Abstract
The phosphatase and tensin homology deleted on chromosome ten (PTEN) gene is severely lost in tissues of endometrial carcinorma, which is a hot topic in research of the tumorigenetic mechanism of endometrial carcinoma. PTEN regulated cell growth, proliferation, apoptosis and angiogenesis by regulating three down stream signaling pathways such as 3-kinase phosphatidylinositol/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mT0R), focal adhesion kinase (FAK) and mitogen-activated protein kinase (MAPK) pathways. The loss or mutation of PTEN causes tumorigenesis. This review summarizes the current research on association of PTEN and epidermal growth factor receptor (EGFR) and their downstream signaling pathways with tumorigenesis and development of endometrial carcinoma to provide theoretical evidence for gene diagnosis and gene therapy of endometrial carcinorma.
| Original language | English |
|---|---|
| Pages (from-to) | 447-449 |
| Number of pages | 3 |
| Journal | Tumor |
| Volume | 30 |
| Issue number | 5 |
| DOIs | |
| Publication status | Published - May 2010 |
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
- Endometrial neoplasms
- Epidermal growth factor
- PTEN
- Phosphatase and tensin homology deleted on chromosome ten
- Receptor
- Signal transduction
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