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Site of action of targeted agents. Signals proceeding from growth factor–related receptor tyrosine kinases (RTKs) such as EGF-R, erbB2, or c-kit can be interrupted by lapatinib, erlotinib, gefitinib, and imatinib, acting at the ATP binding site; or by cetuximab, trastuzumab, or panitumumab acting at the receptor. Tyrosine kinases (TKs) that are not directly stimulated by growth factors such as p210 bcr-abl or src can be inhibited by imatinib, dasatinib, or nilotinib. Signals projected downstream from growth factor receptors can be affected by the multitargeted kinase inhibitor sorafenib, acting on c-raf, and, upon arrival at the nucleus, affect gene expression, which can be affected by the targeted transcriptional modulators vorinostat (targeting histone deacetylase), azacytidine derivatives (targeting DNA methyltransferase), or retinoid receptor modulators all-trans-retinoic acid (ATRA) or bexarotene. Source: Chapter 85. Principles of Cancer Treatment, Harrison's Principles of Internal Medicine, 18e Cytokine receptors (CkRs) are one stimulus for degradation of the inhibitory subunit of the NFκB transcription factor by the proteosome. Bortezomib Citation:and Longo Fauciactivation AS, Kasper DL, Hauser SL, Jameson J, Loscalzo J. Harrison's Principles of Internaland Medicine, 18e; 2012asAvailable inhibits this process can DL, prevent of NFκB-dependent genes, among other growth-related effects. Sorafenib sunitinib, acting inhibitorsat: http://mhmedical.com/ Accessed: August 03, 2017 of vascular endothelial growth factor (VEGF) receptors, can modulate tumor blood vessel function through their action on endothelial cells, while © same 2017 McGraw-Hill Education.with All rights bevacizumabCopyright targets the process by combining VEGFreserved itself.