In many tumors, EGF receptors are over-activated, which leads to a stronger signal and a high rate of proliferation. In order to inhibit the signal and to reduce the rate of proliferation, the EGF receptors can be inhibited by antibodies. Prominent examples are Cetuximab and Trastuzumab, which bind to the extracellular domains of erbB-1 or erbB-2, respectively. While Cetuximab blocks the binding of extracellular EGF and thus prevents dimerization and activation, Trastuzumab inhibits erbB-2 independently of ligand binding and dimerization.
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The EGF receptor tyrosine protein kinases and the therapy of tumors with activated EGF receptors – Part 1: Inhibition of receptor activation via antibodies
