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. 2020 Jun 23;8(3):179–191. doi: 10.1093/gastro/goaa026

Figure 1.

Figure 1.

EGFR signaling and potential regimens in cetuximab- or panitumumab-resistant mCRC. In addition to NRAS/KRAS/BRAF mutations, low expression of EGFR/AREG/EREG, the mutations of extracellular domains of EGFR, PIK3CA, PTEN, TP53, and MEK1 are related to cetuximab or panitumumab resistance. The agents targeting BRAF and MEK1/2 have been approved for the subsequent therapy of advanced or metastatic CRC; some other targeted drugs such as PI3K, Mtor, and RAS inhibitors also deserve our attention, especially the KRAS G12C inhibitors AMG-510 and MRTX849. EGF, epidermal growth factor; EGFR, epidermal growth factor receptor; HB-EGF, heparin-binding EGF; TGF-α, transforming growth factor α; AREG, amphiregulin; EREG, epiregulin; ED, extracellular domains; TKD, tyrosine kinase domains; GRB2, growth factor receptor bound-2; SOS, son of sevenless; MEK1/2, mitogen-activated protein kinase kinase; ERK1/2, extracellular-signal-regulated kinase; PI3K, phosphatidylinositol 3-kinase; mTOR, mammalian target of rapamycin; p, phosphorylation; * have been approved for markets.