Literature DB >> 15121754

Hypermethylation-associated inactivation of the SOCS-1 gene, a JAK/STAT inhibitor, in human pancreatic cancers.

Toshiaki Komazaki1, Hisaki Nagai, Mitsuru Emi, Yoshie Terada, Aya Yabe, Enjing Jin, Ooiti Kawanami, Noboru Konishi, Yukichi Moriyama, Tetsuji Naka, Tadamitsu Kishimoto.   

Abstract

BACKGROUND: SOCS-1, a JAK-binding protein (SSI-1/SOCS-1/JAB), regulates the JAK/STAT signal transduction pathway that relays signals from various cytokines in the extracellular matrix into the cell. Inactivation of the SOCS-1 gene by methylation has been previously described in hepatocellular carcinomas and multiple myeloma. The purpose of the present work was to analyze the expression of the SOCS-1 gene and identify inactivation of this gene by methylation in pancreatic cancers.
METHODS: 20 samples were analyzed. We identified the expression of SOCS-1 gene using RT-PCR and the mechanism of inactivation in this gene by methylation assay.
RESULTS: We documented marked suppression of SOCS-1 mRNA and reduction of SOCS-1 protein in 7 of 14 primary pancreatic cancers examined; moreover, CpG-rich regions upstream of the SOCS-1 gene were hypermethylated in 8 of the 14 tumors.
CONCLUSIONS: The results suggested that this gene is silenced in a substantial portion of pancreatic cancers through mechanisms that cause methylation in the promoter region.

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Year:  2004        PMID: 15121754     DOI: 10.1093/jjco/hyh035

Source DB:  PubMed          Journal:  Jpn J Clin Oncol        ISSN: 0368-2811            Impact factor:   3.019


  25 in total

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5.  Low expression of SOCS-1 and SOCS-3 is a poor prognostic indicator for gastric cancer patients.

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8.  Cancer-Associated Fibroblasts in Pancreatic Cancer Are Reprogrammed by Tumor-Induced Alterations in Genomic DNA Methylation.

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10.  Expression of SOCS-1 in the liver tissues of chronic hepatitis B and its clinical significance.

Authors:  Zhi-Xin Zhao; Qing-Xian Cai; Xiao-Mou Peng; Yu-Tian Chong; Zhi-Liang Gao
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