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The Receptor Tyrosine Kinase AXL in Cancer Progression

1
Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University Medical Center, Stanford, CA 94305, USA
2
Department of Obstetrics and Gynecology, Stanford University Medical Center, Stanford, CA 94305, USA
*
Author to whom correspondence should be addressed.
Academic Editors: Deric L. Wheeler and Toni M. Brand
Cancers 2016, 8(11), 103; https://doi.org/10.3390/cancers8110103
Received: 20 September 2016 / Revised: 26 October 2016 / Accepted: 3 November 2016 / Published: 9 November 2016
(This article belongs to the Special Issue TAM family receptors in cancer biology and therapeutic resistance)
The AXL receptor tyrosine kinase (AXL) has emerged as a promising therapeutic target for cancer therapy. Recent studies have revealed a central role of AXL signaling in tumor proliferation, survival, stem cell phenotype, metastasis, and resistance to cancer therapy. Moreover, AXL is expressed within cellular components of the tumor microenvironment where AXL signaling contributes to the immunosuppressive and protumorigenic phenotypes. A variety of AXL inhibitors have been developed and are efficacious in preclinical studies. These agents offer new opportunities for therapeutic intervention in the prevention and treatment of advanced disease. Here we review the literature that has illuminated the cellular and molecular mechanisms by which AXL signaling promotes tumor progression and we will discuss the therapeutic potential of AXL inhibition for cancer therapy. View Full-Text
Keywords: AXL; GAS6; metastasis; cancer stem cell phenotype; immune suppression; therapy; proliferation; resistance; small molecule; decoy receptor AXL; GAS6; metastasis; cancer stem cell phenotype; immune suppression; therapy; proliferation; resistance; small molecule; decoy receptor
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MDPI and ACS Style

Rankin, E.B.; Giaccia, A.J. The Receptor Tyrosine Kinase AXL in Cancer Progression. Cancers 2016, 8, 103.

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