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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
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of vascular endothelial growth factor (VEGF) receptors, can modulate tumor blood vessel function through their action on endothelial cells, while
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