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Review
. 2009:149:203-26.
doi: 10.1007/978-0-387-98094-2_10.

Activated epidermal growth factor receptor in ovarian cancer

Laurie G Hudson  1 , Reema Zeineldin, Melina Silberberg, M Sharon Stack
Affiliations
Review

Activated epidermal growth factor receptor in ovarian cancer

Laurie G Hudson et al. Cancer Treat Res. 2009.
No abstract available

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Figures

Figure 10.1
Figure 10.1. Model of the EGF Receptor
The extracellular N-terminal domain contains two subdomains that directly interact with ligand and two cysteine-rich subdomains. There is a single transmembrane domain that links the extracellular domain to the intracellular tyrosine kinase domain and the C-terminal tail which contains the autophosphorylation sites. The EGF receptor dimerizes with other ErbB receptors.
Figure 10.2
Figure 10.2. Chronic EGF treatment leads to persistent elevation of mesenchymal markers
OvCa 433 cells were grown as described [117] without (−) or with (+) EGF for 72h (left panel) or continuously for 36 days (right panel). After the indicated exposures, cells were rinsed twice with phosphate-buffered saline and placed in growth medium without EGF as indicated. Protein lysates were resolved by SDS-polyacrylamide gel electrophoresis and the mesenchymal markers N-cadherin and vimentin were detected by immunoblot analysis. GAPDH was used as a loading control.
Figure 10.3
Figure 10.3. Mesenchymal phenotype is reversible after short term EGF treatment
OVCA 433 cells were maintained in serum-free medium containing 0.1% bovine serum albumin (w/v) for 24 h prior to treatment without EGF (control) or with 10 nM EGF for the indicated times. For EGF withdrawal (far right panel), cells were treated with EGF for 24h, rinsed twice in phosphate-buffered saline, then returned to serum free medium. Cell phenotype was documented by phase contrast microscopy and digital imaging.
See this image and copyright information in PMC

References

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