Abstract
Aberrant expression or activation of protein tyrosine kinases, including Src and related Src family kinases, is a common occurrence in many human cancers, resulting in deregulation of expression of numerous mediators of cellular functions, including pro-angiogenic molecules. In addition, Src activation regulates vascular permeability of endothelial cells. How these processes contribute to tumor progression and metastasis are the subjects of this review. As Src-selective inhibitors have entered clinical trials for a number of solid tumors, further understanding of the roles of Src kinases in mediating tumor angiogenesis as well as modulating tumor/microenvironment interactions will provide insights into the best use of these inhibitors in treating patients afflicted with tumors in which Src is activated.
| Original language | English |
|---|---|
| Pages (from-to) | 1207-1217 |
| Number of pages | 11 |
| Journal | Expert Opinion on Therapeutic Targets |
| Volume | 11 |
| Issue number | 9 |
| DOIs | |
| Publication status | Published - 2007 Sept |
| Externally published | Yes |
Bibliographical note
Funding Information:National Cancer Institute grant CA-16672 (GE Gallick), Lockton Foundation (GE Gallick), Gillson Longenbaugh Foundation (GE Gallick), National Institutes of Health T32 CA-09599 (AN Shah), the Eleanor B. Pillsbury Fellowship-University of Illinois Hospital (AN Shah) and the Sowell-Huggins Fellowship (J Zhang). GE Gallick is the Sowell-Huggins Professor of Cancer Biology.
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- Angiogenesis
- Metastasis
- Protein tyrosine kinase
- Src family kinase
- Tumor progression
- Tyrosine kinase inhibitors
- VEGF
- Vascular permeability
ASJC Scopus subject areas
- Molecular Medicine
- Pharmacology
- Drug Discovery
- Clinical Biochemistry
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