Axl as a therapeutic target in metastatic ovarian cancer
Abstract/Contents
- Abstract
- ABSTRACT Axl, Sky, and Mer receptor tyrosine kinases (RTKs) are increasingly implicated in a host of cellular responses including cell survival, proliferation, migration, phagocytosis, chemoresistance, and epithelial-mesenchymal transition (EMT). Furthermore, the Gas6/AXL system is implicated in several types of human cancer as well as inflammatory, autoimmune, vascular and kidney diseases. Since the discovery of Gas6/AXL in 1988 in chronic myelogenous leukemia, many more cancers have been found to express AXL. In chapter 1, I will describe my contribution to the field that includes identifying the role of AXL in metastatic ovarian cancer and validating the therapeutic target in ovarian cancer. In the second chapter, I have investigated the role of AXL in chemoresistance in ovarian cancer. Within the past decade, AXL crosstalk has emerged as a dominant pathway for ligand-independent activation. With the recent identification of AXL as an important factor in mediating tyrosine kinase inhibitor resistance, understanding this cross-talk is important. There has been a recent report of c-MET and AXL cross-talk in breast cancer. c-MET has become a potential target for cancer therapy with numerous clinical trials using c-MET inhibitors as monotherapy or in combination with other targeted agents or chemotherapy. I have further explored this cross-talk in ovarian cancer. In my final chapter, I have identified AXL expression in ovarian cancer tumors formed in a conditional genetically modified invasive ovarian cancer mouse model. In the future, AXL therapy should be further investigated in patients with metastatic ovarian cancer.
Description
| Type of resource | text |
|---|---|
| Form | electronic; electronic resource; remote |
| Extent | 1 online resource. |
| Publication date | 2013 |
| Issuance | monographic |
| Language | English |
Creators/Contributors
| Associated with | Fuh, Katherine Cynthia |
|---|---|
| Associated with | Stanford University, Cancer Biology Program. |
| Primary advisor | Giaccia, Amato J |
| Thesis advisor | Giaccia, Amato J |
| Thesis advisor | Cochran, Jennifer R |
| Thesis advisor | Hu, Mickey |
| Thesis advisor | Sweet-Cordero, Eric |
| Advisor | Cochran, Jennifer R |
| Advisor | Hu, Mickey |
| Advisor | Sweet-Cordero, Eric |
Subjects
| Genre | Theses |
|---|
Bibliographic information
| Statement of responsibility | Katherine Cynthia Fuh. |
|---|---|
| Note | Submitted to the Cancer Biology Program. |
| Thesis | Thesis (Ph.D.)--Stanford University, 2013. |
| Location | electronic resource |
Access conditions
- Copyright
- © 2013 by Katherine Cynthia Fuh
- License
- This work is licensed under a Creative Commons Attribution Non Commercial 3.0 Unported license (CC BY-NC).
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