Cancer epidermal growth factor

Whereas epidermal growth factor (EGF) enhances the radiosensitivity of human squamous ceU carcinoma cells in vitro (197), addition of EGF to hormone-deprived MCE-7 breast cancer cells prior to irradiation results ia iacreased radioresistance (198). An anti-EGE-receptor monoclonal antibody blocks the abiUty of EGE to enhance growth and radioresistance. Tumor cells, the growth of which is stimulated by EGE, appear to be protected those where growth is iohibited are sensitized (198). 

The epidermal growth factor receptor 2 (HER-2) is a protein found on the surface of cells. Heterodimerization of HER-2 activates the enzyme tyrosine kinase, triggering reactions that cause the cells to grow and multiply. HER-2 is found at abnormally high levels on the surface of many types of cancer cells, which may divide excessively. Antibodies targeting HER-2 (e.g., trastuzumab) are used as antineoplastic agents. 

Harari PM (2004) Epidermal growth factor receptor inhibition strategies in oncology. Endocr. Relat. Cancer 11 689-708... 

PETERSON G and BARNES s (1993) Genistein and hiochanin A inhibit the growth of hiunan prostate cancer cells but not epidermal growth factor receptor tyrosine autophosphorylation. Prostate. 22 (4) 335-45. 

EGFR or ERB-BI Codes for epidermal growth factor (EGFR) receptor Glioblastoma, breast cancer, squamous carcinoma... 

Cetuximab is a human/mouse antibody that binds to the epidermal growth factor receptor to block its stimulation. The pharmacokinetics of cetuximab demonstrate a volume of distribution that approximates the vascular space and a terminal half-life of 70 to 100 hours. Cetuximab has shown clinical activity in the treatment of colorectal cancer. An acnelike rash may appear on the face and upper torso 1 to 3 weeks after the start of therapy. Other side effects include hypersensitivity reactions, interstitial lung disease, fever, malaise, diarrhea, abdominal pain, and nausea and vomiting. 

Additional genes and protein receptors are believed to be important in colorectal tumorigenesis. Cyclooxygenase 2 (COX-2), which is induced in colorectal cancer cells, influences apoptosis and other cellular functions in colon cells, and overexpression of the epidermal growth factor receptor (EGFR), a transmembrane glycoprotein involved... 

More recently attempts to generate highly selective quiescent affinity labels have been made for a number of protease and kinase targets. As examples, inhibitors of the Rhinovirus 3C protease (Mathews et al 1999) and of the epidermal growth factor receptors (Boschelli, 2002), both incorporating Michael acceptors to covalently inactivate cysteine residues in their target enzymes (Lowry and Richardson, 1981 Figure 8.6), have entered human clinical trials for the treatment of rhinovirus infection and cancer, respectively. 

Wolff AC, Hammond MEH, Schwartz JN, et al. American Society of Clinical Oncology/College of American Pathologists Guideline Recommendations for Human Epidermal Growth Factor Receptor 2 Testing in Breast Cancer. Arch. Pathol. Lab. Med. 2007 131 18-43. 

Wolff A, Hammond M, Schwartz J, et al. American Society of Clinical Oncology/ College of American Pathologists guideline recommendations for human epidermal growth factor receptor 2 testing in breast cancer. J. Clin. Oncol. 2007 25 118-145. 

Johnstone, P. 2002. The epidermal growth factor receptor a new target for anticancer therapy - introduction. Current Problems in Cancer 26(3), 114-164. 

Kane, S. 2006. Cancer therapies targeted to the epidermal growth factor receptor and its family members. Expert Opinion on Therapeutic Patents 16(2), 147-164. 

Filardo EJ (2002) Epidermal growth factor receptor (EGFR) transactivation by estrogen via the G-protein-coupled receptor, GPR30 a novel signaling pathway with potential significance for breast cancer. J Steroid Biochem Mol Biol 80 231... 

Lee AV, Cui X, Oesterreich S (2002) Cross-talk among estrogen receptor, epidermal growth factor, and insulin-like growth factor signaling in breast cancer. Clin Cancer Res 7(12 Suppl) 4429s... 

The unbound fraction of the epidermal growth factor receptor tyrosine kinase inhibitor gefitinib has been extensively studied in cancer patients [39]. The drug was found to bind to serum albumin, oq-acid glycoprotein, and red blood cells with a mean unbound fraction of 3.4% which was constant over 28 days of dosing. Unbound fraction ranged from 2.2% to 5.4% and was inversely correlated with pre-treatment levels of oq-acid glycoprotein. 

Koyama, S., Maruyama, T., and Adachi, S. (1999). Expression of epidermal growth factor receptor and CD44 splicing variant sharing exons 6 and 9 on gastric and esophageal carcinomas a two flow-cytometric analysis. J. Cancer Res. Clin. Oncol. 125, 47—54. 

Sizemore N and Rorke EA [1993] Human papillomavirus 16 immortalization of normal human ectocervical epithelial cells alters retinoic acid regulation of cell growth and epidermal growth factor receptor expression. Cancer Res 53 4511-4517... 

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