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J Thorac Oncol. 2015 Sep;10(9):1319-1327. doi: 10.1097/JTO.0000000000000607.
2
Targeting the phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) pathway: an emerging treatment strategy for squamous cell lung carcinoma.针对磷脂酰肌醇 3-激酶 (PI3K)/AKT/哺乳动物雷帕霉素靶蛋白 (mTOR) 通路:治疗鳞状细胞肺癌的新兴策略。
Cancer Treat Rev. 2014 Sep;40(8):980-9. doi: 10.1016/j.ctrv.2014.06.006. Epub 2014 Jul 3.
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Invest New Drugs. 2014 Aug;32(4):670-81. doi: 10.1007/s10637-014-0082-9. Epub 2014 Mar 21.
4
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Mol Cancer Ther. 2014 May;13(5):1078-91. doi: 10.1158/1535-7163.MCT-13-0709. Epub 2014 Mar 14.
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Phase II study of everolimus-erlotinib in previously treated patients with advanced non-small-cell lung cancer.依维莫司联合厄洛替尼治疗晚期非小细胞肺癌患者的 II 期研究。
Ann Oncol. 2014 Feb;25(2):409-15. doi: 10.1093/annonc/mdt536. Epub 2013 Dec 23.
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Phosphorylated Akt expression is a prognostic marker in early-stage non-small cell lung cancer.磷酸化 Akt 表达是早期非小细胞肺癌的预后标志物。
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J Clin Oncol. 2013 Sep 20;31(27):3327-34. doi: 10.1200/JCO.2012.44.2806. Epub 2013 Jul 1.
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Crizotinib versus chemotherapy in advanced ALK-positive lung cancer.克唑替尼与化疗用于治疗晚期 ALK 阳性肺癌。
N Engl J Med. 2013 Jun 20;368(25):2385-94. doi: 10.1056/NEJMoa1214886. Epub 2013 Jun 1.

磷脂酰肌醇 3-激酶-AKT-雷帕霉素靶蛋白(PI3K-Akt-mTOR)信号通路在非小细胞肺癌中的作用。

Phosphatidylinositol 3-kinase-AKT-mammalian target of rapamycin (PI3K-Akt-mTOR) signaling pathway in non-small cell lung cancer.

机构信息

1 Department of Medical Oncology, Chris O'Brien Lifehouse, Camperdown, NSW, Australia ; 2 Department of Medical Oncology, Macarthur Cancer Therapy Centre, Campbelltown, NSW, Australia.

出版信息

Transl Lung Cancer Res. 2015 Apr;4(2):165-76. doi: 10.3978/j.issn.2218-6751.2015.01.04.

DOI:10.3978/j.issn.2218-6751.2015.01.04
PMID:25870799
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4384220/
Abstract

Non-small cell lung cancer (NSCLC) is a devastating disease with poor prognosis. Systemic chemotherapy has been the mainstay of treatment in advanced disease for many decades. Personalized targeted therapy such as epidermal growth factor receptor tyrosine kinase inhibitors (EGFR TKIs) and crizotinib has significantly changed the treatment paradigm in NSCLC. The future success of development of molecular targeted therapy relies on the understanding of signal transduction pathways. The PI3K-Akt-mTOR pathway is commonly deregulated in human malignancy including NSCLC. Therefore, this pathway is a target for many therapeutic developments. This review will provide an overview of PI3K-Akt-mTOR signaling pathway, genetic alterations activating the pathway and clinical therapeutic development of pathway inhibitors.

摘要

非小细胞肺癌(NSCLC)是一种预后不良的毁灭性疾病。几十年来,系统化疗一直是晚期疾病的主要治疗方法。表皮生长因子受体酪氨酸激酶抑制剂(EGFR TKIs)和克唑替尼等个性化靶向治疗已显著改变了 NSCLC 的治疗模式。分子靶向治疗的未来成功取决于对信号转导途径的理解。PI3K-Akt-mTOR 途径在包括 NSCLC 在内的人类恶性肿瘤中通常失调。因此,该途径是许多治疗开发的目标。本文综述了 PI3K-Akt-mTOR 信号通路、激活该通路的遗传改变以及通路抑制剂的临床治疗进展。