Targeting non-small cell lung cancer: driver mutation beyond epidermal growth factor mutation and anaplastic lymphoma kinase fusion

The identification of driver mutations in epidermal growth factor receptor, anaplastic lymphoma kinase, the BRAF and ROS1 genes and subsequent successful clinical development of kinase inhibitors not only significantly improves clinical outcomes but also facilitates the discovery of other novel driv...

Full description

Saved in:
Bibliographic Details
Published in:Therapeutic Advances in Medical Oncology 2020-01, Vol.12, p.1758835919895756-1758835919895756
Main Author: Chu, Quincy S.
Format: Article
Language:English
Subjects:
1-Phosphatidylinositol 3-kinase
AKT protein
Epidermal growth factor
Epidermal growth factor receptors
ErbB-2 protein
Fibroblast growth factor receptor 1
Gene amplification
K-Ras protein
Kinases
Lung cancer
Lymphoma
Mutation
Neuregulin
Neuregulin 1
Non-small cell lung carcinoma
Protein-tyrosine kinase
Review
Small cell lung carcinoma
TOR protein
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The identification of driver mutations in epidermal growth factor receptor, anaplastic lymphoma kinase, the BRAF and ROS1 genes and subsequent successful clinical development of kinase inhibitors not only significantly improves clinical outcomes but also facilitates the discovery of other novel driver mutations in non-small cell lung cancer. These driver mutations can be categorized into mutations in or near the kinase domain, gene amplification or fusion. In this review, BRAF V600E, EGFR and HER-2 exon 20 mutation, FGFR1–4, K-RAS, MET, neuregulin-1, NRTK, PI3K/AKT/mTOR, RET and ROS1 gene aberration and their therapeutics will be discussed.
ISSN:1758-8359
1758-8340
1758-8359
DOI:10.1177/1758835919895756