Abstract.
 We recently demonstrated inactivation in hepatocellular carcinomas (HCCs) of the gene encoding SOCS1/JAB1/SSI-1, a JAK-binding protein that regulates the JAK/STAT signal-transduction pathway. In a follow-up immunochemical investigation of expression of SOCS-1 in hepatoblastomas (HBLs), the protein was markedly reduced in half of the HBL tumors we examined. CpG-rich regions upstream of the SOCS-1 gene were hypermehylated in 7 of the 15 HBL cases. The results suggest that hypermethylation may play an important role in silencing the SOCS-1 gene, not only in adult HCCs, but also in liver tumors arising in childhood.
Similar content being viewed by others
Log in or create a free account to read this content
Gain free access to this article, as well as selected content from this journal and more on nature.com
or
Author information
Authors and Affiliations
Additional information
Received: November 6, 2002 / Accepted: November 11, 2002
Correspondence to:M. Emi
Rights and permissions
About this article
Cite this article
Nagai, H., Naka, T., Terada, Y. et al. Hypermethylation associated with inactivation of the SOCS-1 gene, a JAK/STAT inhibitor, in human hepatoblastomas. J Hum Genet 48, 65–69 (2003). https://doi.org/10.1007/s100380300008
Published:
Issue date:
DOI: https://doi.org/10.1007/s100380300008
This article is cited by
-
DNA methylation in Hepatoblastoma-a literature review
Italian Journal of Pediatrics (2020)
-
Targeting JAK kinase in solid tumors: emerging opportunities and challenges
Oncogene (2016)
-
Towards an international pediatric liver tumor consensus classification: proceedings of the Los Angeles COG liver tumors symposium
Modern Pathology (2014)
-
Potent antitumor activity of oncolytic adenovirus-mediated SOCS1 for hepatocellular carcinoma
Gene Therapy (2013)
-
Aberrant promoter methylation and loss of Suppressor of Cytokine Signalling-1 gene expression in the development of uterine cervical carcinogenesis
Cellular Oncology (2011)
