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Epidermal Growth
Factor Receptor (EGFR)
Soluble Level


EFGr is a receptor found on the surfaces of many cell types. It is often over-produced on the cells of skin, bladder, breast and Lung Cancers, where it triggers the process of tumour progression. The EGFr can also be shed from the cell surface and remain in the blood in soluble form. Soluble EGFr blocks the cancer-promoting effects of cell-surface EGFr by acting as innate anti-tumour therapy.

This assay is able to provide information regarding the activation of EGFr in the context of specific cancer therapy:

- A patient can be treated with substitute “partner” proteins that will bind with cell-surface EGFr and so prevent their partnering with the ligands that activate their cancer-promoting effects.

- EGFr levels can be measured before and after the application of these molecular substitutes. Detection of high levels of blood-soluble EGFr after this form of cancer therapy demonstrates the resulting success of this treatment. On the other hand, low levels of the protein either before or after treatment reveal that EGFr cannot be considered a contributing factor to the patient’s cancer.


This assay will provide extremely valuable and accurate information relating to all forms of cancer.


EGFr is a very complex transmembrane protein and is expressed on many types of cells. Very often it becomes over expressed on the cells of epithelial tumours as well as cancers in the bladder, breast and lung. Activation of EGFr results in DNA replication and cell proliferation leading to tumour progression. Any activation of EGFr occurs during binding with its ligand, the epidermal growth factor, or EGF-like ligands. In addition some toxic environmental stimuli, such as ultraviolet irradiation, could activate EGFr.

The EGFr can be shed from the cell surface and appears in the blood in soluble form. The soluble receptor is an Antagonistic for the transmembrane receptor located on the cell surface because EGFr in the blood binds the ligand quicker than EGFr on the cell surface and this prevents the induction of signals by the ligand in the cells leading to tumour development. This natural therapeutical action of soluble EGFr is insufficient if there is activation of EGFr on the cell surface by some toxic stimuli. This assay is able to provide information relating to the activation of EGFr.

High levels, before an application of anti-EGFr preparations, indicate an active state of the EGF receptors followed by increased shedding of these receptors from the cell surface. However, there is a risk that an application of the preparations designed to block the EGF receptors on a cancerous cell surface will block the soluble EGF receptors in the blood stream. This will reduce the anti-tumour effects to both the soluble EGF receptors and the anti-EGFr preparation. High levels of EGF soluble receptors after tumour treatment indicate the effectiveness of the anti-tumour therapy. Very low levels of EGFsr are such that they cannot be considered as a contributing factor to tumour growth.
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