Therapeutic targeting of AXL/Gas6 signaling in metastatic and primary cancer

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Abstract/Contents

Abstract
AXL is a receptor tyrosine kinase shown to be involved in driving metastasis and disease progression in many of solid and hematologous human cancers. Our lab has previously shown that inhibiting the activation of AXL by trapping its only ligand, Gas6, can reduce metastatic disease burden in several aggressive cancer models. Using engineered high-affinity AXL decoy receptors, we show that inhibiting AXL downstream signaling by preventing the binding of Gas6 to native AXL receptors can halt disease progression in acute myeloid leukemia (AML). Collectively, these results validate AXL as a therapeutic target in metastatic disease and highlight the potential clinical value of the engineered AXL decoy receptors as novel anti-metastatic therapies. We further examine the validity of AXL as a therapeutic target in canine melanoma, an alternative model of melanoma that mirrors many of the features of human melanoma

Description

Type of resource text
Form electronic resource; remote; computer; online resource
Extent 1 online resource
Place California
Place [Stanford, California]
Publisher [Stanford University]
Copyright date 2020; ©2020
Publication date 2020; 2020
Issuance monographic
Language English

Creators/Contributors

Author Diep, Anh Ngoc
Degree supervisor Giaccia, Amato J
Thesis advisor Giaccia, Amato J
Thesis advisor Ford, James M. (James Matthew)
Thesis advisor Graves, Edward (Edward Elliot), 1974-
Thesis advisor Rankin, Erinn
Degree committee member Ford, James M. (James Matthew)
Degree committee member Graves, Edward (Edward Elliot), 1974-
Degree committee member Rankin, Erinn
Associated with Stanford University, Cancer Biology Program.

Subjects

Genre Theses
Genre Text

Bibliographic information

Statement of responsibility Anh Ngoc Diep
Note Submitted to the Cancer Biology Program
Thesis Thesis Ph.D. Stanford University 2020
Location electronic resource

Access conditions

Copyright
© 2020 by Anh Ngoc Diep
License
This work is licensed under a Creative Commons Attribution 3.0 Unported license (CC BY).

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