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EGFR, also known as transmembrane ERBB 1 or HER1, is a member of a family of receptor tyrosine kinases. EGFR is controlled by signaling cascades Involved slow cell growth, differentiation and proliferation, and YM155 is used in many types of confinement normal tissues and various types of tumors, Expressed Lich CRC. Figure 1 summarizes the major EGFR signaling pathways described shows. When a ligand binds to EGFR, is the receiver singer a dimer resulting in a signaling cascade inside cells by tyrosine kinase activity t. This cascade of signaling occurs through the activation of receptor autophosphorylation, a series of intracellular Ren Signaling pathways regulate proliferation foreign Avoid st, apoptosis, and the F Promotion of invasion metastasis, and neovascularization.
The proto-oncogene c-erb B code for EGFR activation of oncogenes and proto-EGFR expression results in many tumors. It was an interest in exploring this pathway as a potential target for cancer therapy. Pharmacologically, there are two classes of EGFR antagonists in clinical use: antiEGFR monoclonal body against the extracellular re ne Cathedral of the receptor and oral small molecule EGFR tyrosine kinase inhibitors that block Rezeptoraktivit t TK wettbewerbsf HIGEN addressed. The monoclonal Body antiEGFR, cetuximab and panitumumab act by binding to the extracellular Re region of EGFR, and thus the block ligand binding region prevents activation ligandinduced TK. These monoclonal Bodies recognize only the EGFR, which makes them highly selective for their target.
The small molecule EGFR tyrosine kinase inhibitors, erlotinib and gefitinib, inhibit the catalytic activity of t Of TK by competing with adenosine triphosphate in the intracellular Re Dom to bind ne. These small molecule inhibitors are not the canal and EGFR receptor may differ, as Vaskul block Re endothelial growth factor receptor-factor and other members of the EGFR family. Anti-EGFR monoclonal Bodies were evaluated both treated and chemotherapy refractory metastatic CRC Rer disease. Figure 2 shows the current treatment paradigm of metastatic colorectal cancer, including normal involvement of the appropriate therapy antiEGFR monoclonal antique Body improves survival in Selected Hlten patients with fa Reasonable one. Table 1 summarizes some of the clinical studies of antique AntiEGFRmonoclonal body inmetastatic CRC.