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. Author manuscript; available in PMC: 2020 Apr 1.
Published in final edited form as: Cancer Res. 2019 Aug 15;79(19):5074–5087. doi: 10.1158/0008-5472.CAN-19-0244

Figure 7. Model of drug resistance mechanisms.

Figure 7.

We have shown that N-terminal truncation of either RAF1 or BRAFV600E leads to vemurafenib resistance (A) that can be overcome with a pan-RAF inhibitor (e.g. LY3009120) (B). Our genetic screen identified a DBL-RAC1-PAK resistance mechanism that can drive proliferation in the presence of either BRAF inhibitor (e.g. vemurafenib) or a pan-RAF inhibitor (C). However, the combination of a SRC inhibitor (e.g. saracatinib) and a pan-RAF inhibitor can block both mechanisms identified by our screen (D).