步研究是有必要的,以提高NSCLC的治疗疗效和患者的治疗结果.
更多相关视频
09:38Establishment and Characterization of Three Afatinib-resistant Lung Adenocarcinoma PC-9 Cell Lines Developed with Increasing Doses of Afatinib
Published on: June 26, 2019
13:34A Combined 3D Tissue Engineered In Vitro/In Silico Lung Tumor Model for Predicting Drug Effectiveness in Specific Mutational Backgrounds
Published on: April 6, 2016
相关概念视频
Mitogens and the Cell Cycle
The Tumor Microenvironment
Tumor Immunotherapy
Targeted Cancer Therapies
There are several types of targeted therapies against...
Treatment Resistant Cancers
Combination Therapies and Personalized Medicine
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
