AXL

Balazs Halmos; Xue wen Liu

doi:10.1007/978-1-4419-0717-2_114

AXL

Balazs Halmos, Xue wen Liu

Oncology

Research output: Chapter in Book/Report/Conference proceeding › Chapter

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	https://doi.org/10.1007/978-1-4419-0717-2_114
State	Published - Jan 1 2017

Keywords

AXL
Acquired TKI resistance
Activated mechanisms
Epithelial-mesenchymal transition (EMT)
Gas6
Overexpression
Point mutations
Receptor tyrosine kinase (RTK)
TAM family
Targeted inhibitors

ASJC Scopus subject areas

General Pharmacology, Toxicology and Pharmaceutics
General Biochemistry, Genetics and Molecular Biology
General Medicine

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1007/978-1-4419-0717-2_114

Cite this

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title = "AXL",

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.",

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year = "2017",

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doi = "10.1007/978-1-4419-0717-2_114",

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AU - Halmos, Balazs

AU - Liu, Xue wen

PY - 2017/1/1

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N2 - 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.

AB - 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.

KW - AXL

KW - Acquired TKI resistance

KW - Activated mechanisms

KW - Epithelial-mesenchymal transition (EMT)

KW - Gas6

KW - Overexpression

KW - Point mutations

KW - Receptor tyrosine kinase (RTK)

KW - TAM family

KW - Targeted inhibitors

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AXL