EGFR as a Pharmacological Target in EGFR -Mutant Non-Small-Cell Lung Cancer: Where Do We Stand Now?

T790米 表皮生长因子受体 肺癌 医学 癌症研究 吉非替尼 酪氨酸激酶 临床试验 肿瘤科 癌症 内科学 受体
作者
E-E Ke,Yi‐Long Wu
出处
期刊:Trends in Pharmacological Sciences [Elsevier BV]
卷期号:37 (11): 887-903 被引量:74
标识
DOI:10.1016/j.tips.2016.09.003
摘要

EGFR-TKI monotherapy has been regarded as standard first-line therapy for patients with NSCLC and EGFR-sensitive mutations. To maximize the survival benefit from first-line treatments and delay the occurrence of resistance, EGFR-TKI-based combinations are reasonable strategies that have been explored. Third-generation EGFR-TKIs designed to specifically target T790M mutations may lead to dramatic changes in the treatment paradigm for patients with EGFR mutations over the next few years. Newer EGFR-targeting agents with better penetration of the central nervous system are in development. Targeting the epidermal growth factor receptor (EGFR) using tyrosine kinase inhibitors (TKIs) is highly effective in terms of tumor response rate, survival, and quality of life. However, acquired resistance to EGFR-TKIs is inevitable. Ongoing clinical trials will provide evidence for optimal strategies for patients with EGFR mutant non-small-cell lung cancer (NSCLC) in the near future. Numerous new agents are specifically addressing resistance mechanisms; mature data are related to the T790M mutation and MET pathway activation. Here, we provide a comprehensive review of new perspectives on how to optimize the management of this molecular disease. Targeting the epidermal growth factor receptor (EGFR) using tyrosine kinase inhibitors (TKIs) is highly effective in terms of tumor response rate, survival, and quality of life. However, acquired resistance to EGFR-TKIs is inevitable. Ongoing clinical trials will provide evidence for optimal strategies for patients with EGFR mutant non-small-cell lung cancer (NSCLC) in the near future. Numerous new agents are specifically addressing resistance mechanisms; mature data are related to the T790M mutation and MET pathway activation. Here, we provide a comprehensive review of new perspectives on how to optimize the management of this molecular disease.

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