Epidermal Growth Factor Receptor: Difference between revisions
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[[Image:3i2t1.png|left|200px|thumb|Crystal Structure of unliganded Drosophila Epidermal Growth Factor Receptor ectodomain, [[3i2t]]]]{{ | <StructureSection load='3i2t' size='450' side='right' scene='Epidermal_Growth_Factor_Receptor/Cv/1' caption=''> | ||
[[Image:3i2t1.png|left|200px|thumb|Crystal Structure of unliganded Drosophila Epidermal Growth Factor Receptor ectodomain, [[3i2t]]]] | |||
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[[Epidermal Growth Factor Receptor]] (EGFR or ERBB1) is found on the cell surface and associates to homodimers upon binding of its ligands such as the Epidermal Growth Factor (EGF) to its extracellular domain. The dimerization stimulates autophosphorylation of several tyrosine residues in the intracellular kinase domain which signal downstream transduction cascades. A human EGFR-2 (HER-2 or ERBB2) is involved in breast [[Cancer|cancer]] and is a major target for breast cancer [[Pharmaceutical Drugs|therapeutics]]. ERBB3 uses neuregulin as a ligand. ERBB4 is a closely related receptor tyrosine kinase. The images at the left and at the right correspond to one representative EGFR, ''i.e.'' crystal structure of unliganded Drosophila Epidermal Growth Factor Receptor ectodomain ([[3i2t]]). | [[Epidermal Growth Factor Receptor]] (EGFR or ERBB1) is found on the cell surface and associates to homodimers upon binding of its ligands such as the Epidermal Growth Factor (EGF) to its extracellular domain. The dimerization stimulates autophosphorylation of several tyrosine residues in the intracellular kinase domain which signal downstream transduction cascades. A human EGFR-2 (HER-2 or ERBB2) is involved in breast [[Cancer|cancer]] and is a major target for breast cancer [[Pharmaceutical Drugs|therapeutics]]. ERBB3 uses neuregulin as a ligand. ERBB4 is a closely related receptor tyrosine kinase. The images at the left and at the right correspond to one representative EGFR, ''i.e.'' crystal structure of unliganded Drosophila Epidermal Growth Factor Receptor ectodomain ([[3i2t]]). | ||
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== '''EGFR and Lung Cancers of "Never Smokers"''' == | == '''EGFR and Lung Cancers of "Never Smokers"''' == | ||
Tyrosine kinases in general control critical cellular activities through regulation of signal pathways (3). This regulation is essential for controlling the cell and making sure it acts normally and goes through the normal cell cycle. However, when these kinases are mutated, they can lead to cancer as a result (3). Mutations in EGFR as a result can also lead to cancers, and this is why understanding how EGFR works is an essential aspect for the treatment of certain cancers. In cancer, cells divide rapidly without control and an uncontrolled or unregulated EGF receptor will and can result in uncontrolled cell division. Therefore, inhibition of EGFR can be an essential part of controlling cancers caused by mutations in EGFR. | Tyrosine kinases in general control critical cellular activities through regulation of signal pathways (3). This regulation is essential for controlling the cell and making sure it acts normally and goes through the normal cell cycle. However, when these kinases are mutated, they can lead to cancer as a result (3). Mutations in EGFR as a result can also lead to cancers, and this is why understanding how EGFR works is an essential aspect for the treatment of certain cancers. In cancer, cells divide rapidly without control and an uncontrolled or unregulated EGF receptor will and can result in uncontrolled cell division. Therefore, inhibition of EGFR can be an essential part of controlling cancers caused by mutations in EGFR. | ||
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Ten percent of lung cancers occur in patients who are deemed to be "never smokers" which are people who have smoked less than 100 cigarettes in lifetime (3). Therefore, a large number of people are affected by lung cancer without smoking, and this is quite important. What do these people have in common if they are not smoking cigarettes? A study showed that 75% of cancers with a mutation in EGFR were from these "never smokers" (3). This means that gefitinib and erlotinib are most likely going to be effective on people who have not smoked because there is a high correlation of them having these mutations in EGFR. Studying these mutations and what causes them could be the next step in understanding how to prevent these types of lung cancers. | Ten percent of lung cancers occur in patients who are deemed to be "never smokers" which are people who have smoked less than 100 cigarettes in lifetime (3). Therefore, a large number of people are affected by lung cancer without smoking, and this is quite important. What do these people have in common if they are not smoking cigarettes? A study showed that 75% of cancers with a mutation in EGFR were from these "never smokers" (3). This means that gefitinib and erlotinib are most likely going to be effective on people who have not smoked because there is a high correlation of them having these mutations in EGFR. Studying these mutations and what causes them could be the next step in understanding how to prevent these types of lung cancers. | ||
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== 3D Structures of Epidermal Growth Factor Receptor == | == 3D Structures of Epidermal Growth Factor Receptor == | ||