Abstract |
Cell signaling pathways, responsible for maintaining a balance between cell proliferation and death, have emerged as rational targets for the management of cancer. Emerging data amassed from various laboratories around the world suggests that green tea, particularly its major polyphenolic constituent (-)-epigallocatechin-3-gallate (EGCG), possesses remarkable cancer chemopreventive and therapeutic potential against various cancer sites in animal tumor bioassay systems and in some human epidemiologic studies. EGCG has been shown to modulate multiple signal transduction pathways in a fashion that controls the unwanted proliferation of cells, thereby imparting strong cancer chemopreventive as well as therapeutic effects. This review discusses the modulations of important signaling events by EGCG and their implications in cancer management.
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Authors | Naghma Khan, Farrukh Afaq, Mohammad Saleem, Nihal Ahmad, Hasan Mukhtar |
Journal | Cancer research
(Cancer Res)
Vol. 66
Issue 5
Pg. 2500-5
(Mar 01 2006)
ISSN: 0008-5472 [Print] United States |
PMID | 16510563
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Review)
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Chemical References |
- Anticarcinogenic Agents
- NF-kappa B
- Protease Inhibitors
- Tea
- Vascular Endothelial Growth Factor A
- Catechin
- epigallocatechin gallate
- ErbB Receptors
- Receptor, IGF Type 1
- Mitogen-Activated Protein Kinases
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Topics |
- Animals
- Anticarcinogenic Agents
(pharmacology, therapeutic use)
- Apoptosis
(drug effects)
- Catechin
(analogs & derivatives, pharmacology, therapeutic use)
- Cell Cycle
(drug effects)
- Clinical Trials as Topic
- ErbB Receptors
(antagonists & inhibitors)
- Humans
- MAP Kinase Signaling System
(drug effects)
- Mitogen-Activated Protein Kinases
(antagonists & inhibitors)
- NF-kappa B
(antagonists & inhibitors)
- Neovascularization, Pathologic
(drug therapy)
- Protease Inhibitors
(pharmacology, therapeutic use)
- Receptor, IGF Type 1
(antagonists & inhibitors)
- Signal Transduction
(drug effects)
- Tea
- Vascular Endothelial Growth Factor A
(antagonists & inhibitors)
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