Abstract
The identification of oncogenic driver mutations underlying sensitivity to epidermal growth factor receptor and anaplastic lymphoma kinase tyrosine kinase inhibitors has led to a surge of interest in identifying additional targetable oncogenes in non-small-cell lung cancer. A number of new potentially oncogenic gene alterations have been characterized in recent years, including BRAF mutations, HER2 insertions, PIK3CA mutations, FGFR1 amplifications, DDR2 mutations, ROS1 rearrangements, and RET rearrangements. In this review, we will discuss the techniques used to discover each of these candidate oncogenes, the prevalence of each in non-small-cell lung cancer, the preclinical data supporting their role in lung cancer, and data on small molecular inhibitors in development.
Publication types
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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Carcinoma, Non-Small-Cell Lung / genetics*
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Class I Phosphatidylinositol 3-Kinases
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DNA Mutational Analysis
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Discoidin Domain Receptor 1
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Gene Expression Regulation, Neoplastic
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Genetic Techniques*
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Humans
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Lung Neoplasms / genetics*
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Oncogenes*
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Phosphatidylinositol 3-Kinases / genetics
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Protein-Tyrosine Kinases / genetics
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Proto-Oncogene Proteins / genetics
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Proto-Oncogene Proteins B-raf / genetics
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Proto-Oncogene Proteins c-ret / genetics
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Receptor Protein-Tyrosine Kinases / genetics
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Receptor, ErbB-2 / genetics
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Receptor, Fibroblast Growth Factor, Type 1 / genetics
Substances
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Proto-Oncogene Proteins
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Phosphatidylinositol 3-Kinases
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Class I Phosphatidylinositol 3-Kinases
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PIK3CA protein, human
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DDR1 protein, human
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Discoidin Domain Receptor 1
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FGFR1 protein, human
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Protein-Tyrosine Kinases
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Proto-Oncogene Proteins c-ret
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ROS1 protein, human
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Receptor Protein-Tyrosine Kinases
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Receptor, ErbB-2
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Receptor, Fibroblast Growth Factor, Type 1
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BRAF protein, human
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Proto-Oncogene Proteins B-raf