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Japanese Journal of Clinical Oncology 34:191-194 (2004)
© 2004 Foundation for Promotion of Cancer Research

Hypermethylation-associated Inactivation of the SOCS-1 Gene, a JAK/STAT Inhibitor, in Human Pancreatic Cancers

Toshiaki Komazaki1,3, Hisaki Nagai1, Mitsuru Emi1, Yoshie Terada1, Aya Yabe1, Enjing Jin2, Ooiti Kawanami2, Noboru Konishi4, Yukichi Moriyama3, Tetsuji Naka5 and Tadamitsu Kishimoto5,+

1 Department of Molecular Biology and 2 Department of Pathology, Institute of Gerontology, Nippon Medical School, Kawasaki, Kanagawa, 3 Center for Digestive Diseases, Nippon Medical School, Kawasaki, Kanagawa, 4 Department of Pathology, Nara Medical University, Kashihara, Nara and 5 Department of Medicine III, Osaka University Medical School, Osaka, Japan

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.

+ For reprints and all correspondence: Mitsuru Emi, Department of Molecular Biology, Institute of Gerontology, Nippon Medical School, 1–396, Kosugi-cho, Nakahara-ku, Kawasaki 211–8533, Japan. E-mail: memi{at}nms.ac.jp


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