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Fig. 1 | Clinical and Translational Medicine

Fig. 1

From: KRAS mutant lung cancer: progress thus far on an elusive therapeutic target

Fig. 1

The RAS-RAF-MEK-ERK Signaling Cascade in NSCLC. In a normal cell, the activation of the KRAS protein through binding of GTP and translocation to the plasma membrane is a tightly controlled process. However, in NSCLC, the KRAS protein is often mutated at codons 12, 13, and 61 leading to the inactivation of its intrinsic GTPase activity resulting in constitutive activation of KRAS. Mutant KRAS can then promote tumorigenesis through multiple downstream signaling pathways

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