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EGFR: The Epidermal Growth Factor Receptor

Writer: RRHS ScienceNHSRRHS ScienceNHS


By: Gargi Sharma

EGFR, also known as epidermal growth factor receptor, produces a protein that is a member of the protein kinase superfamily. It is a receptor for ligands from the epidermal growth factor family. It is a cell surface protein that, when binds to a receptor, leads to tyrosine kinase getting activated inside the cellular region of the receptor, leading to phosphorylation. Phosphorylation

allows cells growth and proliferation, and oncogenes such as fos and jun are expressed. It is located at 7p11.2 on the chromosome. EGFR is commonly associated with causing cancer because it is often mutated or

overexpressed in cancer cells.

The EGFR gene is mostly mutated in meninges and the lungs, and copy number variation is most prominent in the central nervous system. Mutations in the EGFR gene mostly cause lung cancer. Mutations in this gene particularly cause lung adenocarcinoma.

There are several other causes for lung cancer as well. The leading cause of lung cancer is

smoking. Cigarette smoke is full of carcinogens, and when a person inhales it, it damages the lining of the lungs. At first, the body is able to repair the damage to the lining. But, as the smoking continues, it becomes harder to repair the damage, and the cells lining the lungs may start acting abnormally, leading to cancer. Targeted drug therapy is useful in treating cancer with particular mutations. The therapy will focus on killing the cells with mutations, like EGFR

mutations.

When there is a mutation in EGFR, it can lead to cancer, mainly due to uncontrolled

proliferation. In addition to promoting proliferative signaling, it deregulates cellular energetics, and enables cell death escape. EGFR most commonly suppresses escaping immune system, invasion and metastasis, and angiogenesis. This can lead to several factors that will help the cancer grow, and it can go unnoticed by the immune system because certain mutations in EGFR induce apoptosis of T-cells.

 
 
 

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