Abstract
In the past two decades, several molecular targeted inhibitors have been developed and evaluated clinically to improve the survival of patients with cancer. Molecular targeted inhibitors inhibit the activities of pathogenic tyrosine kinases. Particularly, aberrant receptor tyrosine kinase (RTK) activation is a potential therapeutic target. An increased understanding of genetics, cellular biology and structural biology has led to the development of numerous important therapeutics. Pathogenic RTK mutations, deletions, translocations and amplification/over-expressions have been identified and are currently being examined for their roles in cancers. Therapies targeting RTKs are categorized as small-molecule inhibitors and monoclonal antibodies. Studies are underway to explore abnormalities in 20 types of RTK subfamilies in patients with cancer or other diseases. In this review, we describe representative RTKs important for developing cancer therapeutics and predicting or evaluated resistance mechanisms.
Highlights
Numerous drugs have been developed to target the receptor tyrosine kinase (RTK) family of growth factor receptors containing aberrations such as mutations, deletions, translocations and amplification/overexpression
Receptors for epidermal growth factor (EGF), leukocyte tyrosine kinase (LTK) (ALK), platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), hepatocyte growth factor (HGF) (MET) and insulin are significantly associated with oncogenic aberrations and are suitable targets for molecular-targeting therapy
These results strongly suggest that the understanding of heterogeneity of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) resistance mechanisms will contribute to the development of more effective therapeutic strategies for patients with non-small cell lung cancer (NSCLC)
Summary
Numerous drugs have been developed to target the receptor tyrosine kinase (RTK) family of growth factor receptors containing aberrations such as mutations, deletions, translocations and amplification/overexpression. All RTKs contain an extracellular domain, containing the ligand-binding site, single transmembrane region and cytosolic domain, which includes the region with protein tyrosine kinase activity. These RTKs receive and transmit signals from the environment in nature. We discuss the recent development of molecular targeting drugs for RTK aberrations in cancers, including potential or established molecular targets of EGFR, HER2, ALK, ROS1, vascular endothelial growth factor receptor (VEGF(R)), MET, insulin-like growth factor 1 receptor (IGF1R) and fibroblast growth factor receptor (FGFR), focusing on therapies for individual patients with cancer
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