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Site of action of targeted agents. Signals proceeding from growth factor–related receptor tyrosine kinases (RTKs) such as epidermal growth factor receptor (EGF-R), erbB2, or c-kit can be interrupted by lapatinib, erlotinib, gefitinib, and imatinib, acting at the adenosine triphosphate (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 Source: PRINCIPLES OF CANCER TREATMENT, Harrison's Hematology and Oncology, 2e modulators all-trans-retinoic acid (ATRA) or bexarotene. Cytokine receptors (CkRs) are one stimulus for degradation of the inhibitory subunit of the NFκB DL. Harrison's Hematology andthis Oncology, Available at:activation http://mhmedical.com/ Accessed: May 05, 2017 transcription Citation: factor byLongo the proteosome. Bortezomib inhibits process 2e; and0can prevent of NFκB-dependent genes, among other growth-related Copyright © 2017 McGraw-Hill Education. All rights reserved effects. Sorafenib and sunitinib, acting as inhibitors of vascular endothelial growth factor (VEGF) receptors, can modulate tumor blood vessel function through their action on endothelial cells, while bevacizumab targets the same process by combining with VEGF itself.