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• W3044184498 abstract "418 The signal transducers and activators of transcription (STATs) are latent cytoplasmic proteins that are activated to participate in gene control by phosphorylation on a single tyrosine which results from activation of the Janus kinase (JAK) when cells encounter various extracellular cytokine, growth factor and hormones. Tyrosine phosphorylation of STAT proteins induces dimmer formation, followed by translocation to the nucleus, where they bind to specific DNA response elements in target gene promoters and thereby regulate gene expression. Seven types of STAT proteins have been identified so far; STATs 1, 2, 3, 4, 5A, 5B and 6. A growing number of tumor-derived cell lines and samples from human cancers are reported to contain constitutively activated STAT proteins, very frequently STAT3. Some target genes of STAT3 include those encoding the antiapoptotic proteins, the proliferation-associated proteins, and the proangiogenic factor. STAT3 was proposed to be an oncogene, based on evidence that a constitutively dimerized/active form of STAT3 transformed immortalized mouse and rat fibroblasts and bestowed upon these cells the ability to grow into tumors in nude mice. In addition, it has been recently reported that the expression of tyrosine-phosporylated STAT3 (p-STAT3) is associated with poor prognosis in head and neck cancer and lymphoma. In our study, we investigated expression of the p-STAT3 in primary breast cancer by immunohistochemistry and analyzed the relation between p-STAT3 expression and clinicopathological and molecular features of breast cancer. It was reported that the suppressor of cytokine signaling-1 (SOCS-1), which was identified as a protein involved in a negative feedback loop for STAT pathway, is silenced by CpG island methylation. Therefore, we also investigated methylation status of SOCS-1 and analyzed the relation between p-STAT3 and SOCS-1 methylation status. P-STAT3 was overexpressed in 39 of 74 breast cancers. There was no significant correlation the p-STAT3 expression and clinicopathological features including age, tumor size, histology, lymph node metastasis. However, the p-STAT3 expression showed a significant correlation with VEGF-C (p=0.0015), although there was no significant correlation between p-STAT3 and the other molecular findings such as hormone receptors and HER2. Next, we investigated methylatin status of SOCS-1 in 57 breast cancers available for DNA. SOCS-1 methylation was detected in 25 of 57 cases. There was a significant correlation between SOCS-1 methylation and p-STAT3 expression. Our results suggest that STAT3 signalings may be one of the major pathways that contribute to tumorigenesis in breast cancer." @default.
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• W3044184498 date "2006-04-15" @default.
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• W3044184498 title "Activated STAT3 due to SOCS-1 methylation contributes to breast tumorigenesis" @default.
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