Literature DB >> 22296598

Activation of c-Jun N-terminal kinase in non-cancerous liver tissue predicts a high risk of recurrence after hepatic resection for hepatocellular carcinoma.

Satoru Hagiwara1, Masatoshi Kudo, Hobyung Chung, Kazuomi Ueshima, Tatsuo Inoue, Seiji Haji, Tomohiro Watanabe, Ah-Mee Park, Hiroshi Munakata, Toshiharu Sakurai.   

Abstract

AIM: Hepatocellular carcinoma (HCC) ranks as the third leading cause of cancer deaths worldwide. Hepatic resection is the mainstay of curative treatment for early stage HCC. Although c-Jun N-terminal kinase (JNK) activation contributes to hepatocyte proliferation and HCC development in mice, the extent of involvement of JNK in human HCC development is unknown. The aim of this study is to assess the predictive value of JNK for postoperative recurrence in HCC.
METHODS: From April 2005 to March 2008, 159 patients underwent curative resection for HCC. From the 159 patients, 20 patients each matched for age, gender and etiology were registered as three groups: (i) without recurrence (no recurrence group), (ii) with recurrence within one year after surgery (early recurrence group), and (iii) with recurrence at one year or more after surgery (late recurrence group) (a cross-sectional control study). We investigated factors contributing to postoperative early and late phase recurrence.
RESULTS: Multivariate analysis using a Logistic regression model showed that JNK activity in non-cancerous liver tissue was correlated with postoperative late recurrence. (P = 0.02, odds ratio; 5.79, 95% confidence interval [CI]; 1.33-25.36).
CONCLUSIONS: JNK activity in non-cancerous liver tissue is considered as a reliable predictive biomarker for post-operative recurrence in HCC.
© 2012 The Japan Society of Hepatology.

Entities:  

Year:  2012        PMID: 22296598     DOI: 10.1111/j.1872-034X.2011.00932.x

Source DB:  PubMed          Journal:  Hepatol Res        ISSN: 1386-6346            Impact factor:   4.288


  5 in total

1.  Activation of JNK and high expression level of CD133 predict a poor response to sorafenib in hepatocellular carcinoma.

Authors:  S Hagiwara; M Kudo; T Nagai; T Inoue; K Ueshima; N Nishida; T Watanabe; T Sakurai
Journal:  Br J Cancer       Date:  2012-05-17       Impact factor: 7.640

2.  Molecular mechanisms of liver injury and hepatocarcinogenesis: focusing on the role of stress-activated MAPK.

Authors:  Hayato Nakagawa; Shin Maeda
Journal:  Patholog Res Int       Date:  2012-05-14

3.  Gankyrin induces STAT3 activation in tumor microenvironment and sorafenib resistance in hepatocellular carcinoma.

Authors:  Toshiharu Sakurai; Norihisa Yada; Satoru Hagiwara; Tadaaki Arizumi; Kosuke Minaga; Ken Kamata; Mamoru Takenaka; Yasunori Minami; Tomohiro Watanabe; Naoshi Nishida; Masatoshi Kudo
Journal:  Cancer Sci       Date:  2017-09-02       Impact factor: 6.716

4.  GRP75-mediated upregulation of HMGA1 stimulates stage I lung adenocarcinoma progression by activating JNK/c-JUN signaling.

Authors:  Guo-Bing Qiao; Ren-Tao Wang; Shu-Nan Wang; Shao-Lin Tao; Qun-You Tan; Hua Jin
Journal:  Thorac Cancer       Date:  2021-03-23       Impact factor: 3.500

5.  ABCB6 mRNA and DNA methylation levels serve as useful biomarkers for prediction of early intrahepatic recurrence of hepatitis C virus-related hepatocellular carcinoma.

Authors:  Ryouichi Tsunedomi; Norio Iizuka; Kiyoshi Yoshimura; Michihisa Iida; Masahito Tsutsui; Noriaki Hashimoto; Shinsuke Kanekiyo; Kazuhiko Sakamoto; Takao Tamesa; Masaaki Oka
Journal:  Int J Oncol       Date:  2013-03-08       Impact factor: 5.650

  5 in total

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