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The tumor suppressor NPRL2 in hepatocellular carcinoma plays an important role in progression and can be served as an independent prognostic factor
Author(s) -
Otani Satoshi,
Takeda Shin,
Yamada Suguru,
Sakakima Yoshikazu,
Sugimoto Hiroyuki,
Nomoto Shuji,
Kasuya Hideki,
Kanazumi Naohito,
Nagasaka Tetsurou,
Nakao Akimasa
Publication year - 2009
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.21241
Subject(s) - hepatocellular carcinoma , univariate analysis , medicine , multivariate analysis , biology , pathology , oncology
Background/Aims Hepatocarcinogenesis is a multifactorial, multistep process that involves the activation of oncogenes or the inactivation of tumor suppressor genes throughout the different stages of hepatocellular carcinoma (HCC) progression. NPRL2 is one of the candidate tumor suppressor genes identified on chromosome 3p21.3, a region which frequently contains genetic abnormalities found in the early stages of the development of various human cancers. In the current study, we aimed to evaluate NPRL2 expression in HCC and to explore the prognostic significance of NPRL2. Method We investigated NPRL2 mRNA expression in 70 HCC specimens, using quantitative real‐time reverse transcription polymerase chain reaction analysis, and the correlation between NPRL2 expression and clinicopathologic parameters. Results NPRL2 mRNA was found to be expressed equally in both HCC tissues and corresponding non‐cancerous liver tissues. However, higher NPRL2 expression correlated significantly with tumor size ( P = 0.0062) and serum PIVKA‐II levels ( P = 0.0002). Univariate and multivariate analyses revealed that higher NPRL2 mRNA expression was an independent prognostic factor for overall survival (risk ratio 0.39; P < 0.0001). Conclusion Our results suggest that NPRL2 mRNA expression has prognostic significance for the survival of patients with HCC. J. Surg. Oncol. 2009;100:358–363. © 2009 Wiley‐Liss, Inc.