Abstract
AXL is a member of the TAM family, a receptor tyrosine kinase (RTK) subfamily composed of AXL, TYRO-3, and MER. Its main ligand is the vitamin K-dependent protein named growth arrest-specific gene 6 (Gas6). AXL is abnormally activated in many cancers by protein overexpression, point mutations, and gene fusions. The Gas6-AXL axis contributes to tumor progression, invasion, metastasis, and resistance both to chemotherapeutic and targeted anticancer therapies in a wide variety of cancers. In this review, we describe the biology of AXL, review diverse mechanisms of activation and the established and putative roles of AXL as a biomarker and therapeutic target in cancer therapy. Pre-clinical and clinical data for anti-AXL therapies to date are also summarized.
| Original language | English (US) |
|---|---|
| Title of host publication | Cancer Therapeutic Targets |
| Publisher | Springer New York |
| Pages | 661-671 |
| Number of pages | 11 |
| Volume | 2-2 |
| ISBN (Electronic) | 9781441907172 |
| ISBN (Print) | 9781441907165 |
| DOIs | |
| State | Published - Jan 1 2017 |
Keywords
- Acquired TKI resistance
- Activated mechanisms
- AXL
- Epithelial-mesenchymal transition (EMT)
- Gas6
- Overexpression
- Point mutations
- Receptor tyrosine kinase (RTK)
- TAM family
- Targeted inhibitors
ASJC Scopus subject areas
- Medicine(all)
- Biochemistry, Genetics and Molecular Biology(all)
- Pharmacology, Toxicology and Pharmaceutics(all)
