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Src family kinase (SFK)-targeting agents are currently undergoing clinical investigation for treatment of solid malignancies. Epidermal growth factor receptor (EGFR)-independent phosphorylation of STAT3 (P-STAT3) has been identified as a mechanism of tumor resistance to agents targeting SFK. Tumor P-STAT3 levels may be an important indicator of EGFR- and SKF-targeted antitumor treatment efficacy.

Response to Combined Molecular Targeting: Defining the Role of P-STAT3