Published online Jun 15, 1997. doi: 10.3748/wjg.v3.i2.117
Revised: January 31, 1997
Accepted: March 1, 1997
Published online: June 15, 1997
AIM: To study the relationship between insulin-like growth factor II (IGF-II), IGF-II receptor, and chronic liver diseases and to investigate the clinical mechanisms of human hepatocellular carcinoma (HCC) development.
METHODS: We analyzed IGF-II and IGF-II receptor poly (A)+ mRNA in dysplasia liver cell (DLC; n = 10), liver cirrhosis (LC; n = 9), and chronic active hepatitis (CAH; n = 9) specimens by Northern blot using human IGF-II and IGF-II receptor DNA probes labeled with 32P through nick translation.
RESULTS: Expression of IGF-II in DLC samples (10/10, 100%) was higher than in CAH (3/9, 33%) and LC samples (3/9, 33%) (P < 0.01). Expression of IGF-II receptor in DLC samples (7/10, 70%) was significantly higher than in CAH (2/9, 22%) and LC samples (3/9, 33%). Data on hepatitis B virus (HBV) infection status from different chronic liver disease samples were also analyzed.
CONCLUSION: Overexpression of IGF-II and IGF-II receptor in DLC samples was associated with a preceding step to malignant phenotype hepatocyte transformation and may be of diagnostic value for early detection of hepatocellular carcinoma (HCC). Persistent HBV infection was strongly associated with abnormal IGF-II and IGF-II receptor mRNA expression, suggesting that an autocrine or paracrine mechanism is involved in the regulation of growth in liver cell carcinogenesis.