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Constitutive Stat3 activity up-regulates VEGF expression and tumor angiogenesis
Non-receptor and receptor tyrosine kinases, such as Src and EGF receptor (EGFR), are major inducers of vascular endothelial growth factor (VEGF), one of the most potent mediators of angiogenesis.Expand
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Inhibiting Stat3 signaling in the hematopoietic system elicits multicomponent antitumor immunity
The immune system can act as an extrinsic suppressor of tumors. Therefore, tumor progression depends in part on mechanisms that downmodulate intrinsic immune surveillance. Identifying theseExpand
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Regulation of the innate and adaptive immune responses by Stat-3 signaling in tumor cells
Although tumor progression involves processes such as tissue invasion that can activate inflammatory responses, the immune system largely ignores or tolerates disseminated cancers. The mechanismsExpand
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Constitutive activation of Stat3 by the Src and JAK tyrosine kinases participates in growth regulation of human breast carcinoma cells
Constitutive activation of signal transducer and activator of transcription (STAT) proteins has been detected in a wide variety of human primary tumor specimens and tumor cell lines including bloodExpand
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Targeting Stat3 blocks both HIF-1 and VEGF expression induced by multiple oncogenic growth signaling pathways
Vascular endothelial growth factor (VEGF) upregulation is induced by many receptor and intracellular oncogenic proteins commonly activated in cancer, rendering molecular targeting of VEGF expressionExpand
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Roles of activated Src and Stat3 signaling in melanoma tumor cell growth
Activation of protein tyrosine kinases is prevalent in human cancers and previous studies have demonstrated that Stat3 signaling is a point of convergence for many of these tyrosine kinases.Expand
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Persistently activated Stat3 maintains constitutive NF-kappaB activity in tumors.
NF-kappaB (RelA) is constitutively active in many cancers, where it upregulates antiapoptotic and other oncogenic genes. While proinflammatory stimulus-induced NF-kappaB activation involvesExpand
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Role of Stat3 in Regulating p53 Expression and Function
ABSTRACT Loss of p53 function by mutation is common in cancer. However, most natural p53 mutations occur at a late stage in tumor development, and many clinically detectable cancers have reduced p53Expand
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Tumor-induced upregulation of Twist, Snail, and Slug represses the activity of the human VE-cadherin promoter.
Endothelial integrity is dependent on intracellular adherens junctions formed by complexes of vascular endothelial (VE)-cadherin and catenins. We have previously demonstrated that exposingExpand
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Inhibition of Bcr–Abl kinase activity by PD180970 blocks constitutive activation of Stat5 and growth of CML cells
Chronic myelogenous leukemia (CML) is a myeloproliferative disease characterized by the BCR–ABL genetic translocation and constitutive activation of the Abl tyrosine kinase. Among members of theExpand
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