Mass General Hospital Cancer Center treats patients with many cancer types. To learn more about the different cancer types that can be treated at the Cancer Center, please visit the Cancer Center website at the following page:
http://www.massgeneral.org/cancer/services/
CLICK IMAGE FOR MORE INFORMATIONThe EGFR gene encodes for a cell-surface protein known as the epidermal growth factor receptor, which is found in many normal epithelial tissues such as the skin and hair follicles. When epidermal growth factor ligand bind to EGFR, they activate several different cell signaling pathways that control various cell functions, including cell growth and proliferation.
Mutations in EGFR can lead to unregulated activation of the protein. These types of activating mutations are often found in NSCLC (non-small cell lung cancer), glioblastoma and head and neck squamous cell carcinoma. Sometimes, excess EGFR protein is produced due to the presence of too many copies of the EGFR gene, leading to excessive cell division and growth in the presence of epidermal growth factor. Among the human cancers in which EGFR overabundance is present are cancers of the head and neck (squamous cell), colon, rectum, lung (NSCLC), central nervous system (glioblastoma), pancreas and breast (HER2-positive metastatic). Blocking EGFR in tumors may keep cancer cells from growing. The FDA has approved several therapies that target EGFR in one or more cancers. Testing for genetic alterations of EGFR is available at the MGH genetics lab. Treatment for EGFR-mutant tumors, along with clinical trials testing new drugs for the treatment of EGFR-mutant tumors are available at the MGH Cancer Center.
Tumor mutation profiling performed clinically at the MGH Cancer Center has indicated that EGFR mutations occur primarily in lung cancer (~15%), but also in a minor subset of gastric (2%), brain (1%) and pancreatic (1%) cancers.
Source: Genetics Home Reference
The EGFR gene encodes for a cell-surface protein known as the epidermal growth factor receptor, which is found in many normal epithelial tissues such as the skin and hair follicles. When epidermal growth factor ligand bind to EGFR, they activate several different cell signaling pathways that control various cell functions, including cell growth and proliferation.
Mutations in EGFR can lead to unregulated activation of the protein. These types of activating mutations are often found in NSCLC (non-small cell lung cancer), glioblastoma and head and neck squamous cell carcinoma. Sometimes, excess EGFR protein is produced due to the presence of too many copies of the EGFR gene, leading to excessive cell division and growth in the presence of epidermal growth factor. Among the human cancers in which EGFR overabundance is present are cancers of the head and neck (squamous cell), colon, rectum, lung (NSCLC), central nervous system (glioblastoma), pancreas and breast (HER2-positive metastatic). Blocking EGFR in tumors may keep cancer cells from growing. The FDA has approved several therapies that target EGFR in one or more cancers. Testing for genetic alterations of EGFR is available at the MGH genetics lab. Treatment for EGFR-mutant tumors, along with clinical trials testing new drugs for the treatment of EGFR-mutant tumors are available at the MGH Cancer Center.
Tumor mutation profiling performed clinically at the MGH Cancer Center has indicated that EGFR mutations occur primarily in lung cancer (~15%), but also in a minor subset of gastric (2%), brain (1%) and pancreatic (1%) cancers.
Source: Genetics Home Reference
PubMed ID's
15864276,
15118073,
15118125,
15329413,
18772890,
15837736,
16720329,
21057220The EGFR G719C mutation arises from the nucleotide change c.2155G>T in exon 18, resulting in an amino acid substitution of the glycine (G) at position 719 by a cysteine (C).
The EGFR G719C mutation arises from the nucleotide change c.2155G>T in exon 18, resulting in an amino acid substitution of the glycine (G) at position 719 by a cysteine (C).