Wangari-Talbot J , Hopper-Borge E .

P30 CA006927 NCI NIH HHS , T32 CA009035 NCI NIH HHS

Figure 1. A simplified illustration of mechanisms of resistance to conventional therapeutics and TKIs in NSCLCResponse to TKIs targeting epidermal growth factor receptor (EGFR) can be affected by mechanisms that include the development of drug insensitive secondary mutations (T790M) in the kinase domain of the receptor; crosstalk with insulin-like Growth Factor Receptor 1 (IGFR-1); cross talk of amplified MET with epidermal growth factor receptor 3 (ERBB3) and mutations in KRAS. These mechanisms result in activation of signaling effectors such as STAT3, ERK1/2 and PI3K/AKT which support the proliferation and survival of drug resistant cells. ABC transporters such as ABCG2 and ABCB1 have been shown to efflux both TKIs and conventional therapeutics. The resulting decrease in intracellular drug concentrations is a factor in drug resistance. Targeting the oncogenic fusion protein echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase (EML4-ALK) with TKIs such as crizotinib has also been shown to be negatively affected by the development of secondary gate keeper residue mutations such as L1196M, and the emergence of fusion negative tumors that render the disease insensitive to the drug. EGF (epidermal growth factor), IGF (insulin-like growth factor, HGF (hepatocyte growth factor), GTP (guanosine triphosphate).

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