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Association of circulating insulin‐like growth factor 1 with hepatocellular carcinoma: one cross‐sectional correlation study
Author(s) -
Su WeiWen,
Lee KingTeh,
Yeh YaoTsung,
Soon MawSoan,
Wang ChaoLing,
Yu MingLung,
Wang ShenNien
Publication year - 2010
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/jcla.20320
Subject(s) - hepatocellular carcinoma , correlation , cross sectional study , medicine , association (psychology) , insulin , insulin like growth factor , oncology , endocrinology , cancer research , growth factor , chemistry , psychology , pathology , mathematics , receptor , geometry , psychotherapist
Deregulation of insulin‐like growth factor‐1 (IGF‐1) has been implicated in the pathogenesis of several malignancies. This study aimed to investigate the association of changes in circulating IGF‐1 with hepatocellular carcinoma (HCC). The radioimmunoassay was used to analyze serum IGF‐1 levels of 65 HCC patients and 165 healthy subjects. Serum IGF‐1 levels were significantly decreased in the HCC patients as compared with the healthy subjects (158.46±105.07 vs. 247.63±149.96 ng/mL, P <0.001). Furthermore, insulin resistance was significantly higher in the HCC patients than the healthy subjects ( P =0.027). In addition, the significant correlations of serum IGF‐1 levels with age and insulin resistance in the healthy subjects were not noted in the HCC patients. Intriguingly, individuals with hepatitis C virus (HCV), not hepatitis B virus, had remarkably decreased IGF‐1 levels in both groups of the HCC patients and healthy subjects. Moreover, in the HCV subgroup, serum IGF‐1 levels were significantly reduced in the HCC patients than the healthy subjects (113.14±71.28 vs. 172.42±74.02 ng/mL, P =0.003). In conclusion, decreased serum IGF‐1 levels were associated with HCC and the decrease was remarkably noted in those patients concomitant with chronic hepatitis C. J. Clin. Lab. Anal. 24:195–200, 2010. © 2009 Wiley‐Liss, Inc.

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