EGFR mutations and the terminal respiratory unit
EGFR mutations and the terminal respiratory unit
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DOI：
10.1007/s10555-010-9205-8
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发表时间：
2010-02
影响因子：
9.2
通讯作者：
Y. Yatabe
中科院分区：
文献类型：
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作者：
Y. Yatabe
自 2004 年首次发现表皮生长因子受体 (EGFR)-酪氨酸激酶结构域突变以来，人们已经积累了大量关于这些突变的知识。携带这种突变的非小细胞肺癌患者对 EGFR-酪氨酸激酶抑制剂的治疗显示出显着的临床反应，其有效性最近已在大型临床试验中得到证实。大多数反应者最终都会经历的大多数导致治疗耐药的机制已经被阐明，并且克服耐药性的方法也已经被开发出来。除了临床益处之外，了解 EGFR 突变还为该腺癌亚型的分子和病理学方面提供了新的线索，其中包括非吸烟者或女性中的频繁发展，以及肺癌分子分类中的特定簇。与肺腺癌发展早期阶段 EGFR 突变的参与相反，EGFR 扩增叠加在侵袭性癌症的进展中。在这篇综述中，我总结了肺癌EGFR突变的临床病理特征。我还概述了目前对携带 EGFR 突变的肺腺癌亚型的理解，特别提到了肺癌的分子分类和“终末呼吸单位”的新概念。
Considerable knowledge has accumulated about mutations of the epidermal growth factor receptor (EGFR)-tyrosine kinase domain since these were first identified in 2004. Patients with nonsmall cell lung cancer with this mutation show dramatic clinical responses to treatment with EGFR-tyrosine kinase inhibitors, whose effectiveness has been established recently in large clinical trials. Most of the mechanisms responsible for resistance to treatment, which most responders experience eventually, have been elucidated, and methods to overcome resistance have been developed. In addition to the clinical benefit, understanding EGFR mutations sheds new light on the molecular and pathological aspects of this adenocarcinoma subset, which include frequent development in nonsmokers or females, and particular clusters within the molecular classification in lung cancer. In contrast to the involvement of EGFR mutations in the early stage of lung adenocarcinoma development, EGFR amplification is superimposed on the progression to invasive cancer. In this review, I summarize the clinicopathological characteristics of EGFR mutations in lung cancer. I also provide an overview of the current understanding of the lung adenocarcinoma subset harboring EGFR mutations with special reference to the molecular classification of lung cancer and the novel concept of the “terminal respiratory unit.”