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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
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Oncology,
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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.