Molecular pathology of lung cancer: key to personalized medicine
Molecular pathology of lung cancer: key to personalized medicine
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DOI：
10.1038/modpathol.2011.215
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发表时间：
2012-03-01
期刊：
影响因子：
7.5
通讯作者：
Zhang, Shaobo
中科院分区：
文献类型：
--
作者：
Cheng, Liang;Alexander, Riley E.;Zhang, Shaobo
大多数表皮生长因子受体（EGFR）突变或EML 4-ALK再表达阳性的肺腺癌患者对酪氨酸激酶抑制剂敏感。这些患者中相当多的患者对这些疗法的原发性和获得性耐药仍然是一个主要的临床问题。与酪氨酸激酶抑制剂耐药相关的具体分子机制尚未完全了解。临床病理学观察表明，涉及所谓的“驱动突变”的分子改变可用作标记，有助于选择最有可能从靶向治疗中获益的患者。在这篇综述中，我们总结了最近的发展，涉及特定的分子机制和标记物，已与原发性和获得性耐药EGFR靶向治疗肺腺癌。了解这些机制可能会提供新的治疗途径，并改善目前的治疗算法。Modern Pathology（2012）25，347-369; doi：10.1038/modpathol.2011.215; 2012年1月27日在线发表
The majority of lung adenocarcinoma patients with epidermal growth factor receptor-(EGFR) mutated or EML4-ALK rearrangement-positive tumors are sensitive to tyrosine kinase inhibitors. Both primary and acquired resistance in a significant number of those patients to these therapies remains a major clinical problem. The specific molecular mechanisms associated with tyrosine kinase inhibitor resistance are not fully understood. Clinicopathological observations suggest that molecular alterations involving so-called 'driver mutations' could be used as markers that aid in the selection of patients most likely to benefit from targeted therapies. In this review, we summarize recent developments involving the specific molecular mechanisms and markers that have been associated with primary and acquired resistance to EGFR-targeted therapy in lung adenocarcinomas. Understanding these mechanisms may provide new treatment avenues and improve current treatment algorithms. Modern Pathology (2012) 25, 347-369; doi:10.1038/modpathol.2011.215; published online 27 January 2012