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For example, combined inhibition of both c-Met and EGFR pathways could repress the tumor growth of HCC ( Recently, a growing body of evidence suggests that aberrant activation of HGF/c-Met signaling is associated with resistance of target therapies ( In conclusion, although the tivantinib phase III trial failed and the reason is not clear, the role of c-Met inhibitors in treating HCC can not be denied

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