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Comment
. 2011 Feb 1;17(3):393-5.
doi: 10.1158/1078-0432.CCR-10-2925. Epub 2011 Jan 25.

Response to combined molecular targeting: defining the role of P-STAT3

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Comment

Response to combined molecular targeting: defining the role of P-STAT3

Ann Marie Egloff et al. Clin Cancer Res. .

Abstract

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.

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Figures

Fig. 1
Fig. 1
EGFR- and SFK-independent activation of STAT3 provides a mechanism for Overcoming EGFR- and SFK-targeted therapies. Solid arrows indicate activation of signaling components or pathways. Dashed arrow indicates phosphorylation independent of activation. Inhibition is represented by a red T.

Comment on

References

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