Targeted therapies for advanced non-small cell lung cancer

Xiaojuan Ai, Xialing Guo, Jun Wang, Andreea L. Stancu, Patrick M.N. Joslin, Dianzheng Zhang and Shudong Zhu _

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Oncotarget. 2018; 9:37589-37607. https://doi.org/10.18632/oncotarget.26428

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Xiaojuan Ai1, Xialing Guo2, Jun Wang1, Andreea L. Stancu3, Patrick M.N. Joslin4, Dianzheng Zhang5 and Shudong Zhu1,2

1National Key Discipline of Genetics, School of Life Sciences, Central South University, Changsha, China

2Argus Pharmaceuticals, Changsha, China

3Department of Dermatology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA

4Division of Hematology/Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA

5Department of Bio-Medical Sciences, Philadelphia College of Osteopathic Medicine, Philadelphia, PA, USA

Correspondence to:

Shudong Zhu, email: [email protected]

Keywords: NSCLC; molecular target; mTOR; EGFR; PI3K

Received: August 23, 2017     Accepted: February 24, 2018     Published: December 25, 2018


Lung cancer is a serious health problem and the leading cause of cancer death worldwide, due to its high incidence and mortality. 85% of lung cancers are represented by the non-small cell lung cancer (NSCLC). Traditional chemotherapy has been the main treatment option in NSCLC. However, it is often associated with limited efficacy and overall poor patient survival. In recent years, molecular targeting has achieved great progress in therapeutic treatment of cancer and plays a crucial role in the current clinical treatment of NSCLC, due to enhanced efficacy on cancer tissues and reduced toxicity for normal tissues. In this review, we summarize the current targeting treatment of NSCLC, including inhibition of the epidermal growth factor receptor (EGFR), phosphatidylinositol 3-kinase (PI3Ks), mechanistic target of rapamycin (mTOR), epidermal growth factor receptor 2 (ErbB2), vascular epidermal growth factor receptor (VEGFR), kirsten human rat sarcoma protein (KRAS), mesenchymal-epithelial transition factor or hepatocyte growth factor receptor (c-MET), anaplastic lymphoma kinase (ALK), v-Raf murine sarcoma viral oncogene homolog B (BRAF). This article may serve as a guide to clinicians and researchers alike by assisting in making therapeutic decisions. Challenges of acquired drug resistance targeted therapy and imminent newer treatment modalities against NSCLC are also discussed.

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